Kidney symptoms of the disease

Kidney diseases in the modern world represent one of the most serious problems. Many kidney diseases can last for a long time in a hidden or erased form. How to treat kidney disease folk remedies look here.

Some syndromes are distinguished in nephrological practice:

Some syndromes( for example, nephrotic, hypertonic) represent an expanded clinical picture of the disease, when patients, as a rule, have certain complaints and numerous manifestations of the disease. To diagnose other syndromes, you need to use special research methods.

In a number of cases, these syndromes can be a consequence of unilateral kidney damage simulating a two-sided process, so it must always be remembered about asymmetric kidney lesions. It should be borne in mind the often ephemeral nature of the syndrome, which may first occur at the onset of the disease, and then not be repeated( eg, nephrotic syndrome).This possibility makes it necessary to carefully study the patient's anamnesis, since the duration of this or that syndrome often determines the prognosis and characteristics of the treatment.

For the nephrological diagnosis, the detection of proteinuria and hematuria is of great importance.

Proteinuria is an important and most frequent symptom of kidney damage, requiring careful examination of the patient. Normally, protein excretion in urine in adults does not exceed 150 mg / day, and in children under 10 years - 100 mg / day. Sedimentary protein samples can give false positive results in the presence of iodine contrast substances in the urine, a large number of analogues of penicillin or cephalosporin, metabolites of sulfonamides. In the presence of severe leukocyturia and especially hematuria, a positive reaction to a protein can be a consequence of the disintegration of the formed elements with prolonged standing of urine. Examination of urine using test strips reveals proteinuria only if protein excretion exceeds 0.3 g / l. Proteinuria over 3 g / day leads to the development of nephrotic syndrome.

In urine in kidney diseases, various plasma proteins are detected - both low-molecular( albumin, ceruloplasmin, transferrin, etc.), and high-molecular( α2-macroglobulins, γ-globulins).Depending on the content of certain proteins in the plasma and urine, selective and nonselective proteinuria are singled out( the term conditional, it is more correct to talk about the selectivity of the isolation of protein fractions, the selectivity of their clearance).

In addition to plasma proteins in the urine, it is possible to identify proteins of kidney origin - Tamm-Horsfall mucoprotein, secreted by the epithelium of convoluted tubules.

With pathology of the kidneys, proteinuria is most often associated with increased filtration of plasma proteins through glomerular capillaries - the so-called glomerular proteinuria. The filtration of plasma proteins through the capillary wall depends on the structural and functional state of the wall of the glomerular capillaries, the properties of protein molecules, the pressure and blood flow velocity that determine GFR.

The wall of the glomerular capillaries consists of endothelial cells( with rounded holes between the cells), a three-layered basal membrane - a hydrated gel, and also epithelial cells( podocytes) with a tangle of "leg" processes. Due to this complex structure, the glomerular capillary wall can "sift" the plasma molecules from the capillaries into the space of the capsule of the glomerulus, and this function of the "molecular sieve" depends to a large extent on the pressure and current velocity in the capillaries. In pathological conditions, the size of the "pores" can increase, the deposits of immune complexes can cause local changes in the capillary wall, which increase its permeability for macromolecules.

In addition to mechanical obstacles( dimensions "pores"), electrostatic factors also matter. The BMC is charged negatively;The negative charge is borne by the feet of podocytes. Under normal conditions, the negative charge of the glomerular filter repels anions - negatively charged molecules( including albumin molecules).The loss of a negative charge contributes to the filtration of albumin. It is suggested that in the body of patients with the disease of minimal glomerular changes and focal-segmental glomerulosclerosis, humoral factors of permeability that change the charge of BMC and legs of podocytes are produced. It is assumed that the merging of the leg legs is the morphological equivalent of the loss of the negative charge.

Glomerular proteinuria is observed in most kidney diseases - with glomerulonephritis, amyloidosis of the kidneys, diabetic glomerulosclerosis, renal vein thrombosis, as well as hypertension, atherosclerotic nephrosclerosis, and "stagnant" kidney.

Tubular( tubular) proteinuria occurs less frequently. It is associated with the inability of the proximal tubules to reabsorb plasma low-molecular proteins filtered in normal glomeruli. The canalic proteinuria rarely exceeds 2 g / day, the protein is represented by albumin, as well as the fractions with an even lower molecular weight( lysozyme,( 32-microglobulin, ribonuclease, free light immunoglobulin chains), absent in healthy individuals and glomerular proteinuriaIn connection with the 100% reabsorption of the epithelium of the convoluted tubules, the characteristic feature of tubular proteinuria is the predominance of P2-microglobulin over albumin, as well as the absence of high molecular weight proteins.

Tubular proteinIn the case of interstitial nephritis, pyelonephritis, potassium-penic kidney, acute tubular necrosis, chronic rejection of the kidney graft, congenital tubulopathies( Fanconi syndrome).

Overflow proteinuria develops with increased formation of low-molecular-weight plasma proteins( light chains of immunoglobulins,hemoglobin, myoglobin), which are filtered by normal glomeruli in an amount exceeding the ability of the tubules to reabsorb. This is the mechanism of proteinuria in myeloma( Bens-Jones proteinuria, see the clinical analysis of "Bence-Jones's myeloma with" large proteinuria "at the end of the section), myoglobinuria. An example of such proteinuria is lysozymuria, described in patients with leukemia.

Differentiation of types of proteinuria can be carried out only by determining the protein fractions in the urine( biochemical and immunohistochemical methods).

With the glaucoma( non-systemic) and lupus glomerulonephritis, diabetic glomerulosclerosis, proteinuria is usually combined with erythrocytic;pure proteinuric forms are rare.

Isolated proteinuria( or proteinuria combined with a minor erythrocyte) is more typical for renal amyloidosis, renal vein thrombosis, and also for hypertension. With hemorrhagic purpura Shonlein-Genoch, nodular polyarteritis erythrocyturia is usually more expressed than proteinuria.

In addition, proteinuria can have extrarenal origin - be a consequence of cell disintegration in diseases of the urinary tract or genitals, with prolonged standing of urine( false proteinuria).

It should be borne in mind the possibility of the emergence of functional proteinuria, the exact mechanisms of pathogenesis which are not established. These include orthostatic proteinuria, idipathic transient proteinuria, tension proteinuria and febrile proteinuria.

For her, the appearance of a protein in the urine with prolonged standing or walking with a rapid disappearance in a horizontal position is typical.

Characteristics of proteinuria: usually does not exceed 1 g / day, glomerular, non-selective, the mechanism of its occurrence is not clear. More often observed in adolescence, half of patients disappear after 5-10 years.

The diagnosis of orthostatic proteinuria is made with the following criteria:

An orthostatic test is required to confirm the diagnosis. Urine collected in the morning before going up from the bed, then - after a 1-2-hour stay in an upright position( walking, preferably with hyperlordosis, with a stick behind the back to straighten the spine).The sample gives even more accurate results if the morning( night) portion of urine pours out( as there may be residual urine in the bladder), and the first portion is collected after a 1- to 2-hour stay of the examinee in a horizontal position.

In adolescence, idiopathic transient proteinuria can also be observed, which is found in healthy persons in other cases during medical examination and is absent in subsequent urine tests.

The stress protein detected in 20% of healthy individuals( including athletes) after a sharp physical strain with protein detection in the first collected urine sample has a tubular( tubular) character.

It is suggested that the mechanism of this proteinuria is associated with redistribution of blood flow and relative ischemia of proximal and distal tubules.

Feverish proteinuria is observed in acute fever, especially in children and senile individuals;it is predominantly glomerular in nature. The mechanisms of these types of proteinuria have been little studied. Assume a possible role of increased glomerular filtration along with a transient lesion of the glomerular filter immune complexes.

It is important to establish the very fact of proteinuria and the degree of its expression, since in the vast majority of cases proteinuria is one of the main signs of kidney damage.

High proteinuria - excretion of protein with urine in the amount of more than 3 g / day, which often leads to the development of nephrotic syndrome. This type of proteinuria is observed in acute and chronic glomerulonephritis, kidney damage in systemic diseases( SLE, hemorrhagic vasculitis, etc.), with amyloidosis of the kidneys, subacute infective endocarditis. Pronounced proteinuria can also be observed with myeloma and thrombosis of renal veins, as well as diabetic nephropathy.

Moderate proteinuria - excretion of protein in the urine in an amount of 0.5 to 3 g / day;it is observed with all the diseases listed above, as well as malignant arterial hypertension, nodular periarteritis, hypertension, atherosclerosis of kidney vessels( ischemic kidney disease) and other diseases.

Urinary excretion of albumin( microalbuminuria) appears earlier than other signs of renal impairment, which can be established by currently available methods, and reflects the lesion of the microvascular bed of the kidneys( and at the same time other vascular areas - the heart, brain).The diagnostic significance of microalbuminuria is as follows. First, it is the earliest indicator of kidney damage in patients with type I and II diabetes mellitus and in hypertensive patients;thus, it reveals the most severe group prognostically, which requires close monitoring with strict control of blood glucose and blood pressure. Secondly, the appearance of microalbuminuria predicts an unfavorable outcome of cardiovascular diseases( myocardial infarction, stroke), especially in patients with the so-called high-risk group - who have diabetes mellitus, obesity, arterial hypertension or family predisposition to vascular and renal diseases.

In recent years, more and more data are available on the "toxic" effect of proteinuria. It is established that plasma proteins passing through the glomerular membrane in nephropathies are not only a reliable marker of kidney damage, but also a factor that actively damages the structures of the kidney tissue, which increases inflammation and induces fibrosis, primarily tubulointerstitial.

Attention to proteinuria as an important factor in the progression of parenchymal diseases of the kidneys has especially grown after establishing a direct relationship between the magnitude of proteinuria and the risk of progression of renal failure, less dependent on the morphology of the kidney process.

It has long been known that tubulointerstitial inflammation is present simultaneously with glomerular inflammation in patients with proteinuric forms of nephritis. However, until recently it was not clear whether this is a consequence of ischemic obliteration of peri-tubular capillaries or albumin and other proteins accumulating in the lumen of the renal tubules can indeed cause inflammation of the interstitium. In recent years, it has been proved that the pronounced and prolonged proteinuria has a toxic effect on the tubular epithelium. Intensive reabsorption by the epithelium of the proximal tubules of large amounts of filtered proteins leads to the activation of epithelial cells with the expression of the genes of inflammatory and vasoactive substances. The molecules of these substances, produced by the kidney tubules in excess quantities, are secreted through the basal sections of the cells into the interstitium, leading to the development of an inflammatory reaction, which in most forms of nephritis precedes the development of nephrosclerosis.

Hematuria( admixture of blood in urine) is frequent, often the first sign of kidney and urinary tract diseases, as well as diseases and conditions not related to kidney damage( acute leukemia, thrombocytopenia, anticoagulant overdose, severe physical activity, etc.).

Types of hematuria:

Hematuria with nephropathies( renal hematuria), as a rule, persistent bilateral painless, often combined with proteinuria, cylindruria, leukocyturia. Nevertheless, the forms of glomerulonephritis, which proceed with recurrent isolated pain, are described.

The pathogenesis of renal hematuria is not completely clear. It is believed that the involvement of mesangium, as well as the involvement of interstitial tissue and the epithelium of convoluted tubules, are of great importance, since the most common hematuria is observed with mesangial nephritis and interstitial nephritis. Hematuria can be caused by necrotizing inflammation of renal arterioles, renal intravascular coagulation, kidney infarction.

Japanese authors on a series of electronograms have recently been shown that red blood cells can penetrate even through the smallest breaks of BMC, while changing its shape. True macrohematuria should be distinguished from false. Unlike true, false hematuria is caused by the coloration of urine in red not by erythrocytes, but by other substances.

Renal hematuria is observed with OGN, CGN, as well as with many nephropathies arising in the background of systemic diseases.

Acute fever is manifested by hematuria, proteinuria( more often mild), edema, arterial hypertension. . However, at present most of the acute nephritis is atypical, and a number of symptoms, including massive hematuria, may be absent. Recurrent acuteness of the symptoms is often manifested mesangioproliferative variant CGN, which differs from acute nephritis by a morphological pattern.

One of the most common causes of isolated hematuria is IgA-nephropathy, or Berger's disease( focal mesangial nephritis).IgA-nephropathy is detected, as a rule, in children and adults under the age of 30, more often in men;is manifested by attacks of macrohematuria( less often persistent microhematuria) with blunt pain in the lower back, recurring against pharyngitis. Proteinuria is usually minimal. The course of the disease in children is usually benign, in adults the forecast is worse.

Similar hematuric IgA-nephritis with increasing concentration of IgA in serum is characteristic for patients with chronic alcoholism. It is detected mainly in persons over 40 years old on the background of alcoholic liver damage in combination with other systemic manifestations of alcoholism( defeat of the pancreas, heart, polyneuropathy).Unlike Berger's disease, "alcoholic" glomerulonephritis is manifested by persistent painless microhematuria and proceeds more severely - hypertension is often associated with kidney failure.

Hematuria is a characteristic sign of interstitial nephritis, including acute drug. The cause of hematuria can be a variety of drugs, most often sulfonamides, streptomycin, kanamycin, gentamicin, analgesics( phenacetin, analgin), pyrazolidone derivatives( butadione), as well as salts of heavy metals.

A special pain variant of hematuric nephropathy is described - lumbulgic-hematuric syndrome, which is observed mainly in young women who use oral estrogen-containing contraceptives, but single cases of the disease have been described in men. Clinically, this syndrome is manifested by attacks of intense pain in the lumbar region in combination with hematuria( often macrogmaturia) and often intermittent fever. Attacks are provoked by catarrhal diseases, severe physical exertion. In the interstitial period, no pathological changes in the analysis of urine are noted. There are also no signs of immunological activity. In angiographic examination, changes in the intrarenal arteries can be detected in the form of their partial or complete occlusion, tortuosity, fibroelastosis.

Primarily hematuria manifests hereditary nephritis with hearing loss and decreased vision( Alport syndrome), the disease has an unfavorable prognosis.

A much better prognosis is benign familial recurrent hematuria;when biopsies often find unchanged kidney tissue, sometimes focal glomerulonephritis.

In recent years, children have described special forms of chronic interstitial nephritis, manifested by hematuria, - with hyperoxaturia.

Bilateral renal hematuria is characteristic of secondary glomerulonephritis in a number of systemic diseases.

• Jade in hemorrhagic vasculitis can develop from the very beginning of the disease or join a few years after the appearance of cutaneous, articular and abdominal syndromes. Kidney damage in most cases proceeds according to the type of hematuric glomerulonephritis( in 40% of cases, macrohematuria is observed) with an increase in the serum IgA level and is characterized by a persistent or slowly progressive course. With the development of nephrotic syndrome, the prognosis is much worse.

• Glomerulonephritis in infectious endocarditis, which can occur against the backdrop of a detailed clinical picture of the disease( fever, heart valve disease, splenomegaly, anemia), but may be the first manifestation of the disease, usually occurs with hematuria, sometimes with macrogemuria, moderate proteinuria;nephrotic variant of nephritis is less common. In 40-60% of cases of infective endocarditis, infarcts of the kidney with macrohematuria occur.

• Nephropathy with classical nodular periarteritis( Kussmaul-Mayer disease) occurs several months after the common symptoms of fever, weight loss, muscle and joint pain, asymmetric polyneuritis, and is characterized by microhematuria( more than half the time), moderate proteinuria and malignant hypertension. Macrohematuria with severe lower back pain may manifest a rarer form of nephropathy with nodular periarteritis - more often an aneurysm rupture of the intrarenal artery.

• Microscopic polyangiitis is a form of necrotizing vasculitis with damage to small vessels( capillaries, venules, arterioles).In the blood, AT is detected in the cytoplasm of neutrophils( antineutrophilic cytoplasmic AT-ANCA), reacting with myeloperoxidase of their granules and giving a perinuclear type of luminescence in the immunofluorescence test. Most often, the skin( purpura), the lungs( hemorrhagic alveolitis with hemoptysis up to pulmonary hemorrhage), kidneys are affected. Gastrointestinal tract, myalgia, peripheral neuritis are also possible. The kidneys are affected in 90-100% of cases( observe urinary and nephrotic syndromes, arterial hypertension, more than 50% of cases the nephritis acquires a rapidly progressive course).In the renal biopsy, proliferative glomerulonephritis is detected with necrosis foci; in immunofluorescence studies, the absence or insignificant amount of immune deposits( pauci- immune - "low immunity" glomerulonephritis).

• Renal damage in Wegener's granulomatosis develops against a background of granulomatous necrotic lesions of the upper respiratory tract and lungs and is manifested by hematuria( in 25% of cases of macrohematuria) in combination with moderate proteinuria. Arterial hypertension and nephrotic syndrome develop rarely, but already in the first years of the disease in most patients, signs of renal failure are revealed.

• Goodpasture's syndrome is characterized by lung damage( hemorrhagic alveolitis with repeated pulmonary hemorrhage) and usually in a few months the GPGN with massive micro- or macrogmaturia is attached.

• Thrombotic microangiopathies are characterized by a widespread lesion of small vessels that occur with Coombs-negative hemolytic anemia, intravascular coagulation, thrombocytopenia, haematuria, often with the development of arresters. This group includes many similar diseases - thrombotic thrombocytopenic purpura - TTP and hemolytic-uremic syndrome - HUS.

Despite the fact that the list of nephropathies leading to the appearance of blood in the urine is very large, nevertheless, when hematuria is detected, it is first of all necessary to exclude urological diseases( urolithiasis, tumors and tuberculosis of the kidney).It should be remembered that even a minimal hematuria( less than 10 erythrocytes in the field of view of the microscope) may be the first sign of a tumor of the genitourinary system.

For the elimination of urological diseases, it is very important to get familiar with the patient's complaints, anamnesis, as well as physical and laboratory tests.

Hematuria, observed only at the beginning or at the end of the act of urination, is characteristic only for urological diseases;the same diseases are more characteristic of hematuria, accompanied by severe pain in the lower back, especially paroxysmal.

Initial and terminal hematuria can be easily detected using a three-glassed sample. Detection of blood only in the first portion of urine is characteristic for diseases of the urethra, only in the last portion - for diseases of the bladder, prostate gland, and seminal tubercles. In the presence of total hematuria( in all three portions of urine), the source of bleeding can be either the parenchyma of the kidney or the calyx-pelvis system or ureter. Often it is useful to carry out an orthostatic test( a sample with physical activity), consisting in obtaining two portions of urine: the first one - the morning one, taken immediately after awakening, preferably lying down to the transition to a vertical position, and the second - taken 1-2 hours after the transitionin a vertical position and a small physical load( walking, climbing the stairs).In both portions, the number of red blood cells is counted. A significant increase in hematuria is characteristic of nephroptosis, urolithiasis. The presence of erythrocyte cylinders in the sediment is characteristic of renal hematuria. It is assumed that the cylinders can be destroyed during centrifugation, so they suggest that the urinary sediment should be isolated not by centrifugation, but by filtration through finely porous filters.

The question of the importance of unchanged and altered red blood cells in the urinary sediment has been discussed for a long time. In recent decades, the predominance of certain erythrocytes has not been given a diagnostic value. Since the late 70's in the study of erythrocytes of urinary sediment began to apply the method of phase contrast microscopy. It is shown that erythrocytes in kidney diseases are significantly different from erythrocytes in urological diseases. Erythrocytes of glomerular origin appear to be noticeably deformed as a result of their passage through BMP and then through liquid media with sharp changes in pH, osmolarity and electrolyte composition of urine in various sections of the renal tubules. The presence in the urine sediment of more than 70% of the "dysmorphic" erythrocytes indicates their glomerular origin. When bleeding from damaged vessels in patients with urological diseases, erythrocytes, which enter urine, retain the size and shape inherent in normal erythrocytes( "unchanged" erythrocytes).This method can be a primary test of differential diagnosis, which determines the direction of further careful urological examination.

Especially important for the elimination of urological pathology is instrumental and X-ray examination: cystoscopy with catheterization of ureters and separate urine collection, renal ultrasound, excretory urography( preferably lying and standing to exclude pathological mobility of the kidney), if necessary retrograde pyelography, CT, selective angiography. Recently, radioisotope angiography and renoscintigraphy with radioactive Tc99 have been used. These methods are more simple and safe, they allow us to identify local disorders of hemo- and urodynamics characteristic of unilateral hematuria in renal venous hypertension, renal vein thrombosis, and forecanic bleeding.

The cause of approximately 15% of hematuria is a urinary tract tumor. In 60% of cases, these are bladder tumors, which can be accompanied only by painless hematuria;The diagnosis is clarified with cystoscopy. Approximately 20% of tumors of the urinary tract - cancer of the kidney parenchyma( blunt low back pain, fever, anemia or erythrocytosis, hypercalcemia), sometimes occurring with paraneoplastic reactions, including with membranous nephropathy;To confirm the diagnosis, intravenous urography and angiography should be performed.

One of the most common causes of hematuria is urolithiasis. A typical clinical picture includes a sharp paroxysmal pain in the lower back, radiating into the inguinal region, followed by macrogemuria. About 90% of kidney stones contain calcium and can be detected with an overview of the kidney area.

Hematuria in combination with leukocyturia and moderate proteinuria( usually up to 1 g / l) is often found in nonspecific inflammatory diseases of the urinary system. Microhematuria in chronic pyelonephritis is caused by damage to the interstitial tissue of the kidney. In acute pyelonephritis and exacerbation of chronic pyelonephritis, episodes of macrohematuria may develop, usually as a result of necrosis of the renal papillae, in the pathogenesis of which is ischemia of the papillae( embolization of blood vessels) or compression by inflammatory infiltrates. Infection of the lower urinary tract( the number of microbial bodies in 1 ml of urine is not less than 105) sometimes can cause hematuria;with hematuria, a fungal infection can occur. Episodes of macrohematuria can be in women with cystitis and urethritis.

With tuberculosis of the urinary system, hematuria, as a rule, is combined with pyuria and insignificant proteinuria, but sometimes it is isolated. Diagnosis is complex and requires careful bacteriological( repeated urine cultures, sediment microscopy), X-ray and ultrasound studies.

Haematuria is often detected with congestive venous hypertension in the kidney, which can be caused by nephroptosis, renal vein stenosis, renal vein thrombosis, renal vein anomalies, etc. Renal venous hypertension may be manifested by microhematuria, which is significantly enhanced with exercise, in combination with minor proteinuria. Macrogematuria in these conditions in most cases is due to an increase in venous pressure and the breakthrough of a thin septum between the veins and the calyx of the kidney( fork bleeding).

Hematuria( usually unilateral) is observed with a kidney infarction, as well as with renal vein thrombosis. Kidney infarction develops with embolism of the renal artery or its thrombosis, can be observed with infective endocarditis, nodular polyarteritis. Characterized by low back pain, transient hematuria and proteinuria, and sometimes hypertension. For thrombosis of the renal veins pain, massive proteinuria and hematuria with rapid attachment of the nephrotic syndrome are characteristic. In acute complete thrombosis, hematuria is possible, nephrotic syndrome is often combined with transient renal failure. Chronic thrombosis usually occurs with minor pain or without pain, manifested by microhematuria and nephrotic syndrome. For the precise localization of thrombosis, lower wenokavagrafia is used in combination with renal venography and arteriography. Recently, in all these situations, Doppler ultrasound, including color scanning, is increasingly used for diagnostic purposes.

One of the most characteristic and serious manifestations of acute and especially chronic kidney disease is nephrotic syndrome. This is one of the "big" nephrologic syndromes, which represents a prognostically very serious clinical and laboratory symptom complex, including massive proteinuria( above 3.0-3.5 g / day, in children above 50 mg / kgs), hypoproteinemia( hypoalbuminemia - albuminblood less than 30 g / l) and edema. A frequent sign of a nephrotic syndrome is hypercholesterolemia( hyperlipidemia, to be more exact).

A wide range of changes in the body systems responsible for maintaining homeostasis in nephrotic syndrome leads to its isolation as extremely important not only because of the occurrence of significant edema, but also because of the possibility of developing formidable complications( primarily infections, vascular thromboses),complex therapy, the severity of the prognosis.

Nephrotic syndrome develops most often in children aged 2 to 5 years and in adults from 17 to 35 years. Along with this, cases of nephrotic syndrome have been described and in earlier life - in newborns, as well as in senile age( 85-95 years).

Spontaneous remissions in adults are rare, and although there is usually a satisfactory GFR remaining for very long signs of nephrotic syndrome, there is no hypertension, hematuria, but in most cases the disease progresses continuously with the development of CRF.

In this regard, the timely detection of nephrotic syndrome, correct interpretation of its origin and attempts at active treatment are very important.

At the heart of the nephrotic syndrome is usually the defeat of the glomerulus of the kidneys: various variants of glomerular lesions( from minimal, captured only by electron microscopy, to severe variants of glomerular nephritis, including fibroplastic and focal segmental glomerulosclerosis), as well as amyloidosis, diabetic glomerulo-sclerosis.

In most cases, a nephrotic syndrome occurs with "primary" kidney disease - acute and chronic glomerulonephritis. However, at the present time, kidney damage with nephrotic syndrome is often due to systemic diseases( SLE, systemic vasculitis, rheumatoid arthritis, etc.).The development of nephrotic syndrome can cause diseases of infectious etiology( chronic inflammation of the lungs, bone system, tuberculosis, syphilis, actinomycosis, subacute infective endocarditis), parasitic diseases( malaria, schistosomiasis), liver diseases, especially those associated with HBV and HCV infection, diseasesblood( lymphogranulomatosis, non-Hodgkin's lymphomas, mixed cryoglobulinemia, sickle-cell anemia), allergic( atopic) diseases such as pollinosis, food allergies, diabetes mellitus,fever, thrombosis of large veins( not only the kidney, but also the lower hollow, femoral, etc.).

Nephrotic syndrome may be due to exposure to LS.To drugs that can cause kidney damage with the development of nephrotic syndrome, include antiepileptic drugs, bismuth preparations, gold, mercury, D-penicillamine, antibiotics, vitamins, etc. In addition to isolated kidney damage, it is possible to develop severe drug disease involving almost all systems and organs( including kidneys).

It should be noted the possibility of paraneoplastic nephrotic syndrome, which occurs most often with bronchogenic carcinoma, cancer of the kidney parenchyma, stomach and colon.

Finally, there are rare congenital and genetically determined diseases in which the main clinical manifestation is nephrotic syndrome. These diseases include congenital nephrotic syndrome of the Finnish type, nephrotic syndrome, which proceeds with damage to the nail plates and knee cups, etc.

In all of these diseases, the nephrotic syndrome is realized through the above two variants of renal damage: changes in the type of glomerulonephritis and amyloidosis, with orAnother frequency of each of these options, specific to a particular disease. Thus, in case of periodic illness, the nephrotic syndrome is caused by amyloidosis in almost 100% of cases, with glomerulonephritis always forms the basis of the nephrotic syndrome, amyloidosis with nephrotic syndrome usually develops with rheumatoid arthritis, less often glomerulonephritis, including drug, in subacute infective endocarditis, glomerulonephritis and amyloidosis occurapproximately at the same frequency.

Primary kidney disease

Secondary nephrotic syndrome( for other diseases)

Thus, the etiology of the nephrotic syndrome is different, and its numerous manifestations are nonspecific, which is to a certain extent due to the commonness of the pathogenetic mechanisms.

Damage to the glomeruli of the kidneys and massive proteinuria lead to the appearance of other "big" symptoms of nephrotic syndrome, in a complex forming a clinical picture of this condition.

• Hypoalbuminemia, which develops after massive proteinuria, is an indispensable sign of nephrotic syndrome. Most often, the decrease in the level of albumin and total protein in the blood is very significant, which leads to a drop in the oncotic plasma pressure. About hypoalbuminemia say with a serum albumin content of less than 35 g / l;in severe nephrotic syndrome, the albumin content can be reduced to 15-20 and even up to 8-10 g / l. Hypoalbuminization determines the decrease in the amount of total protein in the serum, a decrease in the oncotic pressure of the serum, a decrease in the transport function of albumin as a carrier of a number of substances, including many drugs.

• Hypoproteinemia is a constant symptom of nephrotic syndrome. The content of total protein in the blood serum is reduced to 30-40 and even 25 g / l. Hypoproteinemia is often aggravated by loss of protein by the intestine, increased catabolism of body proteins, including immunoglobulins, a decrease in the protein reabsorption of tubules due to protein blockade of the kidney lymphatic system and edema of renal interstitium.

• In addition to hypoalbuminemia, nephrotic syndrome also shows other signs of disproteinemia - almost always there is pronounced hyper-α2-globulinemia and often hypogammaglobulinemia.

• Important signs of nephrotic syndrome include hyperlipidemia - elevated blood levels of triglycerides, total cholesterol, low-density lipoprotein( LDL), apoprotein B, unesterified fatty acids. Nephrotic hyperlipidemia is aggravated by persistent nephrotic syndrome and HA therapy. The mechanism of the development of hyperlipidemia in nephrotic syndrome is explained by a decrease in the oncotic pressure and viscosity of the plasma, as well as the loss of urine in the liporegulatory substances.

In parallel with the disorders of protein and lipid metabolism in nephrotic syndrome, changes often occur in the coagulation and anticoagulation systems, resulting in the formation of a symptom of hypercoagulable blood.

The nephrotic syndrome is characterized by pronounced disturbances of the water-electrolyte balance, leading to the development of edema. With progressing edemas reach the degree of anasarka with dropsy( cavity, hydrothorax, hydropericardium), which usually determines the main complaints of patients. The immediate cause of edema development is the retention of sodium and water, which is accomplished through various mechanisms, explained by two widely accepted theories.

• The first, the most well-known( "classical") theory places the main importance of hypoproteinemia with a decrease in the oncotic pressure of the plasma and the release of water and electrolytes into the interstitial tissue, which leads to hypovolemia. Hypovolemia causes compensatory inclusion of mechanisms regulating BCC, primarily the system of "renin-angiotensin-aldosterone" and ADH.As a result, the reabsorption of sodium and water by the kidneys increases. This theory is called hypovolemic, or( which is the same thing) the theory of "incomplete bed" and quite convincingly explains the retention of sodium and water in those 30-40% of patients with a truly detectable decrease in BCC.

• In patients with normo- or hypervolemia( 60-70% of patients with nephrotic syndrome) and lack of activation of the renin-angiotensin-aldosterone system, the development of edema is explained primarily by renal sodium retention due to a decrease in its filtration or tubular reabsorption( the theory of "overcrowdedchannel ").The idea of ​​the magnitude of BCC in nephrotic syndrome is of great practical importance, justifying the indications for the appointment of diuretics and ultrafiltration.

Usually, nephrotic edema, like other signs of nephrotic syndrome, develops gradually as proteinuria increases, with nephrotic syndrome occurring at the onset of the disease without recurring or rarely recurring in the future, which is considered the most favorable variant of the course of the disease. The unfavorable variant is the continuously recurring course of the nephrotic syndrome, especially the constantly existing pronounced variant, when often there is also an arterial hypertension. In all cases, the prognosis is largely determined by the duration of remission of the nephrotic syndrome, spontaneous or medically, and the frequency and duration of relapses.

The severity of the condition with nephrotic syndrome can be exacerbated by a number of complications, among which the most serious are the following:

Infections( pneumonia, pneumococcal peritonitis, sepsis) were most often diagnosed in the preantibacterial era of patients with nephrotic syndrome;they are explained primarily by a decrease in immunity and aggravated by the current active immunosuppressive therapy of nephrotic syndrome.

The development of an infection, including a clinical picture of erysipelas, may be affected by a breach of the integrity of the skin( cracks in the swelling of the skin, trauma with subcutaneous injections).The inflammation that arises in these cases is usually due to p-hemolytic streptococcus( erysipelas), as well as staphylococcus or other gram-positive bacteria and requires antibiotic treatment.

Erysipelas should be differentiated from migrating erythem in a nephrotic crisis. If the painful migratory erythema-like erythema of the most diverse localization( more often in the abdomen, lower extremities) is accompanied by severe abdominal pains, often with peritoneal symptoms and a decrease in diuresis, one can think of the development of the so-called nephrotic crisis, one of the initial manifestations of hypovolemic shock.

The nephrotic crisis is an abacterial complication of the nephrotic syndrome, characterized by anorexia, vomiting and abdominal pain in the presence of anasarca and severe hypo-albuminemia, vascular collapse( hypovolemic shock).It is hypovolemia that is the main pathophysiological link of the nephrotic crisis. The nephrotic crisis should be differentiated from vascular thrombosis, which is characterized by severe pain, hemorrhagic eruptions, thrombocytopenia, the corresponding changes in the coagulogram( a dynamic study of the coagulogram is mandatory for a patient with a nephrotic syndrome).

ARF is an important, although rare complication of nephrotic syndrome. It develops as a result of thrombosis of the renal veins, acute crisis of local( renal) hypercoagulation, hypovolemic shock, sepsis, diuretic therapy and NSAIDs, the introduction of large amounts of radiocontrast substances. In children, the more common cause of OPN is sepsis and thrombosis.

Brain edema with nephrotic syndrome occurs very rarely, usually at the height of development of massive edema. It manifests itself as sluggishness, inhibition of the patient, sometimes it can grow into a coma. The prognosis is serious. The condition requires immediate resuscitation. Edema of the retina is often developed in edematous patients. As the total edema decreases and the albumin increases in the blood, the retinal edema decreases.

Vascular complications of the nephrotic syndrome include peripheral phlebothrombosis, pulmonary embolism, thrombosis of the artery of the kidney with the development of infarctions of its parenchyma. Finally, with nephrotic syndrome, taking into account the hyperlipidemia inherent in these patients, it is possible to accelerate atherosclerosis with the development of coronary heart disease( CHD), myocardial infarction and strokes.

Prolonged existing nephrotic syndrome, regardless of its cause, leads to the development of CRF.Persistent "large" proteinuria itself damages renal structures - tubules and interstitium, causing interstitial inflammation and tubulointerstitial fibrosis. In this case, the degree of damage and the risk of progression of renal failure are clearly correlated with the magnitude of proteinuria. Once again, it should be emphasized that persistent "large" nonselective proteinuria is one of the main factors in the progression of chronic kidney diseases. So, the nephrotic syndrome should always be considered as a condition significantly worsening the overall prognosis of the nephrologic patient both from the point of view of rapid development of renal insufficiency and from the point of view of joining a number of complications aggravating the severity of the condition even before the onset of a decrease in renal function.

Since the main factor in the development of hypoproteinemia in nephrotic syndrome is the loss of protein by the kidneys, the value of daily proteinuria is the main laboratory indicator. Together with other biochemical features described above, the diagnosis of nephrotic syndrome becomes relatively simple( in rare cases, proteinuria, which is never "large", can be detected in patients with hypoalbuminemia, ascites, and then it is necessary to exclude the possible association of edema with liver damage).

Differential diagnostics is more complicated, since almost all the signs of a nephrotic syndrome have a nonspecific character. Therapeutic tactics, however, vary greatly depending on the nosological nature of the nephrotic syndrome.

Differential diagnosis should be carried out to clarify the etiology of the disease: first of all, it is necessary to exclude amyloidosis of the kidneys( biopsy of the kidney, gums, rectal mucosa), paraneoplastic nephrotic syndrome. When suspected of multiple myeloma, it should be remembered that the true nephrotic syndrome( with hypoalbuminemia and edema) in this disease is rarely observed, despite the severity of proteinuria( "proteinuria overflow").When combined nephrotic syndrome with fever, anemia, leukopenia should exclude SLE( especially in young women), systemic vasculitis, subacute infective endocarditis. The establishment of a nephrotic syndrome with allergy( including drug) is important for the purpose of elimination treatment.

Refinement of the etiology of nephrotic syndrome is of great practical importance: elimination of the causative factor( infection control, radical removal of the foci of chronic suppuration, tumors) can in itself cause the reverse development of nephrotic syndrome even in amyloidosis. Unfortunately, in most cases, the etiological principle of nephrotic syndrome therapy is not yet possible, and therefore pathogenetic and symptomatic treatment plays an important role.

Kidneys play a major role in the regulation of blood pressure. The emergence of hypertensive syndrome in kidney disease is due to sodium and water retention as a result of activation of pressor( renin-angiotensin-aldosterone) and a decrease in the function of depressor( prostaglandin and kallikrein-kinin) systems. As a result, most kidney diseases are accompanied by hypertensive syndrome. In patients in the terminal stage of renal failure, the incidence of arterial hypertension reaches 80-100%.

Impaired renal function, decreased GFR are accompanied by a decrease in the release of sodium and water. The delay in sodium and water in most cases leads to an increase in BCC, as well as an increase in sodium content in the vessel wall with its swelling and an increase in sensitivity to pressor effects of angiotensin and catecholamines. Following a delay in sodium, calcium accumulates in the vascular wall( in smooth muscle cells) with increased contractility and vascular tone, which leads to an increase in the total peripheral vascular resistance( OPSS).This mechanism with the leading role of hyperhydration, hypervolemia and increased cardiac output is of primary importance in the development of arterial hypertension in patients with OGN and CRF( especially in the terminal stage).It should be noted that the primary role of sodium and water retention, leading to an increase in the volume of extracellular fluid and increased cardiac output, E.M.Tareyev pointed out as far back as 1936, but this position became universally recognized only in the 80s of the XX century.

The second mechanism responsible for the development of arterial hypertension in kidney disease is associated with the activation of the pressor system, which includes:

Renin is an enzyme formed in the juxtaglomerular cells of the nephron. Under the action of renin from angiotensinogen( produced in the liver), angiotensin I is formed, which under the influence of ACE passes into angiotensin II, the latter causes a systemic spasm of arterioles with an increase in OPSS, enhances the reabsorption of sodium( acting directly on the renal tubules, and also enhancing the secretion of aldosterone).

Renin secretion is stimulated by a drop in pressure in the arterial system of the kidneys( blood loss, shock), hypovolemia, sodium deficiency in food, intake of diuretics.

Aldosterone( hormone of the glomerular zone of the adrenal glands) delays sodium, increasing its reabsorption in collecting tubes, and increases the excretion of potassium. Isolation of aldosterone is regulated by the "renin-angiotensin" system and the concentration of Na + and K + ions. The aldosterone's aldosterone action is associated with its effect on the cell membrane with an increase in its permeability to sodium. The accumulation of sodium in the walls of the vessels leads to vasoconstriction.

Increased renin activity plays a role in the development of arterial hypertension in kidney diseases characterized by the preservation of their function, but the presence of ischemia in the region of the juxta-glomerular apparatus. This situation is most pronounced in stenosis of the renal artery. Renin-dependent hypertension is also observed in some patients in the terminal stage of renal failure. Conducting hemodialysis in such patients does not reduce blood pressure, and only bilateral nephrectomy can lead to its reduction. Renin activity is increased in a number of patients with chronic glomerulonephritis, but this is not the only pathogenetic factor of arterial hypertension. Renin-dependent hypertension occurs with a significant increase in OPSS.At the same time, in patients with acute glomerulonephritis, renin activity is reduced and does not increase in response to the administration of diuretics.

Increased secretion of aldosterone contributes to the development of arterial hypertension in all cases of activation of the renin-angiotensin-zine system, as well as hyperaldosteronism - primary( tumors of the glomerular zone of the adrenal cortex) and secondary.

An increase in the activity of the sympathetic adrenal system is associated with an increase in the formation of catecholamines( for example, with pheochromocytoma) or their delay in the violation of the excretory function of the kidneys( eg, CRF).The delay in sodium increases the sensitivity of the receptors of the vascular wall to the pressor effect of catecholamines. The role of catecholamines in the origin of arterial hypertension in diseases of the kidney is associated with vasoconstriction and an increase in OPSS, as well as an increase in cardiac output.

Endothelial endocrine hormones also contribute to the development of arterial hypertension. With damage to the vascular endothelium, the relationship between the mediator systems - vasoconstrictor( endothelin and thromboxane) and vasodilating( prostacyclin and nitrogen oxide) - shifts in favor of activation of vasoconstrictor components. In patients with diffuse kidney disease, if there is a violation of their function in the blood, an increased concentration of endothelin-1 is found.

Decreasing the effect of the depressor system

The depressor system, which opposes the action of pressor factors, includes:

Prostaglandins reduce arterial tone, reduce their reaction to vasopressor substances, exhibit potent natriuretic, and consequently, diuretic action. The final products of the kallikrein-kinin system, bradykinin and callidin, also have pronounced vasodilating properties;the excretion of kallikrein can serve as an indicator of vasodilation and the activity of the natriuretic system. The defeat of the renal parenchyma leads to a decrease in the depressor function of the kidneys - a disorder of the "endothelin-nitrogen oxide" system, which contributes to the development of arterial hypertension due to a sharp increase in OPSS.The delay of sodium in the body further increases the imbalance of this system.

It should be emphasized once again that only with a few pathological conditions can we speak of one leading mechanism for the development of hypertensive syndrome. In most patients with chronic glomerulonephritis, hypertension is of mixed origin.

The development of hypertensive syndrome significantly worsens the prognosis of glomerulonephritis, as it is one of the most important factors in the progression of the disease. Persistent arterial hypertension contributes to sclerotic changes in the blood vessels( arterioles) of the kidney with secondary activation of the pressor mechanisms, as well as an increase in intra-cerebral pressure followed by the development of glomerulosclerosis.

Clinic of hypertensive syndrome in diseases of the kidneys is determined by the degree of increase in blood pressure, severity of heart and vascular lesions. Patients complain of headache, vision impairment, pain in the region of the heart, dyspnea, with labile arterial hypertension( with hyperkinetic circulation) - fast fatigue, excitability, palpitations, less often for a headache. Malignant hypertensive syndrome is characterized by a particularly high and persistent diastolic pressure, expressed by retinopathy( with foci of hemorrhage, edema of the optic nerve, plasmorrhagia, often with reduced vision until blindness), hypertensive encephalopathy, heart failure( first left ventricular and then stagnant in a large circleblood circulation).In chronic renal failure, the development of heart failure contributes to anemia. Compared with hypertension, complications( stroke, myocardial infarction) in a patient with renal hypertensive syndrome are less common.

With a severe lesion of the renal arteries, a rise in plasma levels of renin and aldosterone is noted, hyponatremia syndrome with hypokalemia, thirst, polyuria, weight loss can develop.

Hypertensive crises( caused by ejection of adrenaline), as a rule, are not frequent, are manifested by a sharp headache, nausea, vomiting, and visual impairment.

In the presence of hypertensive syndrome, it is necessary to assess its severity and resistance, as well as( at least roughly) its hemodynamic variant. An approximate idea of ​​the hemodynamic variant can be obtained by measuring the so-called basal pressure, which is carried out twice - sitting( lying) and re sitting( lying) 5 minutes after being in an upright position. Reduction of the initial blood pressure( systolic) by 20-30 mm Hg. Art.indicates rather a hyperkinetic variant;the study is recommended to be conducted in a quiet environment, in a warm room.

For the differential diagnosis of high- and low-grade arterial hypertension, the exception of renovascular high-renal arterial hypertension is a captopril test. With the introduction of captopril( ACE inhibitor), patients with high-grade arterial hypertension after 30-40 min marked a significant decrease in blood pressure;In patients with normo- or low-grade arterial hypertension, blood pressure does not change. The trial with saralazine is used mainly to exclude renous ventricular hypertension.

Renal hypertensive syndrome is observed in parenchymal diseases of the kidneys, lesions of the kidney vessels, as well as in the hyperproduction of aldosterone or catecholamines.

Hypertensive syndrome may be accompanied by virtually all parenchymal diseases of the kidneys. A hypertensive variant is observed in approximately 20% of patients with chronic glomerulonephritis. The disease occurs with a moderate urinary syndrome( proteinuria usually does not exceed 1 g / day, erythrocyturia and cylindruria are minimal).Changes in urine are detected before the registration of elevated blood pressure;the course is moderately progressing( 10-year survival in our observations was 68%).The hypertensive variant of glomerulonephritis should be differentiated from hypertensive disease and renovascular hypertension, which occur in some patients with moderate urinary syndrome( ischemic nephropathy).

Hypertensive syndrome, not prominent in the clinical picture, is met with latent glomerulonephritis in some patients.

When combined with severe nephrotic syndrome with severe hypertension, one should think of mixed CGN or PGHN( in favor of the latter, fast deterioration of renal functions is indicated).In chronic interstitial nephritis, malignant hypertension is noted in 25-30% of patients.

Hypertonic syndrome is characteristic for OGN, and it is often observed in chronic pyelonephritis. Chronic pyelonephritis can often occur with hypokalemia, which, in the presence of increased blood pressure, leads to differential diagnosis with primary hyperaldosteronism.

Persistent arterial hypertension, often malignant, is characteristic of nodular polyarteritis, systemic scleroderma( "scleroderma kidney"), diabetic kidney;it is also observed in SLE, hemorrhagic vasculitis( purpura) of Schönlein-Genoch, gouty kidney, etc. In renal amyloidosis, persistent hypertensive syndrome is noted relatively rarely.

The causes of renovascular arterial hypertension in 85-90% of cases are atherosclerosis of the kidney vessels and fibro-muscular hyperplasia. Significantly less often the cause of renovascular hypertension is aneurysm of the renal artery, aortoarteriitis, embolism or thrombosis of the renal artery, anomalies of the vascular arrangement.

Atherosclerosis usually affects the proximal third of the renal artery, near the aorta;more often it develops in men older than 40 years. Fibromuscular hyperplasia is characterized by areas of fibrous and muscular hyperplasia, alternating with areas of destruction of the media. Usually the middle and distal sections are affected. Women are more often ill at the age of 20-40 years. Aortoarteriitis often affects the thoracic and abdominal parts of the aorta;more often young women.

Renovascular hypertension should be considered in the presence of a marked increase in blood pressure, especially with diastolic or malignant arterial hypertension, resistant to standard antihypertensive therapy, in patients without a clear clinical picture of CGN or chronic pyelonephritis. An important clinical sign is systolic noise( and sometimes diastolic), heard in the area of ​​the projection of the renal arteries in 50% of patients. With atherosclerosis of the renal arteries, the noise is better listened to in the middle line above the navel, in the epigastric region( to listen without pressing the stethoscope);with fibromuscular hyperplasia, the noise is heard a little laterally and upward from the navel. Sometimes the noise is better audible from the back. The symptom is not absolute, since sometimes abdominal noise can be heard in patients and without stenosis of the renal artery. Another clinical sign that makes one suspect a renovascular hypertension is asymmetry of the arterial pressure on the limbs( with atherosclerosis or aortoarteritis).

The first stages of an additional examination for suspected renal arterial hypertension include radioisotope renography with 13h-hippuran, followed by excretory urography. Radioisotope renograms show decreased blood supply to the affected kidney, often with a decrease in its function( reduction of the vascular segment and lengthening of the secretory and excretory segments of the renogram).On urograms reveal:

More convincing results of aortography and selective renal arteriography, allowing to reveal the place of the lesion, its prevalence. New diagnostic methods are of great diagnostic value-radio angiography with albumin, two-dimensional ultrasound of the abdominal aorta in combination with Doppler scanning, digital subtraction angiography, spiral CT, MRI, color duplex sonography.

Additional diagnostic methods include the determination of renin activity in blood plasma, as well as in renal veins( an increase on the side of stenosis);this study is especially informative when it is performed before and after the administration of captopril. The results are more accurate with an additional( repeated) study of renin activity after taking 25-50 mg of captopril. Exceeding the initial indicators several times confirms the diagnosis.

Diagnosis of renal arterial hypertension is important, as it is possible to perform operative treatment( prosthetics of stenotic area or stenosis) or intra-arterial expansion with a balloon catheter.

It should be remembered that patients with bilateral stenosis of the renal arteries are contraindicated with ACE inhibitors.

Special attention has recently been paid to atherosclerosis as a cause of kidney damage, called ischemic kidney disease( IBP), leading to CRF in a fairly large number of patients.

Clinical suspected ischemic kidney disease( IBP) should occur if the patient has coronary artery disease or atherosclerotic peripheral vascular disease( history or at the time of the examination), noises heard during auscultation in the projection of major arteries unexplained by other causes of increased serum creatinine levels, oftenwith minimal changes( or lack thereof) in a routine urinalysis, a significant increase in serum creatinine level when treated with ACE inhibitors. These signs are important to always bear in mind when dynamically observing patients, but especially elderly patients and people with advanced atherosclerosis.

Special attention should be paid to the importance of auscultation of the main arteries in these patients, as well as in elderly people with their hypertension - the detection of noise allows one to assume a vasorenal( renal artery lesions - unilateral or bilateral, damage to their intrarenal branches)arterial hypertension and nephrosclerosis, which is also confirmed by Doppler ultrasound.

Arterial hypertension associated with hyperproduction of pressor substances( endocrine hypertension) is observed in primary hyperaldosteronism and pheochromocytoma.

Primary hyperaldosteronism( Conn's syndrome) in 75% of cases is due to adrenal adenoma, in 15-20% - the result of hyperplasia of the adrenal glands, multiple adenomas. Diagnostic signs:

For differential diagnosis of primary and secondary hyperaldosteronism, samples with stimulation of renin and aldosterone can be used by walking and intravenous administration of furosemide. Primary hyperaldehistonism( aldosterome) is characterized by a decrease in the initially elevated plasma level of aldosterone, while the plasma renin activity( ARP), initially low, remains reduced after the load.

In secondary hyperaldosteronism( stenosis of the renal arteries, renal, heart failure, cirrhosis, nephrotic syndrome), elevated serum aldosterone levels are combined with an adequately elevated level of renin and does not change after exercise. For topical diagnosis using ultrasound, CT, adrenal scintigraphy, aortography, in some cases - selective phlebography.

Arterial hypertension associated with hyperproduction of catecholamines( epinephrine and norepinephrine) by chromaffin cells is usually caused by a tumor of adrenal medulla - pheochromocytoma( less often a tumor of adrenal gland localization - paraganglioma).

It is necessary to exclude pheochromocytoma in the following cases:

Sometimes pheochromocytoma is combined with other diseases - diabetes, hyperparathyroidism;can be observed changes in the psyche.

To confirm the diagnosis, it is necessary to examine the content of catecholamines and vanillin-mandelic acid in daily urine;often show an increase in blood glucose and urine levels - during a crisis and a few hours after it. For topical diagnosis, CT, MRI, and aortography are shown.

Acute cold fever is characterized by sudden onset or build-up of edema, hematuria and proteinuria, signs of azotemia( decreased GFR), salt and water retention, arterial hypertension.

• Acute poststreptococcal glomerulonephritis.

• Other glomerulonephritis associated with infection:

• Primary chronic glomerulonephritis:

Usually the whole clinico-laboratory complex of acute cold syndrome takes place, although only some of its signs( swelling or changes in urine) are sometimes expressed, sometimes considered by the doctor in isolation, outside the framework of the described syndrome.

The mechanism of development of this syndrome( as in many respects the pathogenesis of symptoms with OGN) can not be considered clarified, especially in cases of its appearance, for example, in a patient with glomerulonephritis with a pronounced nephrotic syndrome.

The emergence of acute syndrome is most typical for OGN, when after some time( from several hours to 7-12 days) after exposure to a known etiologic or provoking factor, virtually all of the above signs of acute cold symptoms appear almost simultaneously.

Acutefibrillary syndrome can develop at the beginning of CGN or first occur against the background of a long-existing renal disease, sometimes acquiring a continuously recurrent nature. In any case, the appearance of this syndrome most likely indicates an increased activity of the disease.

Diagnosis of acute cold syndrome in connection with a clear outline of symptoms is not difficult. It is practically important to distinguish, on the one hand, OGN from acute oesophrenic syndrome with chronic kidney disease, on the other hand - acute cold syndrome with CGN from the PGHN, since the volume of therapeutic measures and prognosis for these conditions are different. Suddenly arisen signs of acute cold syndrome in the absence of anamnestic data on them( changes in urinalysis, increased blood pressure, edema) allow first to think about OGN.The presence of anamnestic indications of the listed changes indicates that CGN is the basis of the acute cold syndrome, especially if a decrease in the relative density of urine and the value of GFR is observed, which persists even after the disappearance of signs of acute cold syndrome. Sometimes a biopsy of the kidney helps to finally answer the questions of differential diagnosis in this situation.

In some cases, the clinical picture of acute cold syndrome is aggravated by the occurrence of complications - eclampsia, acute heart failure and anuria, timely and correct diagnosis of which is very important. Renal eclampsia, in contrast to other convulsive conditions - common( eg, with epilepsy) or localized( eg, CRF) - is characterized by a rapidly developing significant increase in blood pressure in combination with urinary syndrome( although small changes in the urine may also occur with epilepsy),Brain symptoms in the form of mental inhibition, followed by a coma. Acute heart failure is usually manifested by typical attacks of cardiac asthma without any signs of classic diseases complicated by acute circulatory insufficiency( myocarditis, heart defects, etc.).Oliguric or anuric arthrosis in acute syndrome in addition to the absence of typical etchological factors for acute renal failure( acute infectious-toxic kidney) is characterized in contrast to the latter by arterial hypertension, swelling, significant changes in the urine.

Thus, the acute syndrome and its complications make the clinical picture of kidney disease more difficult, complicate the differential diagnosis and force to include in the ongoing treatment a number of additional measures.

Nephroptosis is an omission of the kidneys that occurs when their mobility increases. The disease can be associated with a poor development of the ligamentous apparatus and fascias that hold the kidneys. At the same time, other organs of the abdominal cavity( visceroptosis) can also be omitted due to weak development of abdominal muscles.

Nephroptosis often occurs asymptomatically. Sometimes it causes slight pain in the abdominal cavity, especially in persons with neurasthenia. However, in some patients, nephroptosis leads to a violation of urinary outflow, especially with a rapid transition to the vertical position. In such cases, there is acute pain in the lumbar region with nausea, vomiting, a decrease in the excretion of urine. Changing the position of the body can eliminate these symptoms. In rare cases, the omission of the kidney leads to the development of renal hypertension due to impaired circulation of the organ. At the same time there may be protein, erythrocytes in the urine, sometimes secondary infection of the urinary tract is attached.

Types of nephroptosis

Kidney can be of several kinds. Depending on the degree of mobility, the kidneys are secreted:

Fixing;
The moving type of the omitted kidney( another name for this pathology is the wandering kidney).

Development of the fixation type of descent occurs in three stages:

During inspiration, the lower part of the kidney leaves the hypochondrium, and when exhaled it assumes its original location. Similarly, this movement occurs at different positions of the human body: vertical and horizontal.
The kidney moves to the pelvic region, the second stage begins. Due to increased pressure in the renal vessels, erythrocytes and proteins can be detected in the urine. This is a painful period, the patient can feel colic in the lumbar region or dull aching pain.
In the third stage, the renal leg is stretched and twisted, resulting in difficulty urinary excretion and infectious complications appear.

In the case of a low-symptom course - the use of a complex of therapeutic gymnastics to strengthen the abdominal press, wearing a special bandage that fixes the kidney in a certain position. In the presence of severe complications, surgery is necessary.

Acute renal failure( ARF) - a sudden appearance of impaired renal function with delayed excretion of nitrogen metabolism from the body and the disturbance of water, electrolyte, osmotic and acid-base balance. These changes occur as a result of acute severe disorders of renal blood flow, GFR and tubular reabsorption, which usually occur simultaneously.

Currently, several etiological groups of arthritis are distinguished.

• Prerenal arrester( ischemic)

• Renal arrester.

• Emergency arresters.

Clarification of the etiological factors of ARF allows more purposeful therapeutic effects. Thus, prerenal OPN develops mainly in shock states characterized by severe microcirculation disorders due to hypovolemia, low central venous pressure and other hemodynamic changes;on the liquidation of the latter and it is necessary to send the basic medical measures. Close to the mechanism for these conditions and the cases of arthritis associated with a large loss of fluid and NaCl in severe extensive lesions of the gastrointestinal tract( infections, anatomical disorders) with indomitable vomiting, diarrhea, which also determines the range of therapeutic effects. Renal OPN develops in connection with the action of various toxic factors, first of all a number of chemical, medicinal( sulfanilamides, mercury compounds, antibiotics) and radiopaque substances, and can also be caused by renal diseases proper( OGN and nephritis associated with systemic vasculitis).Prevention and treatment of ARI in these cases should include measures that limit the possibility of these factors, as well as effective methods to combat these kidney diseases. Finally, the therapeutic tactics for postrenal arterial hypertension is mainly reduced to the eradication of acute urinary drainage due to urolithiasis, bladder tumors, etc.

It should be borne in mind that the ratios of various causes of arterial hypertension may vary due to the particular characteristics of their effects on the kidneys. Currently, the main group of cases of acute arthritis is acute shock and toxic damage to the kidney, but within each of these subgroups, along with post-traumatic arteries, arthritis with obstetric-gynecological pathology( abortion, complications of pregnancy and childbirth), arthritis in connection with blood transfusion complicationsand the effect of nephrotoxic factors( poisoning with acetic essence, ethylene glycol), ARF is associated with an increase in surgical interventions, especially in older age groups, and also with the use of newx medicines. In endemic foci, the cause of acute renal failure may be a viral haemorrhagic fever with kidney damage in the form of severe acute tubulointerstitial nephritis.

Although a large number of studies have been devoted to the study of the mechanisms of development of acute renal failure, nevertheless the pathogenesis of this condition can not be considered definitively clarified.

However, it has been proved that a variety of aetiological variants of arrester are characterized by a number of general mechanisms:

The resulting morphological changes relate mainly to the tubular apparatus of the kidneys, primarily the proximal tubules, and are represented by dystrophy, often severe necrosis of the epithelium, accompanied by moderate changes in the interstitium of the kidneys. Glomerular disorders are usually minor. It should be noted that even with the deepest necrotic changes, regeneration of the renal epithelium occurs very quickly, which is facilitated by the use of hemodialysis prolonging the life of these patients.

In the community of developing processes, the predominance of one or another pathogenesis link determines the features of the development of arthritis in each of these variants. Thus, with shock arresters, the primary role is played by ischemic damage to the kidney tissue, with nephrotoxic arthrosis, in addition to hemodynamic disorders, the direct action of toxic substances on the tubular epithelium during their secretion or reabsorption is important, with thrombotic microangiopathy predominant in hemolytic-uremic syndrome.

In some cases, OPN develops as a consequence of the so-called acute hepatorenal syndrome and is due to severe liver disease or surgical interventions on the liver and biliary tract.

Hepatorenal syndrome is a variant of acute functional renal failure that develops in patients with severe liver damage( with fulminant hepatitis or far-reaching liver cirrhosis), but without any visible organic changes in the kidneys. Apparently, in the pathogenesis of this condition, a certain role is played by changes in blood flow in the cortical substance of the kidneys of a neurogenic or humoral origin. Precursors of onset of hepatorenal syndrome are gradually increasing oliguria and azotemia. From acute tubular necrosis, hepatorenal syndrome usually distinguishes low concentration of sodium in urine and no significant changes in sediment, but it is much more difficult to differentiate from prerenal arthritis. In doubtful cases, the kidney response to the recovery of bcc helps - if renal failure does not respond to an increase in BCC, it almost always progresses and leads to death. Developing in the terminal stage, arterial hypotension can cause tubulonecrosis, which further complicates the clinical picture.

In the development of acute renal failure, four periods are identified: the period of the initial action of the etiologic factor, the oligoanuric period, the recovery period of diuresis and recovery.

In the first period, symptoms of the condition leading to ARF predominate. For example, fever, chills, collapse, anemia, hemolytic jaundice in anaerobic sepsis associated with community-acquired abortion, or a clinical picture of the general effect of a particular poison( acetic essence, carbon tetrachloride, salts of heavy metals, etc.) are observed.

The second period - the period of a sharp decrease or discontinuation of diuresis - usually develops shortly after the action of the causative factor. Azotemia grows, nausea, vomiting, coma, nausea, vomiting, coma, because of the delay of sodium and water develops extracellular hyperhydration, manifested by increased body mass, cavitary edema, pulmonary edema, brain.

After 2-3 weeks, oligoanuria is followed by a period of diuresis recovery. The amount of urine increases usually gradually, after 3-5 days diuresis exceeds 2 liters / day. First, the liquid accumulated in the body during the oligoanuria is removed, and then, due to polyuria, dangerous dehydration occurs. Polyuria usually lasts 3-4 weeks, after which, as a rule, the level of nitrogenous slag is normalized and a long( up to 6-12 months) recovery period begins. Thus, from the clinical point of view, the most difficult and life-threatening patient with ARF is the period of oligoanuria, when the picture of the disease is characterized primarily by azotemia with a sharp accumulation of urea, creatinine, uric acid and electrolyte imbalances in the blood( primarily hyperkalemia, and alsohyponatremia, hypochloraemia, hypermagnesia, hypersulphate and phosphatemia), the development of extracellular hyperhydration. The oligoanuric period is always accompanied by metabolic acidosis. During this period a number of serious complications can be associated with inadequately conducted treatment, especially with uncontrolled administration of saline solutions, when accumulation of sodium causes first extracellular hydration, and then intracellular hyperhydration leading to coma. The severe condition is often exacerbated by the uncontrolled use of a hypotonic or hypertonic glucose solution, which reduces the osmotic pressure of the plasma and enhances cellular hyperhydration due to the rapid transition of glucose, and, after it, water into the cell.

During restoration of diuresis due to severe polyuria, there is also a danger of severe complications, especially in connection with developing electrolyte disturbances( hypokalemia, etc.).

In the clinical picture of OPN, signs of cardiac and hemodynamic disorders, unfolded uremic intoxication with severe symptoms of gastroenterocolitis, mental changes, anemia may predominate. Often, the severity of the condition is aggravated by pericarditis, respiratory failure, nephrogenic( hyperhydration), and cardiac pulmonary edema, gastrointestinal bleeding, and especially infectious complications.

To assess the severity of a patient's condition with an arrester, the most important are the parameters of nitrogen metabolism, especially creatinine, whose level in the blood does not depend on the characteristics of the patient's nutrition and therefore more accurately reflects the degree of renal dysfunction. The delay in creatinine usually outstrips the increase in urea levels, although the dynamics of the level of the latter is also important for estimating the prognosis for ARF( especially when involved in the process of the liver).However, in many respects the clinical manifestations of arthritis, in particular signs of damage to the nervous system and muscles( primarily the myocardium), are associated with impaired potassium metabolism. Often arising and quite understandable hyperkalemia leads to an increase in myocardial excitability with the appearance of high, with a narrow base and pointed tip of the T wave on the ECG, retardation of the atrioventricular and intraventricular conduction up to cardiac arrest. In some cases, however, hypokalemia( with repeated vomiting, diarrhea, alkalosis) may develop instead of hyperkalemia, the latter is also dangerous for the myocardium.

Chronic renal failure( CRF) is a symptom complex characterized by a constant and gradual deterioration of the glomerular and tubular functions, in which the kidneys can no longer maintain the normal composition of the internal environment. CRF is characteristic of the final phase of any progressive renal lesion;while sometimes the decline in GFR for a long time is asymptomatic, and the patient feels healthy until uremia.

The term "uremia" is used for the terminal stage of impairment of all functions of the kidneys, including metabolic and endocrine.

Among the most common causes of CRF are:

CGN and chronic pyelonephritis are the causes of terminal renal failure in more than 80% of patients. Among the other nosological forms most often the development of uremia leads to diabetes mellitus, amyloidosis and polycystic kidney disease.

The prevalence of CRF( the incidence of chronic renal failure per million population per year) ranges very widely: from 18-19( according to data from individual centers in Switzerland, Denmark, Austria) to 67-84( according to renal centers in the USA, Sweden).

Data on the prevalence of CRF are extremely important in the socio-economic aspect, since they serve as the basis for planning specialized care( the number of beds for hemodialysis and the volume of kidney transplantation performed), so creating a register of patients with chronic renal failure is an urgent task for modern healthcare.

According to the classification of chronic kidney disease( CKD) proposed in the recommendations of the US National Renal Fund, chronic renal failure corresponds to stage III( GFR 30-59 ml / min / 1.73 m2), stage IV( GFR 15-29 ml / min /1.73 m2) and stage V( GFR & lt; 15 mL / min / 1.73 m2, dialysis) of CKD.

If conservative therapy is the main method of treatment of patients in an easy and moderate stage, then there is a need for renal replacement therapy - extrarenal cleansing( hemodialysis, peritoneal dialysis) or kidney transplantation at a severe and terminal stage.

Despite the variety of etiological factors, changes in the kidneys in severe CRF are of the same type and are reduced to the predominance of sclerotic processes, loss of morphological originality of the original process and hypertrophy of the remaining nephrons.

A sharp decrease in the weight of active nephrons in CRF is clinically manifested in the inability of the kidney to maintain a normal water-electrolyte balance.

We briefly dwell on the main violations of homeostasis in chronic renal failure.

In chronic renal failure, the body retains the products of nitrogen metabolism( urea, creatinine, uric acid, etc.), because these substances can not be removed from the body in a different way. Nitrogenous slags have long been considered "uremic toxins" responsible for many clinical symptoms of uremia( dyspepsia, bleeding, damage to the nervous system, etc.).It has now been established that retention of urea, an indicator of the degree of CRF, is not of great clinical importance, although it may play some role in the development of dyspeptic symptoms and encephalopathy. The delay of creatinine is the most accurate indicator of the degree of CRF.Delayed uric acid leads to the development of uremic arthritis.

Not excluding the role of nitrous metabolites as toxic agents, in recent years some scientists consider biologically active substances( parathyroid hormone, insulin, glucagon, natriuretic factor, etc.) as universal "uremic toxins", contributing to the maintenance of homeostasis with uremia.

In early stages of CRF, the ability of the kidneys to concentrate urine is impaired. In the pathogenesis of this disorder, in addition to anatomical causes( damage to the medulla of the kidney), the sensitivity of the collecting tubules to ADH, as well as the development of osmotic diuresis in the remaining nephrons, play a role. The remaining nephrons work under conditions of increased osmotic load and should excrete far more soluble substances in a minute than normal nephrons. To do this, they need to increase the amount of urine output. As a result, polyuria develops, the normal rhythm of urine output is disturbed, nocturia appears. Gradually, the relative density of urine decreases, isostenuria develops( the relative density of urine becomes equal to the relative density of the protein-free filtrate plasma, making 1.010-1.012), then hyposthenuria( the relative density of urine does not exceed 1.008).Violation of the concentration function is especially early detected with interstitial nephritis, pyelonephritis, and polycystic kidney disease. At the terminal stage of renal failure, the amount of urine decreases sharply and oliguria and anuria develop.

Normally, the kidney filters 550-600 g( 24,000 mmol) of sodium per day and releases 3-6 g( 140-280 mmol) of the electrolyte. When 7 g sodium chloride is taken with food, the excreted sodium fraction( ie the ratio of the isolated sodium to the accepted one) is 0.5%, with an increase in the intake of sodium chloride to 14 g, the excreted fraction increases to 1%.

The ability of the kidneys to excrete sodium in the amount of about the same as that received, remains with renal failure for quite some time. The mechanism of adaptation of sodium homeostasis with a significant decrease in the mass of the active nephrons is provided by a sharp decrease in the reabsorption of the electrolyte in both the proximal and the distal nephron and the increase in the excreted sodium fraction.

With the development of the terminal stage of renal failure, when the amount of filtered sodium decreases 15-20 times, with the intake of 7-14 g NaCl per day, the amount of excreted fraction reaches 10-20%.Among the subtle mechanisms of tubular adaptation that provide the release of sodium, distinguish:

As the progression of renal failure, adaptation mechanisms are depleted. The kidneys lose the ability to retain sodium. With the inability of the kidneys to reduce the concentration of sodium in the urine below 40-50 mmol / l, salt depletion may develop( salting kidney), which is observed in pyelonephritis, polycystosis, hyperchloremic acidosis. Clinically, salt depletion is manifested by weakness, arterial hypotension. In other patients with terminal stage of renal failure, on the contrary, the tendency to sodium retention develops. The delay of sodium in the body without the appearance of edemas gradually becomes the main cause of the development of arterial hypertension, which often complicates the course of chronic renal failure.

In the vast majority of patients with CRF, the ability to respond quickly to abrupt changes in sodium and water levels is impaired. Diarrhea, vomiting and other sodium losses do not lead to compensatory retention of sodium. Instead, the loss of sodium in the urine continues, which leads to hyponatremia, a decrease in the volume of extracellular fluid, arterial hypotension, a sharp narrowing of the kidney vessels, and eventually a sharp deterioration in renal function. A vicious circle develops:

In most patients with moderate renal failure, the kidneys are able to maintain a normal potassium balance, i.e.the excretion of potassium is equal to the daily intake of it in the body. Normal excretion of potassium( 1-3 g / day) is preserved as a result of an increase in the excreted fraction of the electrolyte( among the mechanisms for increasing the excreted potassium fraction, there is discussion of an increase in the activity of medullary N +, K + -dependent ATPase, as well as increased secretion of aldosterone).As a rule, the normal content of potassium in the blood is maintained until diuresis exceeds 600 ml / day. With the progression of chronic renal failure, violations of the potassium balance can be manifested by the development of hyperkalemia, less often - hypokalemia.

Hyperkalemia is observed in the terminal stage of renal failure in oligo- or anuria or in severe acidosis. Hyperkaliemia in chronic renal failure may result in increased catabolism( infection, fever, trauma), hemolytic complications, excessive intake of potassium from food, and intake of potassium-sparing diuretics( spironolactone, triamterene, amiloride).Potassium-sparing diuretics especially lead to hyperkalemia in diabetic nephropathy.

Clinical hyperkalemia is manifested by arterial hypotension, bradycardia, muscle weakness. On the ECG, a sign of hyperkalemia is a high T wave;when the potassium concentration is raised above 7 mmol / l, the broadening of the QRS complex is observed.

Concentration of potassium in the blood within 7 mmol / l and above is considered life threatening( potassium concentration above 8.5 mmol / l in most cases leads to cardiac arrest).If the heart lesion with a conduction disorder in the patient was present even before the terminal stage of renal failure developed, cardiac arrest may occur at a potassium concentration of less than 7 mmol / l.

Hypokalemia is more common in the early polyuric stage of CRF, or in the predominantly tubular form of CRF.Hypokalemia can also develop as a consequence of hyperaldosteronism, which is most common in malignant hypertensive syndrome with severe nephrosclerosis. Causes of hypokalemia in chronic renal failure may be low potassium intake from food, loss of potassium in the urine due to the use of potassium-diuretic diuretics, loss of potassium through the digestive tract.

Clinical signs of hypokalemia - pronounced muscular weakness, hypoventilation, dyspnea, convulsions. In ECG studies, abnormalities of the rhythm by the type of various forms of ventricular extrasystole, flattening of the T wave and the appearance of a pronounced denticle U.

Metabolic acidosis in CRF develops with a decrease in GFR to 25% or less from the baseline level. At moderate degrees of CRF, the plasma concentration of bicarbonates is maintained within the limits of normal values. The exception is CGN with a tubulointerstitial component, in which acidosis develops in the early stages of CRF.

The degree of severity of acidosis in CRF depends on the production of hydrogen ions, the total number of buffer compounds in the body, the ability of the lungs to release CO2 and kidneys to restore bicarbonates.

The mechanism of bicarbonate reduction is closely related to the excretion of hydrogen ions by the kidneys. It should be noted that the number of hydrogen ions excreted by the kidney is much less than that released by the lungs. Therefore, impairment of pulmonary function can lead to acidosis within a few minutes, while at the terminal stage of renal failure, even with complete anuria, acidosis develops only after a few days.

Moderate acidosis with uremia does not clinically manifest itself, the pathological breathing of Kussmaul is considered a sign of severe acidosis.

Laboratory signs of metabolic acidosis:

Excretion of titrated acids is usually normal or somewhat decreased, excretion in urine of ammonia is only 50% of normal values, although the values ​​of the indicator exceed the normal level when calculated on the weight of active nephrons. On the one hand, this may be due to a decrease in the mass of the active renal parenchyma leading to a decrease in ammonia production from glutamine, and on the other hand, to a reduction in the amount of renal blood flow that delivers ammonium to the kidneys. However, excretion of ammonium, as well as excretion of titrated acids, in terms of 1 ml of glomerular filtrate with uremia significantly exceeds that in a group of healthy individuals. The hyperfunction of the remaining nephrons does not reach the level providing complete compensation for the function of anatomically altered nephrons.

The development of renal acidosis is largely facilitated by a pronounced loss of bicarbonate in the urine, which arises from violations of the reabsorption of bicarbonates. The cause of these disorders can be anatomical or functional changes in the renal tubules, leading to a decrease in the activity of carbonic anhydrase, a decrease in sodium reabsorption, the development of hyperparathyroidism, etc.

Metabolic alkalosis with uraemia is extremely rare and occurs again, mainly due to extrarenal loss of potassium( with vomiting, diarrhea) or with severe manifestations of secondary hyperaldosteronism.

Kidneys play a leading role in the regulation of calcium, as it is in the kidneys that vitamin D becomes the most active form, 1,25-dihydroxyvitamin D3, which regulates the transport of calcium in the intestines and bones.

Violation of the formation of an active form of vitamin D3 in chronic renal failure, leading to a decrease in calcium absorption in the intestine, is one of the causes leading to hypocalcemia. In addition, the delay of phosphates in renal dysfunction is important( hyperphosphatemia contributes to the deposition of calcium in tissues with secondary hypocalcemia), as well as a decrease in the intake of calcium from food.

Hypocalcemia stimulates the production of parathyroid hormone, followed by partial compensatory increase in the calcium content. However, usually with progression of renal failure, hypocalcemia becomes more pronounced. In some cases, compensatory hyperproduction of parathyroid hormone leads to hyperplasia of parathyroid glands, the development of secondary hyperparathyroidism with an increase in the level of calcium in the blood plasma.

Clinical abnormalities of phosphorus-calcium metabolism in CRF are manifested by changes in the bone system:

Primary tubular defects( renal tubular acidosis, Fanconi syndrome) and hypoalbuminemia can lead to hypercalciuria and hypocalcaemia( a decrease in serum albumin by 10 g / L leads to a decreaseof calcium in the serum by 0.2 mmol / l).

In addition to reducing the formation of active metabolites of vitamin D3 in the pathogenesis of uremia, it is important to reduce other endocrine functions of the kidney - a decrease in the production of erythropoietin, a violation of the production of hormones involved in the regulation of blood pressure( pressor-depressor system).

In the clinical picture of progressing chronic renal failure, general symptoms often come to the fore: weakness, drowsiness, fatigue, apathy( uremic encephalopathy), muscle weakness.

With the delay of "uremic toxins", itching is associated with skin itching( sometimes painful), bleeding( nasal, gum, gastrointestinal, uterine), subcutaneous hemorrhages. With prolonged retention of uric acid, "uremic gout" can develop with gait-related joint pains and tofusias. A clear sign of uremia is dyspeptic syndrome( nausea, vomiting, hiccough, loss of appetite until aversion to food, diarrhea, less frequent constipation).Early signs of renal failure are polyuria and nocturia. Early enough, hypoplastic anemia develops( "anemia of the brothers" according to EM Tareev, 1929), associated with a decrease in the hematopoietic function of the kidneys( a decrease in the production of erythropoietin).Characterized by leukocytosis and moderate thrombocytopenia, which contributes to bleeding.

With severe uremia, a pale yellow complexion( a combination of anemia and urochromes delay), bruises on the hands and feet is revealed during examination, the skin becomes dry, with traces of clefts, a smell of urine( urine or ammonia, rather than urea, which is odorless).Urine is very light( low concentration and, moreover, devoid of urochromes).

With the progression of CRF in 80% of patients, sodium retention leads to hypertension, often with features of malignancy, with retinopathy. Arterial hypertension accelerates the progression of renal failure. Arterial hypertension, anemia, as well as electrolyte shifts lead to the development of severe heart damage. Myocardial infarction with uremia is a result of joint action of arterial hypertension( with left ventricular hypertrophy), anemia and lesions of the coronary arteries. Their contribution is also caused by a violation of calcium metabolism and hyperparathyroidism, which contribute to calcification of the valves and the development of fibrotic changes in the myocardium. Uremic damage of the heart( uremic cardiomyopathy) is forming, leading to congestive heart failure. In severe cases, the clinical picture of cardiomyopathy resembles manifestations of severe myocarditis: the expansion of all parts of the heart, gallop rhythm, arrhythmia, left ventricular failure, diffuse ECG changes. In the terminal stage, there is fibrinous or exudate pericarditis( obviously, a toxic genesis), manifested by severe chest pains, dyspnea. The noise of friction of the pericardium is better heard in the lower third of the sternum.

Diseases of the cardiovascular system, based on atherosclerosis, are one of the leading causes of death in patients with chronic renal failure, including those receiving treatment with various methods of renal replacement therapy. In addition, the incidence of IHD, cerebrovascular diseases, and also, apparently, atherosclerosis of peripheral arteries( including intermittent claudication syndrome) in patients with uremia is significantly higher than in the general population. It is now evident that the significant prevalence of cardiovascular diseases in CRF is associated not so much with the increased life expectancy of patients with persistent impairment of kidney function due to the more accessible chronic hemodialysis, continuous outpatient peritoneal dialysis, and kidney transplantation, due to a significant increase in intensityeffects of known factors of atherogenesis, some of which acquire special significance with uremia.

An epidemiological pattern characteristic of uremia is considered to be an increase in morbidity and mortality from IHD and cerebrovascular diseases in young patients. Thus, the rate of cardiovascular mortality in patients less than 45 years old with terminal renal failure receiving hemodialysis treatment is almost 100 times higher than in the general population.

Progression of atherosclerosis in chronic renal failure is largely determined by known factors of atherogenesis. Arterial hypertension, formed at one of the stages of the evolution of nephropathy, or arisen de novo already with terminal renal failure, leads to a significant increase in the risk of complicated forms of IHD, primarily due to the induction of the development of myocardial hypertrophy of the left ventricle. Thus, in a prospective observation of patients with impaired renal function, it was found that echocardiographic signs of left ventricular hypertrophy are present in 1/3 of patients with CRF( creatinine clearance 50-75 ml / min) and in 1/2 patients with terminal renal insufficiency. It should be emphasized that, in the terminal stage of CRF, the effect of hypertension on left ventricular myocardial remodeling is enhanced by the effect of a number of factors specific for CRF, primarily anemia. In addition, with CRF, the value of arterial hypertension and as an initial mechanism of the pathogenesis of cerebrovascular diseases is preserved.

Thus, it is obvious that active antihypertensive therapy is necessary in patients with irreversibly lost kidney function. As with the choice of other drugs, when appointing patients with CRF antihypertensive drugs should take into account the peculiarities of their pharmacokinetics, due to impaired renal function. A generally accepted rule is a reduction in the doses of most drugs with CRF by a factor of 1.5-2.However, some drugs, "renal" and "hepatic" ways of excretion of which can compensate each other, are used in patients with uremia without correction of doses. However, the number of such drugs is small: for example, fosinopril has the most properties among ACE inhibitors.

In patients with renal dysfunction, lipoprotein lipase function is suppressed, and hypertriglyceridemia and a decrease in high-density lipoprotein( HDL) concentrations occur in patients with CRF.It should be emphasized that the indicators of total cholesterol in patients with uremia and in the general population practically do not differ, since non-hyperlipoproteinemia is typical for CRF, and dyslipoproteinemia, manifested by an increase in the concentrations of LDL and very low density lipoproteins( VLDL), and a decrease in HDL in plasmablood, which appears even with a moderately pronounced decrease in kidney function. Even in the conservative stage of CRF, a 0.1 to 0.2 mmol / l decrease in HDL-C is accompanied by an increase in the risk of coronary artery disease by 1.2-1.4 times regardless of the LDL and VLDL values.

The amount of data supporting the efficacy and safety of various methods of antihyperlipidemic therapy in patients with CRF is not so great, but to date it is clear that the drugs of choice are statins. The results of small-scale clinical studies indicate the advisability of prolonged use of statins in chronic kidney diseases associated with dyslipoproteinemia, both in patients with nephrotic syndrome and CRF.Apparently, the results of large-scale clinical trials of statins can be extrapolated to a population of patients with uremia. Correction of doses of most statins with CRF is not required;the degree of their clearance during the procedure of hemodialysis remains to this day not certain. When using statins, it is necessary to periodically monitor the activity of liver transaminases and CK.

Taking into account the peculiarities of dyslipoproteinemia in CRF( hyper triglyceridemia at low HDL concentration) in patients with uremia, the use of fibrates can be justified. The safety of many fibrates is currently considered insufficient, primarily due to the provocation of rhabdomyolysis. Gemfibrozil - a representative of this group, currently considered as a drug of choice in CRF, accompanied by dyslipoproteinemia. This drug has almost no toxic effect and does not have the ability to cumulate in the body( Wanner, S., 2000).The efficacy of gemfibrozil in patients with hypertriglyceridemia and a decrease in HDL concentration was demonstrated in a relatively large controlled study of VA-HIT.It should be emphasized that the risk of the hepatotropic action, as well as the development of rhabdomyolysis, increases significantly with the combined use of statins and fibrates, and therefore the appointment of a combination of these drugs is considered unjustified.

Diabetes mellitus retains its importance as a factor of atherogenesis in patients with CRF.It is shown that monitoring the concentration of serum glucose leads to a significant increase in the survival rate of patients with terminal renal insufficiency receiving chronic hemodialysis treatment. However, with CRF, the formation of insulin resistance de novo is also possible.

The need to quit smoking patients with impaired renal function is known for a long time. It is now generally accepted that stopping smoking not only leads to a reduction in the risk of coronary heart disease, but also contributes to a certain extent to slowing the progression of CRF.

Hyperhomocysteinemia( an increase in the concentration of homocysteine-an amino acid, a product of methionine demethylation) refers to the proven risk factors for atherosclerosis in chronic renal failure.

The formation of hyperhomocysteinemia in chronic renal failure is determined by a decrease in the filtration of this amino acid in the glomerulus of the kidney, as well as a significant decrease in the intensity of its catabolism in renal interstitium. In addition, patients with chronic renal failure often observe a deficiency of co-factors in the re-methylation of homocysteine ​​- folic acid and vitamin B12, while a significant amount of folic acid is eliminated during hemodialysis sessions.

Mechanisms for the realization of atherogenic action of homocysteine ​​are generally similar to those for oxidized LDL.It was shown that homocysteine ​​causes dysfunction of the endothelium, induces thrombogenesis, and also prevents catabolism of LDL.Hyperhomocysteinemia increases the risk of not only IHD and cerebrovascular diseases, but also cardiovascular complications specific for CRF, for example, thrombosis of the arterio-venous shunt. With a persistent decline in GFR, hyperhomocysteinemia may acquire an independent significance as a factor in the progression of renal damage.

Methods of correction of hyperhomocysteinemia are under study. The expediency of administering folic acid in a dose of 15 mg to patients with terminal renal failure receiving chronic hemodialysis treatment is demonstrated. A favorable effect on the concentration of homocysteine ​​in the plasma of statins is suggested. However, the prognostic validity of the drug correction of hyperhomocysteinemia needs further clarification.

Certain violations in the development of cardiovascular complications in chronic renal failure also have a disruption of phosphorus-calcium metabolism. Calcium deposition in the vascular wall, including atherosclerotic plaques, increases the likelihood of their destabilization with the development of complicated forms of IHD( acute coronary syndromes), as well as acute disorders of cerebral circulation.

Anemia associated with CRF is associated with an increased risk of cardiovascular complications, primarily due to provocation of left ventricular hypertrophy. In this regard, at present, early initiation( before the formation of severe anemia) of therapy with erythropoietin preparations is considered more appropriate, although the data on the effect of correction of anemia on the cardiovascular system in patients with chronic renal failure remain controversial.

Of risk factors for atherosclerosis, which are important for CRF, lipoprotein( a) deserves attention. It is known that in patients with CRF there is an increase in the concentration of lipoprotein( a), especially its fraction with a high molecular weight. After the kidney transplantation, the content of lipoprotein( a) in serum is reduced. However, the introduction of the definition of this substance in clinical practice is difficult due to the high cost of the methods, as well as the uncertainty of the methods of influencing the elevated concentrations of lipoprotein( a).

Thus, patients with CRF require constant monitoring of many risk factors for atherosclerosis. Treatment of coronary artery disease and cerebrovascular disease in chronic renal failure is carried out according to general rules, but recently the role of invasive methods of treatment is increasing, with success even in patients with terminal renal insufficiency permanently receiving renal replacement therapy.

"Classic" factors of atherogenesis

Factors of atherogenesis that are of particular importance in CRF

"New" factors of atherogenesis

Additional factors of the pathogenesis of cardiovascular complications

Prior to the introduction of treatment methods by software hemodialysis, the appearance of pericardial friction noise was considered an extremely poor prognostic sign( "funeral ringing").The use of hemodialysis reduced its prognostic significance, but led to the appearance of forms rarely found in the natural course of uremia( chronic constrictive pericarditis, cardiac tamponade).

With the progression of uremia, neurological symptoms increase, convulsive twitchings appear, encephalopathy increases, until the development of uremic coma with "large" noisy acidic breathing( Kussmaul's breathing).Sometimes severe myopathy is observed, when patients are not able to climb stairs, to be in an upright position.

Characteristic of the propensity to infections. Often noted pneumonia, even more leading to impaired renal function. A picture resembling bilateral pneumonia in x-ray examinations can give uremic lungs( bilateral focal blackouts coming from the lung ganglion, associated with left ventricular failure or increased transudation from pulmonary capillaries).

It is possible to establish the presence of chronic renal failure at the first contact with the patient on the basis of questioning( detection of nocturia, polyuria, complaints of skin itch, bleeding, dyspeptic signs) and examination( skin color, dryness, calculi, bruises, pericardial friction noise, characteristicammonia odor from the mouth).The detection of anemia and low relative density of urine confirms the diagnosis, as well as the detection of azotemia.

Difficulties can arise when delimiting irreversible CRF from transient renal failure caused by exacerbation of kidney disease. The above complaints( with the exception of hemorrhage) speak rather in favor of the terminal stage of renal failure( with pyelonephritis and SLE anemia may be a sign of the disease itself).A significant decrease in the size of the kidneys( a survey image, a tomogram, ultrasound) indicates the terminal stage of renal failure. It should be remembered that even with the current chronic renal failure, episodes of a sharp decrease in kidney function are possible, related to the influence of intercurrent infection, the fall of blood pressure, the addition of drug damage( interstitial nephritis, papillary necrosis), and the development of thrombosis of the kidney vessels.

The diagnosis of CRF in a patient without anamnestic indications of kidney disease is sometimes significantly delayed. This happens in those cases when the kidney disease proceeds for a long time without symptoms and the patient turns for the first time to the doctor only with the appearance of uremic intoxication, about dyspeptic phenomena, arterial hypertension, joint pain, bleeding. The main task of a doctor in this situation is to think about the presence of CRF with a subsequent relatively simple confirmation of this diagnosis.

Treatment with hemodialysis leads to an improvement in a number of vital signs related to the action of dialysable "uremic toxins".In particular, the skin itching decreases, dyspeptic phenomena disappear, encephalopathy, pericarditis, sodium-dependent arterial hypertension decreases. Anemia usually does not respond to hemodialysis treatment.

At the same time, there are some complications that occur rarely in the natural course of uremia. They include a cardiac tamponade( assumed with a sharp decrease in blood pressure, development of right ventricular failure), peripheral neuropathy( the first sign may be a painful burning sensation in the hands and feet, followed by developing numbness and weakness).Bone lesion - uremic osteodystrophy( fibrosing osteitis and / or osteomalacia) - is also more common in patients on hemodialysis. Finally, dialysis treatment with untreated water in some cases develops dialysis dementia, which is associated with the accumulation of aluminum in the brain.

Tubular dysfunctions( tubulopathies) form a group of nephropathies, the course of which is characterized by early partial or generalized damage to the tubular functions with normal or slightly decreased GFR.Tubular changes are primary;Glomerular lesions can develop at later stages of the disease and are secondary in nature.

Recall the main functions of the tubular kidney apparatus( including the proximal tubule, the nephron loop, the distal tubule and the collecting tubes):

Renal tubular diseases can be associated with a violation of any of these processes.

Syndromes of tubular dysfunction are more often hereditary and are observed in childhood, but adults often appear as a late recognized genetic disease or as an acquired defect in a number of kidney diseases( pyelonephritis, interstitial nephritis, glomerulonephritis with tubulointerstitial component, etc.) or with extrarenaldiseases( tumors, autoimmune diseases, etc.).

One of the main functions of the kidneys is participation in the regulation of the acid-base state of the body. The latter is carried out by active secretion of H + ions by tubular cells, which leads to a decrease in the pH of the urine.

In the cells of the proximal and distal sections of the tubules from CO2 and water, H + ions and HCO3 ions are formed. H + ions are actively secreted into the tubular fluid in exchange for Na + ions, which enter the cells passively, and the HCO3 ions diffuse into the plasma. The secreted H + ions in the lumen of the tubule interact with the filtered bicarbonate, forming carbonic acid. The resulting acid with the help of the enzyme carbonic anhydrase is dehydrated, and CO2 diffuses into the cell. Thus, the secretion of hydrogen ions is accompanied by the reabsorption of an equivalent amount of Na + and HCO3_ ions.

A significant part of the secreted H + ions is associated with anions of phosphates, weak acids and ammonia and is released as titratable acids and ammonium ions;Only a small amount is output as free H + ions.

When there is a violation of the secretion of H + ions and the reabsorption of bicarbonate( in conditions of a normal level of nitrogenous slags in the blood), renal tubular acidosis occurs. This clinical syndrome includes:

There are two types of renal tubular acidosis: distal tubular acidosis( type I, "classical") and proximal tubular acidosis( type II).

Disturbance of the ability of the kidney to acidify the urine in the distal nephron leads to the development of distal renal tubular acidosis( type I).Pathogenetically it is associated with the inability of the epithelium of the distal nephron to secrete H + ions in the lumen of the tubule or with the reverse diffusion of H + ions from the lumen of the tubule into the cell. In such patients, the pH of the urine does not fall below 6.0 regardless of the degree of systemic acidosis( and with ammonium chloride loading);while reabsorption of bicarbonates in the proximal tubules is not reduced. Systemic acidosis with a chain of metabolic disorders, leading to severe hypokalemia, hypercalciuria, develops. Excess of calcium in the urine creates the prerequisites for the formation of calcium stones, the development of nephrocalcinosis( at a pH of about 6.0 urinary excreted calcium becomes insoluble and precipitates easily).Nephrolithiasis is often the first sign of a disease.

The result of systemic acidosis is osteomalacia, often severe, accompanied by pain in the bones, pathological fractures. Anorexia, stiffness, muscle weakness, apathy, vomiting, polyuria, dehydration, weakness due to potassium loss, respiratory insufficiency, hyperventilation as a compensatory reaction to metabolic acidosis are possible.

Distal tubular acidosis can be an independent nosological form( Battler-Albright Syndrome).This is a hereditary disease transmitted autosomal dominant way. The first symptoms of the disease usually occur in the 2-3rd year of life, but they can appear for the first time in adults, and in this connection they distinguish the "adult" type of distal tubular acidosis. A complete clinical picture of the Buttler-Albright syndrome includes a delay in growth, muscle weakness( in severe cases up to paralysis), polyuria, osteomalacia in adults and rickets in children, nephrocalcinosis and nephrolithiasis with concomitant pyelonephritis or recurrent UTI.

In addition to the primary, genetically determined form, distal tubular acidosis may occur a second time in a number of autoimmune diseases:

Sometimes it is difficult to differentiate the primary distal tubular acidosis from the secondary, associated with urolithiasis or pyelonephritis. In these cases, some help can determine the excretion of calcium in the urine. In patients with genetically determined renal tubular acidosis, this indicator will be within the norm or increased, and in patients with acquired form of distal tubular acidosis, it is usually lowered. In addition, hypokalemia often occurs with a hereditary form of the disease.

Correction of distal tubular acidosis requires the introduction of small doses of bicarbonates( 1-3 mmol / kg / day), i.e.about 0.2 g of sodium bicarbonate per 1 kg of body weight.

This variant is characterized by a decrease in tubular reabsorption of bicarbonates with the preserved ability of the distal tubules to acidify urine. In this case, significant bicarbonaturia, high urine pH, hyperchloremic acidosis are determined. However, the ability of the distal tubules to acidify the urine remains, therefore, in severe systemic acidosis, the urine pH may still decrease, in contrast to the distal tubular acidosis.

Proximal acidosis, as well as distal acidosis, is accompanied by high potassium excretion.

The clinical spectrum of diseases accompanied by proximal acidosis is quite diverse and includes:

Proximal tubular acidosis, characterized by growth retardation, in rare cases, observed bone changes, gait disorders and bone pain due to calcium metabolism disorders, nephrocalcinosis, nephrolithiasis, hypokalemia, hypercalcemia, is one of the components of the Fanconi syndrome. Diagnostic test - determination of bicarbonates in the urine.

Treatment involves the administration of large doses of alkalis - up to 10 mmol / kg per day( ie about 1 g of sodium bicarbonate per 1 kg of body weight);smaller doses are ineffective. Assignable high doses of sodium bicarbonate can enhance the existing hypokalemia.

Disruption of glucose transport in the proximal part of the nephron leads to the development of renal glucosuria - one of the most frequent tubular dysfunctions. The diagnosis of renal glucosuria is based on the following symptoms:

To confirm the diagnosis, it is desirable to identify glucose using enzyme and chromatographic methods that make it possible to distinguish glucose from fructose, pentose, galactose. In some cases, the disease has a family, hereditary nature. Renal glucosuria can occur as an independent disease or be combined with other tubulopathies - aminoaciduria, phosphate-diabetes - and be one of the symptoms of Fanconi syndrome.

Isolated renal glucosuria is a benign disease that does not usually require special treatment, except for severe cases caused by significant sugar losses.

Differential diagnosis of isolated renal glucosuria with other tubular dysfunctions, accompanied by a violation of glucose reabsorption, and diabetes mellitus usually presents no difficulties.

Phosphate-diabetes( hypophosphatemic rickets) is a hereditary disease caused by a violation of the reabsorption of phosphorus in the proximal renal tubules;characterized by osteoporosis, osteomalacia, deformity of bones, unresponsive to usual doses of vitamin D, hypophosphatemia and high activity of alkaline phosphatase in the blood. The disease is hereditary, inherited by a recessive type, manifested usually in childhood.

The main clinical signs:

The disease must be suspected in cases when the treatment of rickets with usual doses of vitamin D( 2000-5000 IU / day) has no effect, and bone deformation progresses. It should be differentiated from other causes of rickets( vitamin D deficiency, malabsorption syndrome, renal tubular acidosis, Fanconi syndrome).

For treatment, large doses of vitamin D( 10,000-25,000 IU / day) are prescribed together with phosphates. When taking long doses of vitamin D for a long time, you should remember about the possibility of developing nephrocalcinosis.

Fanconi syndrome( more correctly - de Toni-Debreu-Fanconi syndrome) - generalized dysfunction of the proximal tubules, which are as follows:

In addition, Na +, K +, Ca2 + loss is observed, and uric acid clearance is increased with a decrease in serum levels.

Fanconi syndrome may be primary( hereditary or acquired), but more often secondary, developing in a number of common diseases.

The cause of Fanconi syndrome may be hereditary metabolic disorders( cystinosis, galactosemia, Wilson-Konovalov's disease), poisoning with toxic substances( for example, salicylates, tetracycline with expired shelf life) and heavy metals( lead, cadmium, bismuth, mercury), malignant neoplasmsmyeloma, lung disease, ovarian, liver, lung, pancreatic cancer), lymphogranulomatosis. Fanconi syndrome can also develop with certain kidney diseases, including viral etiology, hyperparathyroidism, paroxysmal nocturnal hemoglobinuria, severe burns.

Bone lesion( skeletal deformation, bone pain, fractures, diffuse osteomalacia), rickets develop in children, growth retardation. There may be polyuria, thirst, in rare cases, muscle weakness( up to paralysis), associated with hypokalemia, hypocalcemic convulsions. Infants are less resistant to infections.

Clinical signs may be absent;the diagnosis in such cases is based on laboratory data revealing a complex violation of tubular functions.

Despite the fact that in hereditary forms the first signs appear in childhood, the disease is sometimes recognized at an older age. There are no clinical or laboratory signs that distinguish the primary Fanconi syndrome from the secondary syndrome, therefore, in each case a thorough etiological search should be carried out.

Treatment is carried out in large doses of bicarbonates, citrate mixtures are prescribed, vitamin D, potassium preparations, potato-cabbage diet is indicated.

This syndrome, including polyuria with inability to concentrate urine and polydipsia, develops in the absence of response of the epithelial cells of the distal tubules and collecting tubules to ADH.Despite the normal concentration of biologically complete vasopressin( ADH) in the blood and normal osmolality of the plasma, a large amount of hypotonic urine is excreted. In severe cases, severe dehydration may develop( convulsions, fever, vomiting).

A test with vasopressin is used to confirm the diagnosis of vasopressin-resistant diabetes insipidus.

In treatment, the main place is given to the introduction of an adequate amount of fluid. Hydrochlorothiazide is also used;The latter, by inhibiting the reabsorption of sodium chloride in the ascending section of the nephron loop, reduces the production of osmotically free water. When taking hydrochlorothiazide should limit the intake of sodium and add potassium.

Kidney anomalies include a number of anatomical changes relating to the structure and position of the organ, and even its quantitative characteristics. Quantitative anomalies in the direction of increase are a doubling of the kidney( from one or both sides), as well as an additional kidney, in the direction of decrease - aplasia( that is, the absence of one kidney).The wrong anatomical position of the kidneys is a dystopia. An abnormal structure of the kidneys is dysplasia, as well as replacement of all or part of normal renal tissue with cystic formations - multicystosis and polycystic kidney disease.

Kidney Disease is the most common kidney anomaly. As a rule, most often it occurs in women. Doubling is one-sided or two-sided, as well as complete and incomplete. With a full doubling, there are two kidneys with two calyx-pelvis systems and two ureters, each of which is opened by a separate mouth in the bladder. With incomplete doubling, most often there is a fusion of the two ureters into one, which is respectively opened by one mouth in the bladder. Often such an anomaly is combined with any malformation of the ureter, as a result of which very often there arises vesico-ureteral-pelvis reflux, that is, a reverse transfer of urine from the bladder to the renal pelvis.

As a rule, with kidneys doubling there is a violation of urinary outflow for one reason or another, which very often leads to the development of chronic pyelonephritis and other diseases, including tuberculosis of the kidney. If, however, doubling of the kidney is detected by chance and there are no kidney diseases, the patient does not need treatment.

Aplasia - complete absence of the kidney. Aplasia of both kidneys is not compatible with life. Aplasia of one kidney is relatively common( 4-8% of all kidney anomalies), and in men it is 2 times more likely than in women. As a rule, it is impossible to detect the absence of one kidney without a special examination. The remaining single kidney completely takes upon itself all the "work", it is more functionally active and adapted to various kinds of negative influences, so the diseases develop less often in it. However, if the disease in a single kidney does occur, then it is difficult. This requires the use of the most sparing types of treatment, so it is very important to establish the presence of a single kidney in a timely manner. For these purposes, ultrasound, excretory urography, radioisotope examination is used.

Additional kidney - the presence in the body, in addition to a full two, another kidney. This is extremely rare. The size of the additional kidney is significantly reduced in comparison with the normal ones, as a rule, it is detected accidentally during examination on other occasions.

Dystopia is an abnormality of the position of the kidneys, which develops in the prenatal period due to impaired movement of the kidney from the pelvis into the lumbar region. As a rule, the dystopia is one-sided, and the kidney can stop at its level from the bottom upwards at any level. Extremely rare bilateral dystopia of the kidneys, which is accompanied by a cross between the ureters: the right ureter falls into the bladder on the left side, and the left - on the right. Distinguish pelvic, iliac and lumbar dystopia.

Most often, the main manifestation of dystopia in childhood is abdominal pain and digestive disorders. Dystopic kidney can be felt in the abdomen as a tumor-like formation. With lumbar dystopia, pain is localized in the lower back. Pelvic dystopia presents the greatest difficulties for diagnosis, because in this case the kidney is located in the men between the bladder in front and the rectum behind, in women between the uterus in front and the rectum behind. Such localization of the dystopic kidney can sometimes cause very intense pain in the lower abdomen, which can be mistaken for acute surgical pathology.

In dystopic kidneys pyelonephritis, hydronephrosis, urolithiasis can develop. In such cases, the treatment is carried out in accordance with the diagnosis. If the dystopic kidney is not affected by the disease, no treatment is required.

Kidney Dysplasia is a one-sided anomaly of the structure in which the kidney is greatly reduced in size, and its tissue is significantly different from normal and does not function. There are 2 types of dysplasia - a rudimentary kidney and a dwarf kidney. The rudimentary kidney stops in its development during the intrauterine period. In place of the organ, a connective tissue formation of 1-3 cm in size is found, in which, under a special examination, the remains of underdeveloped glomeruli and tubules are found under the microscope.

The dwarf kidney is slightly larger - 2-5 cm, in its tissue the number of glomeruli is significantly reduced, and the surrounding connective tissue, on the contrary, is developed excessively.

The anomalies of the structure also include multicystosis and polycystic kidney disease. Bilateral multicystosis is incompatible with life, because such a kidney consists of immature and inefficient, stagnant nephrons and a number of cysts filled with fluid. In the presence of unilateral multicystosis, the function of the affected kidney is taken by the second, remaining normal. Multicystosis occurs with some unknown failure in the intrauterine period of development. In contrast, polycystosis is a hereditary disease, which should be discussed separately.

Polycystic kidney disease is a congenital hereditary disease characterized by the presence in both kidneys of multiple cyst-globular extensions in the tubules, the wall of the glomerulus capsule, the collecting tubules. There are 2 main forms of the disease: infant( transmitted by autosomal recessive type) and polycystic kidneys of adults( transmitted by autosomal dominant type).

The reason for the development of any form of polycystosis is not completely clear. It is known that in polycystic adults the mutation of one of the genes located in the 16th chromosome occurs, as a result of which the normally formed renal tissue undergoes the formation of a number of cysts. Cysts can grow in size with age. And, of course, these areas of kidney tissue are not able to perform their natural functions. In the future, the conditions of activity of the remaining renal tissue remain normal. They are squeezed by growing cysts, in addition, very often an infection is attached, chronic pyelonephritis is formed, which in most cases leads to the development of renal failure.

Infant form of polycystic is rare, than polycystosis of the kidneys of adults. Difference of this disease is the location of cysts only in tubules and collecting tubes, and the kidney can grow in size, but retains its characteristic shape. Besides the kidneys, the liver suffers. There the bile ducts expand, it is possible the development of periportal fibrosis. As a result, the portal vein suffers, portal hypertension arises - increased pressure in the vein, which leads to an increase in the size of the liver and spleen, as well as bleeding from varicose veins of the esophagus. The predominance of liver symptoms is characteristic of the later development of the disease, whereas in infancy, the signs of kidney damage are in the foreground. The earlier the disease manifested itself, the worse the prognosis. Survive only 50% of newborn children who developed polycystic.

Hepatic disturbances are not noticed in all, they are often detected in case of accidental examination. The development of the terminal stage of renal failure in all children with the infantile form of polycystosis is usually observed at an older age, and in 50% of cases - in adolescence.

Polycystic kidney disease occurs usually after 20 and even 30 years. There are other differences from the infant form of the disease. For example, all parts of the nephron undergo a cystic change, and not just tubules and collecting tubes. As a result, the contour of the kidney changes, becomes bumpy, irregular. An important difference is also the presence of cysts in other organs and tissues. It is believed that polycystic disease is a systemic disease in which the liver is affected( most often), the pancreas, the spleen, the arachnoid membrane of the brain, the thyroid gland of the testicles, the seminal vesicles and the ovaries. In all these organs there are also cystic changes. In addition, there may be an aneurysm in the vessels of the brain, the so-called berry-shaped form.

Despite the fact that the first signs of the disease can be detected in patients older than 20-30 years, the unfolded stage of polycystic kidneys of adults and, accordingly, the main complaints fall at the age of 45-55 years. More than half of all patients notice pain in the lumbar region or in the side, which arise as a result of the dilatation of the renal capsule with increasing volume of cysts. The appearance of erythrocytes in the urine( sometimes to the degree of macrohematuria) is noted in a third of patients as the first manifestation of the disease. Macrogematuria is usually caused by bleeding in the cyst. A persistent increase in blood pressure occurs in most patients, with the frequency of hypertension increasing with an increase in impaired renal function. This is associated with the activation of the renin-angiotensin system, since compression of normal renal tissue with cysts leads to the appearance of a relative oxygen deficiency in it.

Urolithiasis with its characteristic manifestations is observed in about a fifth of all patients. Significantly more often( 50-60%), especially in women( 90%), the signs of recurrent urinary infection come to the forefront.

The development of pyelonephritis adversely affects the functional state of the preserved renal tissue, usually at the age of 60 in such patients there are symptoms of chronic renal failure( CRF), which is particularly unfavorable for women. Among them, at this age in half of the cases, the phenomena of the terminal stage of CRF are already observed.

Urine in patients with polycystic kidney disease is most often detected erythrocytes( microhematuria), leukocytes and bacteria, the protein usually does not exceed 1 g per day, the relative density of urine is low, indicating a violation of the concentration ability of the kidneys. In the blood, anemia is usually noted, and with the appearance of unfolded stages of chronic renal failure - signs of azotemia.

Ultrasound can help to detect polycystic kidney disease with a high degree of reliability, but more informative is computerized tomography, which determines both the increase in the size of the kidneys, and the presence of a multitude of cysts in them, as well as changes in the bowl-pelvic apparatus. Excretory urography also makes it possible to determine the characteristic signs of cystic changes in both kidneys with a violation of the contours of their collection systems, but these results are often questionable, and still require an additional CT scan.

Since polycystosis is most often detected already in the stage of complications, the treatment is aimed at individual correction of various manifestations of the disease. Primarily, a full-fledged treatment of urinary infections( pyelonephritis, etc.).With persistent renal hypertension, drugs that reduce blood pressure are prescribed. Among them, preference is given to a group of ACE inhibitors( kapoten, enam, enap, etc.).With the development of the terminal stage of renal failure, patients need hemodialysis and kidney transplantation. Surgical methods of treatment( the so-called cyst decompression, or percutaneous aspiration of their contents) can not significantly improve the course of the disease and delay the appearance of signs of renal failure.

Before discussing the future of kidney disease, it is necessary to note this detail: based on the characteristics of the structure of the kidneys, doctors allocate diseases that primarily affect the glomerular part of the nephron and the collecting system - calyx and pelvis( pyelonephritis, urolithiasis).Traditionally, glomerulonephritis is treated by nephrologists, and diseases of the collecting system are urologists. We will look at both of them in turn.

Glomerulonephritis is a group of diseases in which the glomerular part of the nephron suffers. Isolate acute, subacute and chronic glomerulonephritis.

Acute glomerulonephritis is a serious kidney disease, which basically has damage mainly to the glomerular apparatus of the immune-inflammatory nature.

Here, special attention should be paid to the word "immunoinflammatory".In this context, it means that inflammation in the kidneys develops due to impaired immunity. As a rule, most of us associate immunity disorders with its decrease, that is, low reactivity. However, in the case of acute glomerulonephritis, there is, on the contrary, a sharply increased activity of the immune system, which we know by another "name" - an allergy.

Allergen or a provoking factor in the development of acute glomerulonephritis in most cases is beta-hemolytic streptococcus of group A, the same streptococcus, which is the causative agent of angina, chronic tonsillitis, otitis, maxillary sinusitis, furunculosis and other forms of local streptococcal infection. In other words, first develops, for example, angina, and then, again, in the body with altered immunity and allergic mood, glomerulonephritis occurs.

In some cases, other bacteria instead of streptococci lead to the development of the disease - pneumococci, staphylococci, etc. In addition to them, various viruses, in particular hepatitis B, herpes, rubella, infectious mononucleosis, adenoviruses can contribute to damage to the kidney tissue.

Less common among the causes of acute glomerulonephritis are non-infectious factors that also act like allergens and lead to a significant restructuring of the immune system. Among them we can note the repeated introduction of vaccines or serums, bee or snake bites, intoxications with alcohol, organic solvents, mercury, lithium, etc.

Predisposing factors for the development of the disease are hypothermia, especially in conditions of high humidity, surgery, trauma, excessive physical exertion.

What happens in the nephron before the onset of the disease? Initially, streptococcal toxins slightly damage the wall of the capillaries in the glomeruli, and as a result of the reaction of the immune system, specific autoantigens and antibodies arise. Then the acute streptococcal infection passes, and the antibodies remain. And with repeated exposure to infection( eg exacerbation of chronic tonsillitis) or the influence of other unfavorable factors of a nonspecific nature - most often hypothermia - a violent allergic reaction develops. It leads to the development of acute inflammation in the glomeruli of the kidneys. This inflammation is not directly associated with streptococcal or other infection, it is caused by the malfunction of the immune system due to its allergic alteration. Damaged in the first place are the smallest suction vessels - the capillaries of the renal glomeruli, and as a result, the entire organ is disrupted, as all nephrons of both kidneys suffer equally. Blood can not flow normally through the affected glomeruli, the walls of the capillaries become more permeable, the Bowman capsule can not fully function, and proteins and blood elements( mainly leukocytes and erythrocytes) enter the final urine. In the renal capillaries are formed microblots of blood, as a result, for a certain period of time the kidneys cease to perform their functions and remove nitrogen slag from the body, so the disease is characterized by severe intoxication due to self-poisoning of the body. However, we will talk about the main symptoms of acute glomerulonephritis below.

Acute glomerulonephritis develops, as a rule, 1-3 weeks after the effect of the causative factor. Most often, the disease is characterized by the presence of 3 main symptoms: pressure, swelling and changes in the urine. This course of the disease is recognized as classical. For him, acute( sudden) onset, as well as complaints of weakness, thirst, headache, pain in the lumbar region, nausea, vomiting are typical. The urine thus acquires a reddish tint - the so-called color of "meat slops".The patient's skin becomes pale, swelling( "bags") is expressed under the eyes, blood pressure does not usually exceed 150/90 mm Hg. Art.(at a rate of 120/80 mm Hg), but can reach the figures of 180/120 mm Hg. Art.and higher. During this period, special attention should be paid to the reduction in the volume of urine that is separated from the usual amount of fluid consumed. This indicates a violation of the main function of the kidneys.

As a result of the accumulation of fluid in the body there are swelling. Edema in acute glomerulonephritis can be very common, fluid accumulates in the abdominal cavity( ascites), in the thoracic cavity( hydrothorax), less often in the heart bag( hydropericardium).However, in a number of cases, so-called latent edema can occur, which can be detected only when taking into account the drunk and secreted fluid and careful weighing of the patient.

In the future, the patient's health worsens, intoxication with nitrogenous slags increases, which is accompanied by an increase in the blood plasma of residual nitrogen and potassium levels. However, the relative density of urine with a decrease in its daily amount remains quite high( up to 1030), indicating a preserved concentration of kidney function. If the specific gravity of urine decreases significantly on the background of a pronounced decrease in its volume for more than 2-3 days, there is a high probability of acute renal failure, which requires emergency measures. The decrease in daily urinary secretion of less than 500 ml / day is also an indicator of the development of acute renal failure.

Intoxication with nitrogenous slags and violation of water-salt metabolism lead to deterioration of the patient's condition. He becomes sluggish, does not move, he has spontaneous muscle twitchings, a decrease in heart rate. Perhaps the development of convulsive syndrome( renal eclampsia) and acute heart failure.

Due to the presence of a high level of potassium in the blood, the development of cardiac rhythm disturbances, including flickering and fluttering of the atria and ventricles, is a particular danger, which can cause death.

In urine, a protein is usually determined, the amount of which can vary from trace to 3 grams per day or more. In addition, in large quantities there are erythrocytes, rarely cylinders( hyaline, granular, erythrocyte), epithelial cells. In the blood, the level of leukocytes and ESR, immunoglobulins, as well as residual nitrogen( nitrogenous slags) and potassium was increased.

With a positive outcome of the disease after a while, the daily volume of urine gradually increases, the period of polyuria begins, when the kidneys begin to actively work, and the body is finally freed of toxins. However, improving the patient's well-being, as well as a full recovery of all renal functions, is very slow. Recovery period after acute acute glomerulonephritis lasts at least one year. About full recovery of the patient can speak only after 3-5 years with a complete absence of complaints and normal laboratory indicators. If laboratory and other signs of glomerulonephritis persist during the year, it is believed that the disease has become chronic.

In addition to the typical, classical course of acute glomerulonephritis, the disease can also appear in an atypical form. It is characterized by the presence of only changes in the urine, whereas edema and increased blood pressure are not always present and if present, are poorly expressed. When the urinary sediment is examined, a moderate amount of protein, erythrocytes, and cylinders is detected. The patients feel moderately sick, however, this variant of the disease course most often tends to chronize the process and form a chronic glomerulonephritis.

Another variant of acute glomerulonephritis - nephrotic - is characterized by massive swelling( up to anasarca, a common swelling of the whole body and its cavities).At the same time, blood pressure rises slightly. In the study of urine, a significant amount of protein and few red blood cells are detected, and in the blood, in addition to the changes typical for glomerulonephritis, a decrease in the total amount of protein and an imbalance of its fractions, as well as an increase in cholesterol level, are revealed. The nephrotic variant of the disease is characterized by persistent and prolonged course( 6 to 12 months) and also a tendency to transition to a chronic form.

A severe complication of acute glomerulonephritis is renal eclampsia. After a cry or a deep sigh, the patient begins to have convulsions of skeletal muscles, respiratory muscles and diaphragm. Consciousness is lost completely, pallor and cyanosis of the face and neck, swelling of the cervical veins, dilated pupils are noted. Breath noisy, snoring, from the mouth follows pink foam( due to the bite of the tongue).The pulse is rare and tense, blood pressure reaches high figures, muscles are hard, as if petrified. Seizures can last from a few seconds to 2-3 minutes, after which the consciousness is usually restored, but the patients do not remember what happened, are long slowed down, sleepy. During the day, repeated seizures can be repeated. The outcome can be hemorrhages in the brain, which even with adequate resuscitation measures cause irreversible consequences and death of the patient.

A patient with acute glomerulonephritis should be treated only in a nephrological or therapeutic department of a hospital. For a period of not less than 2-4 weeks, a strict bed rest is prescribed. Of great importance is therapeutic nutrition. Since everyone knows that salty food contributes to edema even in healthy people, patients with acute glomerulonephritis are prescribed a salt-free diet with the exception of table salt, during the recovery period the amount of salt is limited to 72 teaspoons per day. At the same time, food for the patient is prepared without salt at all, then it is dosed.

Given that nitrogenous slags are in fact a product of protein breakdown, the intake of food protein in the body is also limited to 1 g per kilogram of the patient's weight per day, and in severe cases to 0.5-0.6 g / kg inday. In the acute period, preference is given to milk proteins( sour cream, cream, cottage cheese, dairy products), while meat, fish and eggs are introduced into the diet gradually, as they recover, and in very small quantities. Predominantly the needs of the patient in the diet are met by the high-calorie carbohydrate food. The fluid is limited to 800 ml per day, with severe swelling - up to 400-600 ml per day.

During the recovery period, the diet expands somewhat, the liquid is allowed in a volume of 1-1.2 liters per day. However, products and dishes containing extractive substances are completely excluded: meat, fish and mushroom broths, fried meat and fish, refractory fats( beef, pork, mutton), drinks that excite the central nervous system are restricted - strong tea, coffee, cocoa, andalso beer and alcohol.

In the recovery period, the following foods and dishes are allowed to enter the diet:

As an additional source of vitamins, a decoction of hips, fresh fruits, vegetables, berries, berry and fruit juices is used. It is recommended to take food 4-5 times a day.

Currently, individual approach to each patient is applied in treatment. If a direct relationship between the disease and streptococcal infection is proved with an insignificant time interval between the latter and the development of a typical glomerulonephritis pattern, antibacterial agents, antibiotics of the penicillin series( ampicillin, amoxicap, etc.) are used in optimal therapeutic doses for 10-14 days. Contraindicated nephrotoxic drugs, negatively affecting the function of the kidneys( for example, gentamicin), as well as the means of the nitrofuran series( furagin, furadonin, etc.) and sulfonamides.

In parallel to suppress allergic inflammation, non-steroidal anti-inflammatory drugs - indomethacin, voltaren, etc. - 25 mg 4-6 times a day for 4-8 weeks are used, but they are ineffective in the nephrotic form of acute glomerulonephritis. In this case it is necessary to resort to the most powerful anti-inflammatory drugs to date - analogues of the hormones of the adrenal cortex - glucocorticosteroids. These remedies are also used in cases of protracted disease and the low effectiveness of other treatments. Most often, prednisolone is used in a daily dose of 60-80 mg for 3-4 weeks.

Begin the introduction of the drug with a dose of 10-20 mg and gradually increase it to an effective dose, also arrive before drug withdrawal, gradually reducing the dose of 2.5-5 mg every 2-3 days to avoid the so-called withdrawal and deterioration of the patient. The total duration of prednisolone is 4-6 weeks. In the absence of effect or development of complications, stronger drugs that suppress the excessive activity of the immune system are used, such as immunosuppressants, for example, imarant( azathioprine) in a daily dose of 2-3 mg / kg of body weight, cyclophosphamide at 1.5-2 mg / kg. Treatment with these drugs is conducted up to 8-10 weeks under the control of blood indicators. You can use the preparations of the aminoquinoline series( delagil, plakvenil) in a daily dose of 0.5-0.75 g in a course of 3-6 weeks, with the best effect achieved when combined with indomethacin( methindol).

To improve blood circulation in the kidneys use drugs that reduce blood clotting, the so-called anticoagulants( heparin) and antiaggregants( quarantil).Heparin in a daily dose of 20 to 40 thousand ED is administered subcutaneously for 5-10 thousand units every 4 to 6 hours, the course is from 3 to 10 weeks under the control of blood coagulability. Curantyl( dipyridamole) in a dose of 200-400 mg / day, 6-8 weeks course is often prescribed in combination with anticoagulants( heparin) or with indomethacin. To reduce the severity of allergies used antihistamine( antiallergic) drugs( suprastin, tavegil), in addition, apply ascorbic acid, rutin, calcium preparations.

To eliminate edema in acute glomerulonephritis diuretics are used( diuretics), with increased pressure - antihypertensive agents, usually use a combination of calcium antagonists( nifedipine, corinfar, cordafen) with furosemide( lasix).With a slight increase in blood pressure, you can use antispasmodics( dibazol, papaverine, but-shpu).For the treatment of edematous syndrome, furosemide( 40-80-120 mg / day) or a combination of 2-3 diuretic drugs is used. Long-term use of diuretics requires the appointment of corrective doses of potassium preparations.

In the development of complications( heart failure, eclampsia, acute renal failure), treatment is performed in the intensive care unit. In acute heart failure, cardiac glycosides( strophanthin, korglikon), intravenous euphyllin, diuretic( intramuscular or intravenous lasix) are prescribed.

In eclampsia, a complex of emergency measures is used: intravenously, euphyllin, dibazol, lasix, mannitol, magnesium sulfate, hexonium or pentamine, aminazine, concentrated glucose solution;microclysters with chloral hydrate;In severe cases, tracheal intubation and inhalation anesthesia are indicated.

Chronic glomerulonephritis is an immune-inflammatory kidney disease with a primary glomerular lesion characterized by a steadily progressing course with an outcome in chronic renal failure. The variant of the disease course is subacute malignant glomerulonephritis, which is resistant to treatment and quickly leads to an unfavorable outcome.

The causes and mechanism of the development of chronic glomerulonephritis differ little from the acute form, often there is a transition of an acute disease to a chronic one under the repeated action of various adverse factors, with insufficient or untimely treatment, and against the background of a changed reactivity of the immune system. That is, there is any preliminary allergic mood of the body. In connection with the last factor in the development of chronic glomerulonephritis, more pronounced immune-inflammatory mechanisms dominate, leading to self-progression of the process. Unlike acute glomerulonephritis, the chronic form of the disease affects not only the glomeruli, but also tubules, which suffer from prolonged release of protein. Other structural elements of the kidney are involved in the chronic inflammatory process, and the glomeruli themselves are damaged additionally as a result of developing arterial hypertension and the constantly increasing burden on the nephrons that retained the function.

The nature of subacute( malignant) glomerulonephritis remains unclear. It can develop after a streptococcal infection, bacterial endocarditis, systemic lupus erythematosus, abscesses of various locations, viral infections, therefore in most cases it is regarded as an autoimmune process.

Chronic glomerulonephritis can occur in various forms, among which latent, nephrotic, hypertensive, hematuric and mixed are isolated. The latent form of the disease progression is characterized by periodically arising changes in urinalysis in the absence of other extrarenal signs of the disease.

The nephrotic form is generally similar to the nephrotic variant of acute glomerulonephritis with massive swelling, large amounts of protein in the urine and high cholesterol.

In the hypertensive form of the disease, persistent and non-compensable high blood pressure comes to the fore. The hematuric form is characterized by the predominance in the urinary sediment of erythrocytes in large quantities. In the mixed form of chronic glomerulonephritis, various renal and extrarenal manifestations of the disease may be present.

The latent form of chronic glomerulonephritis occurs with a satisfactory general condition of the patient. This is the most favorable form of the disease, since the most negative extrarenal signs of glomerulonephritis are edema, an increase in blood pressure, changes in the fundus are absent. In the study of urinary sediment, a moderate amount of protein is detected-no more than 1-2 g per day, a small amount of erythrocytes and cylinders, the specific gravity of urine remains quite high.

The nephrotic form of chronic glomerulonephritis differs marked edematic syndrome. The patient is concerned about weakness, decreased appetite, edema, up to the development of ascites and dropsy. Blood pressure can be increased( unstable).When studying urine, a significant number of cylinders are detected, a small amount of erythrocytes( small amount) can be noted, and protein losses amount to 4-5 g per day or more. In the general analysis of blood, there is an increase in ESR, anemia, in the biochemical blood test - a marked decrease in the total protein and an imbalance of protein fractions with predominance of alpha and beta globulins, as well as high cholesterol.

The hypertonic form of chronic glomerulonephritis is characterized by an early and persistent increase in blood pressure( unlike the symptomatic hypertension that occurs with any form of glomerulonephritis with the addition of signs of chronic kidney failure).Patients are concerned about persistent headaches, flickering "flies" or fog in front of the eyes, reduced visual acuity. Arterial pressure often rises moderately( up to 160/100 mm Hg), less often up to 180/110 mm Hg.st., but in some cases can reach 200 / 115-250 / 120 mm Hg. Art. In the future, there are complaints of pain in the heart, dyspnea, palpitations. From this moment, signs of hypertrophy of the left ventricle of the heart are recorded clinically, radiological and by ECG results. When examining the fundus, various degrees of changes in the retinal vessels are noted, and retinopathy later develops. In this case, a small amount of protein, erythrocytes, is noted in the general analysis of urine. The density of urine decreases rather quickly, like glomerular filtration. The hypertonic form of chronic glomerulonephritis can be complicated by left ventricular heart failure. This is one of the unfavorable forms of the disease, which quickly leads to chronic kidney failure.

The hematuric form of chronic glomerulonephritis is manifested by the constant presence of urinary sediment of a significant( sometimes very significant) amount of red blood cells. Protein, by contrast, is small, there is no edema, blood pressure does not increase. The hematuric variant of chronic glomerulonephritis is considered as a diagnosis only after excluding all other possible causes of bleeding from the urinary tract. In general, this is also a favorable variant of the course of the disease.

Mixed form of chronic glomerulonephritis is characterized by a combination of nephrotic and hypertensive forms. These signs can appear both simultaneously and sequentially. There are marked swelling, biochemical changes in blood, characteristic of nephrotic form, as well as persistent increase in blood pressure. This is the most severe form of chronic glomerulonephritis.

During any variant of chronic glomerulonephritis, the stage of exacerbation is distinguished, which is usually characterized by the signs typical for the corresponding form of acute glomerulonephritis, and the stage of remission, during which there is insignificant hematuria and proteinuria, stabilization of arterial pressure and minimal biochemical changes in blood serum.

The course of chronic glomerulonephritis is usually benign, that is, the disease progresses slowly and irreversible changes in the kidneys develop over the years. This is typical of latent, hematological and partially hypertensive forms. In addition, a fast-progressing course of the disease with frequent exacerbations and an average period of development of chronic renal failure is 3-5 years.

The special form of glomerulonephritis is subacute malignant glomerulonephritis, which is characterized by extremely rapid progression, the formation of renal failure and death within 2 years from the onset of the disease. The disease begins as acute glomerulonephritis, but after 4-6 weeks, there are signs of nephrotic syndrome and hypertension, a decrease in the density of urine( according to Zimnitsky's trial), the growth of nitrogenous slags and cholesterol in the blood. Patients complain of general weakness, headache, decreased vision, pain in the heart, swelling, increased blood pressure. Pale skin, early decrease in urination is noted. In the general blood test, anemia, high leukocyte count, and an increase in ESR are noted. In the blood serum - increased content of nitrogenous slags, an imbalance of protein fractions with a decrease in albumins and an increase in globulins, mainly due to gamma fractions, increased cholesterol and other changes. In the general analysis of urine - a consistently high amount of protein, erythrocytes, cylinders. The specific gravity of urine is low, the glomerular filtration progressively decreases, which is an indicator of the development of chronic renal failure.

Chronic glomerulonephritis in children, as in adults, is characterized by a cyclic course with a change in periods of exacerbation and remission. There are 3 main forms of the course of this disease:

You can talk about recovery in chronic glomerulonephritis with complete well-being in the child's condition and its laboratory tests for at least 5 years.

Treatment of chronic glomerulonephritis is continuous, but the choice of methods and medications is carried out individually, depending on the form and stage of the disease. During the exacerbation of the disease, treatment is performed only in conditions of a specialized nephrological or therapeutic department of the hospital. The diet should provide for the correction of the amount of protein, liquid and table salt, depending on the variant of the course of the disease. General dietary recommendations include the elimination of all foods that can cause allergies( citrus fruits, except lemons, chocolate, greenhouse vegetables, honey, strawberries, raspberries, etc.), and foods that already havean allergy in this patient. In addition, the use of fried foods is limited, preference is given to products in boiled, stewed or baked form. Also, smoked and marinades, rich broths and the following vegetables are completely excluded: radish, radish, spinach and sorrel. Diet in the period of remission should be full and provide the body's needs for protein, fats and carbohydrates, as well as vitamins and trace elements.

During the period of exacerbation of the disease, it is recommended to observe strict bed rest for a period of 3 to 6 weeks( until the patient's condition improves).From medicines the same groups of agents are used as with the corresponding form of acute glomerulonephritis: glucocorticosteroids, cytostatics, antimetabolites, anticoagulants, antiaggregants. All these agents to some extent change the immune status of the body, which allows to suppress the inflammatory-allergic reactions underlying the damage to the kidney tissue. In addition, diuretics and hypotensive( pressure-lowering) drugs are used to influence the main symptoms of the disease, an important role is played by antiallergic drugs, high doses of vitamin C.

Non-steroidal anti-inflammatory drugs( indomethacin, voltaren) are contraindicated in the hypertensive form of chronic glomerulonephritis and decreased kidney function,their effectiveness is low and with other forms of the disease, so these funds are used only in combination with anticoagulants and antiaggregants.

Corticosteroids are effective in the nephrotic form of chronic glomerulonephritis and are not indicated in hypertensive and mixed forms. A treatment regimen is used with long-term administration( several months) of maintenance doses( 10-20 mg / day in terms of prednisolone) after the usual course of treatment according to standard inpatient regimens. In extremely severe disease, corticosteroids are administered in very high doses intravenously( the so-called pulse therapy).

Cytotoxic drugs are used in nephrotic and mixed forms, usually as part of complex therapy. Anticoagulants and antiaggregants are also used in these forms, both alone and in combination with cytostatics and corticosteroids. Preparations of the aminoquinoline series( delagil, plaquenil) are effective in latent form with isolated urinary syndrome, in the remaining cases they act weakly.

In severe and refractory flow of chronic glomerulonephritis, plasmapheresis is used according to the usual scheme - 3-5 sessions with a frequency of 1-2 times a week.

Treatment of patients with subacute malignant glomerulonephritis is carried out in a complex manner, using a combination of corticosteroid drugs( if necessary - in the form of pulse therapy), anticoagulants( heparin), antiplatelet agents( quarantil, dipyridamole) and cytostatics( azathioprine, cyclophosphamide, etc.), as well as plasmapheresis.

At an early start, it is considered possible to slow the progression of the disease and increase the life expectancy of patients, but the prognosis remains disappointing.

In the treatment of chronic glomerulonephritis, phytotherapy is widely used, the rich arsenal of which allows diversifying effects on the course of the disease. It is important to regularly use herbal teas and teas to prolong remission or to achieve it as soon as possible. The replacement of one collection by another is carried out once a month.

Below is the composition of some fees that have anti-inflammatory, anti-allergic and diuretic effects.

Collection No. 1

Seed flax seed - 4 parts, root of the stalker - leaves, a sheet of birch white - 3 parts.

Collection No. 2

A sheet of wild strawberry - 1 part, nettle grass - 1 part, a birch leaf layer - 2 parts, a flax seed - 5 parts.

Collection No. 3

Leaf of birch white - 4 parts, sweet potato grass - 2 parts, leaf of strawberry forest - 3 parts, goose foot grass - 3 parts, flax seed - 3 parts, peppermint leaf - 1 part, rhizomes and licorice roots- 4 parts, grass swamp grass - 6 parts, the grass of the violet tricolor - 2 parts, the grass of the clear-eyed white - 4 parts.

Showing and charges with mixed effect.

Gathering No. 4

Watermelon rind - 3 parts, blackberry flowers - 2 parts, sweet clover grass - 3 parts, common oregano grass - 4 parts, St. John's wort - 3 parts, flax seed - 1 part, mother-and-Stepmothers - 3 parts, a sheet of peppermint - 2 parts, a herb of the motherwort five-lobed - 7 parts, cinnamon - 2 parts.

Collection № 5

Kidney tea - 1 part, a leaf of a plantain of the big - 1 part, a grass of a yarrow ordinary - 1 part, flowers of a calendula - 2 parts, a grass of a sequence of tripartite - 1 part, cinnamon - 1 part.