• Renal Failure Symptoms

    Distinguish between acute and chronic renal failure.
    Acute renal failure( ARF) is a sudden impairment of renal function with a delay in excretion of nitrogen metabolism products 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. How to apply traditional medicine with this disease look here.

    Acute renal failure occurs when both kidneys suddenly stop functioning. Kidneys regulate the balance of chemicals and fluids in the body and filter waste from the blood, removing them into the urine. Acute kidney failure can occur for various reasons, including kidney disease, partial or complete blockage of the urinary tract and a decrease in blood volume, for example, after a severe loss of blood. Symptoms can develop for several days: the amount of urine output can drastically decrease, and the fluid that must be eliminated accumulates entirely in the tissues, causing weight gain and swelling, especially at the ankles.

    Acute renal failure is a life-threatening disease because excessive amounts of water, minerals( in particular potassium) and wastes that are usually excreted by the bundles into the urine accumulate in the body. The disease is usually well treatable;the function of the kidneys can be completely restored after a few days or weeks, if the cause is correctly determined and the appropriate treatment is prescribed. However acute renal failure because of kidney disease can sometimes lead to chronic kidney failure, in which case the prospect of the disease depends on the ability to cure the underlying disease.

    Currently, several etiological groups of arthritis are distinguished.

    • Prerenal arrester( ischemic)

    • Renal arrester.

    • Emergency arresters.

    Symptoms of

    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, the 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 recovery period of diuresis. 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 OPN 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 that 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 the restoration of diuresis due to severe polyuria, there is also a risk of severe complications, especially in connection with developing electrolyte disorders( hypokalemia, etc.).

    In the clinical picture of acute renal failure, 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 the condition of the patient with ARF, the most important are the parameters of nitrogen metabolism, especially creatinine, the level of which 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.

    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 due to the action of various toxic factors, first of all a number of chemical, medicinal( sulfanilamides, mercury compounds, antibiotics) and radiocontrast 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 the 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 arthritis, arthritis with obstetric-gynecological pathology( abortion, complications of pregnancy and childbirth), arthrosis due to 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 arthritis are characterized by a number of general mechanisms:

    The resulting morphological changes concern mainly the tubular apparatus of the kidneys, primarily the proximal tubules, and are represented by dystrophy, often with 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 the above 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 prevailing in hemolytic-uremic syndrome.

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

    Hepatorenal syndrome is a variant of acute functional renal failure developing 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.

    • Treatment of a disease that can be the cause of acute renal failure.

    Chronic renal failure( CRF) is a renal dysfunction caused by a significant decrease in the number of adequately functioning nephrons and leading to self-poisoning of the body with products of its own vital activity.

    Chronic renal failure is observed when both kidneys gradually stop functioning. In the kidneys there are numerous tiny structures( glomeruli) that filter waste from the blood and store large substances such as proteins in it. Unnecessary substances and excess water accumulate in the bladder and then are excreted in the form of urine. In chronic renal failure, the kidneys are damaged gradually over many months or years. Since the kidney tissue is destroyed as a result of damage or inflammation, the remaining healthy tissue compensates for its work. Additional work leads to overloading of previously undamaged parts of the kidney, causing even more damage until the entire kidney ceases to function( a condition known as the final stage of kidney failure).

    Kidneys have a great safety margin;more than 80-90 percent of the kidney may be damaged before symptoms appear( although symptoms may appear earlier if the weakened kidney is subjected to sudden stress, such as infection, dehydration or the use of a drug that has a destructive effect on the kidneys).As excessive amounts of liquid, potassium type minerals, acids and waste accumulate in the body, chronic renal failure becomes life-threatening disease. However, if the underlying disease is cured and further damage to the kidneys can be controlled, the onset of the final stage of renal failure may be delayed. At the terminal stage, renal failure is treated with dialysis or kidney transplant;any of these ways can prolong life and allow a person to lead a normal life.

    Various diseases and kidney disorders can lead to the development of chronic renal failure. These include chronic glomerulonephritis, chronic pyelonephritis, polycystic kidney, renal tuberculosis, amyloidosis, as well as hydronephrosis due to the presence of various obstacles to the outflow of urine.

    In addition, CRF can occur not only due to kidney disease, but also for other reasons. Among them, we can note the diseases of the cardiovascular system - arterial hypertension, stenosis of the renal arteries;endocrine system - sugar and diabetes insipidus, hyperparathyroidism. The cause of CRF can serve as a systemic disease of connective tissue - systemic lupus erythematosus, scleroderma, etc., rheumatoid arthritis, hemorrhagic vasculitis.

    It should be noted that, regardless of the cause, chronic renal failure is associated, on the one hand, with a decrease in the number of active nephrons and, on the other hand, a decrease in working activity in the nephron. External manifestations of CRF, as well as laboratory signs of renal insufficiency, begin to be revealed with the loss of 65-75% of nephrons. However, the kidneys have amazing reserve capabilities, because the vital activity of the body is preserved even with the death of 90% of nephrons. Compensation mechanisms include increased activity of surviving nephrons and adaptive restructuring of all other organs and systems.

    The ongoing process of nephron death causes a number of disorders, primarily of an exchange character, on which the patient's condition depends. These include violations of water-salt metabolism, delay in the body products of its vital activity, organic acids, phenolic compounds and other substances.

    A characteristic feature of CRF is an increase in the volume of excreted urine - polyuria, which occurs even in the early stages with the primary damage to the tubular nephron. In this case, polyuria is of a permanent nature even when the fluid intake is restricted.

    Disorders of salt metabolism in CRF affect, primarily, sodium, potassium, calcium, phosphorus. Excretion of sodium in urine can be either increased or decreased. Potassium is normally excreted mainly by the kidneys( 95%), so in chronic renal failure, potassium can accumulate in the body, despite the fact that the intestine takes over the function of removing it. Calcium, on the contrary, is lost, so in his blood with chronic renal failure it is not enough. In addition to water-salt imbalance, the following factors play an important role in the mechanism of CRF development:

    • impaired renal excretion results in a delay in the products of nitrogen metabolism( urea, uric acid, creatinine, amino acids, phosphates, sulfates, phenols), which are toxic to all organsand tissues and, first of all, for the nervous system;

    • impairment of the hematopoietic function of the kidneys causes the development of anemia;

    • activation of the renin-angiotensin system and stabilization of arterial hypertension;

    • acid-base balance is disturbed in the blood.

    As a result, in all organs and tissues there are profound dystrophic disorders.

    It should be noted that the most frequent direct cause of chronic renal failure is chronic pyelonephritis.

    In the asymptomatic course of chronic pyelonephritis, chronic renal failure develops relatively late( 20 or more years after the onset of the disease).The cyclical course of bilateral chronic pyelonephritis is less favorable when unfolded manifestations of renal failure appear 10-15 years later, and its early signs in the form of polyuria are already 5-8 years after the onset of the disease. An important role belongs to the timely and regular treatment of the inflammatory process, as well as the elimination of its immediate cause, if possible.

    CRF caused by chronic pyelonephritis is characterized by a wave-like course with periodic deterioration and improvement of kidney function. Deterioration, as a rule, are associated with exacerbations of pyelonephritis. Improvements come after full-fledged treatment of the disease with restoration of the disturbed outflow of urine and suppression of the activity of the infectious process. It aggravates the disturbances of renal functions in chronic pyelonephritis arterial hypertension, which often becomes a factor determining the intensity of nephron death.

    Urolithiasis also leads to the development of CRF, usually with late or inadequate treatment, as well as with concomitant arterial hypertension and pyelonephritis with frequent exacerbations. In such cases, chronic renal failure develops slowly, within 10-30 years from the onset of the disease. However, with special forms of urolithiasis, for example, with coral calculous kidney stones, the death of nephrons accelerates. Provoke the development of CRF in urolithiasis re-stone formation, a stone of large size, a prolonged finding of it in the kidney in the latent course of the disease.

    At any rate of development of chronic renal failure, a number of stages are sequentially passed: latent, compensated, intermittent and terminal. The main laboratory indicator that separates one stage from another is the clearance of endogenous( own) creatinine, which characterizes the rate of glomerular filtration. Normally, the creatinine clearance is 80-120 ml per minute.

    The latent stage of CRF is detected with a decrease in glomerular filtration( by creatinine clearance) to 60-45 ml / min. During this period, the main clinical signs of CRF are polyuria and nocturia - the allocation of more urine at night, and not in the afternoon. It is possible to develop mild anemia. Other complaints are usually not presented by patients or they indicate increased fatigue, weakness, and sometimes dry mouth.

    The compensated stage is characterized by a decrease in glomerular filtration to 40-30 ml / min. Complaints of weakness, drowsiness, fatigue, apathy are added. Daily urine output usually reaches 2-2.5 liters, increased sodium excretion in the urine, as well as changes in phosphorus-calcium metabolism with the development of the first signs of osteodystrophy can begin. At the same time, the level of residual nitrogen in the blood corresponds to the upper limit of the norm.

    The intermittent stage is characterized by an undulating course with alternating periods of deterioration and a distinct improvement after full treatment. The rate of glomerular filtration rate is 23-15 ml / min. In the blood, the level of residual nitrogen is steadily increased. Patients constantly complain of weakness, sleep disorders, increased fatigue. A typical symptom is anemia.

    The terminal stage is characterized by intoxication of the body with its own nitrogenous slags - uremia. The glomerular filtration rate is 15-10 ml / min. Typical signs are itchy skin, bleeding( nasal, uterine, gastrointestinal, subcutaneous hemorrhages), "uremic gout" with joint pains, nausea, vomiting, loss of appetite, including aversion to food, diarrhea. Skin pale, yellowish hue, dry, with traces of scratching, bruises. The tongue is dry, brown, from the mouth comes a specific sweetish "uremic" smell. Most of these symptoms occur because other organs, for example, the skin, the gastrointestinal tract, etc., try to take on the function of the kidneys to remove nitrogenous slags and do not cope with it.

    The whole body suffers. Violations of the balance of sodium and potassium, persistently increased blood pressure and anemia lead to deep damage to the heart. As the amount of nitrogenous slags in the blood increases, the symptoms of the central nervous system increase: convulsive muscle twitching, encephalopathy right up to uremic coma. In the lungs at the terminal stage, uremic pneumonia can develop.

    Disturbances of phosphorus-calcium metabolism cause calcium leaching out of bone tissue. Osteodystrophy develops, which is manifested by pains in the bones, muscles, spontaneous fractures, arthritis, compression of the vertebrae and deformation of the skeleton. Children stop growing.

    There is a decrease in immunity, which significantly increases the susceptibility of the organism to bacterial infections. One of the most common causes of death of patients with CRF in the terminal stage are purulent complications, up to sepsis, caused by opportunistic bacteria, for example, intestinal daddy.

    In the initial stages, the treatment of CRF coincides with the treatment of the underlying disease, the goal of which is to achieve a stable remission or slow the progression of the process. If there are obstacles to the outflow of urine, it is best to eliminate them by surgery. In the future, with the continuation of the treatment of the underlying disease, the so-called symptomatic means - antihypertensive( pressure-lowering) drugs of ACE inhibitor groups( capoten, enam, enap) and calcium antagonists( cordarone), antibacterial, vitamin drugs, play a big role.

    An important role is played by the restriction in the nutrition of protein foods - no more than 1 g of protein per kilogram of the weight of the patient. Further, the amount of protein in the diet is reduced to 30-40 g per day( or less), and at a glomerular filtration rate of 20 ml / min the amount of protein should not exceed 20-24 g per day. Table salt is also limited to 1 g per day. However, the calorie content of the diet should remain high - depending on the weight of the patient from 2200 to 3000 kcal( using a potato-egg diet without meat and fish).

    For the treatment of anemia, iron preparations and other agents are used. With a decrease in diuresis, it is stimulated with diuretics - furosemide( lasix) in doses up to 1 g per day. In hospital in order to improve blood circulation in the kidneys, intravenously drip-concentrated solutions of glucose, hemodez, reopoliglyukin with the introduction of euphyllin, curantyl, trental, papaverine are prescribed. Antibiotics are used in CRF with caution, reducing doses 2-3 times, aminoglycosides and nitrofurans in chronic renal failure are contraindicated. In order to detoxify the washing of the stomach, intestines, and gastrointestinal dialysis are used. The washing liquid can be a 2% solution of drinking soda or solutions containing sodium, potassium, calcium, magnesium salts with the addition of soda and glucose. Gastric lavage is performed on an empty stomach, using a gastric tube, for 1-2 hours.

    In the terminal stage, the patient is shown regular( 2-3 times a week) hemodialysis - an "artificial kidney" device. The appointment of regular hemodialysis is necessary when the level of creatinine in the blood is more than 0.1 g / l and its clearance is less than 10 ml / min. Kidney transplantation significantly improves the prognosis, however, in the terminal stage, a poor survival of the organ is possible, so the question of transplanting the donor kidney should be addressed in advance.

    The prognosis of chronic renal failure has recently lost its fatalities due to the use of hemodialysis and kidney transplantation, but the life expectancy of patients remains significantly lower than the average for the population.