Renal insufficiency acute - Causes, symptoms and treatment. MF.

Renal failure is a violation of the excretory function of the kidneys with the accumulation of nitrogenous slags in the blood, normally removed from the body with urine. Can be acute and chronic. Below, acute renal failure is considered, and chronic chronic kidney failure is described in the article: Chronic renal failure.

Acute renal failure

Acute renal failure ( OPN) is a syndrome of sudden, rapid reduction or termination of the function of both kidneys( or a single kidney), leading to a sharp increase in nitrogen metabolism in the body, a violation of the total metabolism. Violation of the function of the nephron( a structural unit of the kidney) occurs due to a decrease in blood flow in the kidneys and a sharp decrease in the delivery of oxygen.

Acute renal failure develops within a few hours and up to 1-7 days, lasting more than 24 hours. With timely treatment and properly conducted treatment results in complete restoration of kidney function. Acute renal failure is always a complication of other pathological processes in the body.

Causes of development of acute renal failure

1. Shock bud. Acute renal failure develops with traumatic shock with massive tissue damage, due to a decrease in the volume of circulating blood( loss of blood, burns), reflex shock. This is observed in case of accidents and injuries, severe operations, with damage and decay of liver and pancreatic tissue, myocardial infarction, burns, frostbites, transfusion of incompatible blood, abortions.
2. Toxic kidney. OPN occurs when poisoning with nephrotropic poisons, such as mercury, arsenic, bertholet salt, snake venom, insect venom, fungi. Intoxication with drugs( sulfonamides, antibiotics, analgesics), X-ray contrast substances. Alcoholism, drug addiction, toxicomania, professional contact with salts of heavy metals, ionizing radiation.
3. Acute infectious kidney. Develops with infectious diseases: leptospirosis, hemorrhagic fever. It occurs with severe infectious diseases, accompanied by dehydration( dysentery, cholera), with bacterial shock.
4. Obstruction( obstruction) of the urinary tract. It occurs with tumors, stones, compression, ureter injury, with thrombosis and embolism of the renal arteries.
5. It develops with acute pyelonephritis( inflammation of the renal pelvis) and acute glomerulonephritis( inflammation of the renal glomeruli).

Prevalence of acute renal failure

• 60% of all cases of acute renal failure are associated with surgery or trauma.
• 40% of cases of acute renal failure in a patient develops during treatment in medical institutions.
• 1-2% - in women during pregnancy.

Symptoms of acute renal failure

In the initial period, the symptoms of the disease that led to the development of acute renal failure are at the forefront. These are symptoms of poisoning, shock, the disease itself. Simultaneously, the amount of urine output( diuresis) begins to decrease to 400 ml per day( oliguria), and then to 50 ml per day( anuria).Nausea, vomiting, and appetite decrease. There is drowsiness, a blocking of consciousness, there may be convulsions, hallucinations. The skin becomes dry, pale with hemorrhages, edema appears. Breath deep, frequent. Tachycardia, violation of the heart rhythm, arterial pressure is heard. It is characterized by abdominal distension, loose stools.

With timely treatment, a recovery period of diuresis begins. The amount of excreted urine increases to 3-5 liters per day. Gradually, all the symptoms of acute kidney failure. For complete recovery it is necessary from 6 months to 2 years.

Treatment of acute renal failure

All patients with acute renal failure need urgent hospitalization in the department of nephrology and dialysis or in the intensive care unit.
Determining importance is the earliest possible treatment of the underlying disease, elimination of factors that caused damage to the kidneys. Since in most cases the cause is a shock, it is necessary to start anti-shock activities as soon as possible. With massive blood loss, the loss of blood is compensated by the introduction of blood substitutes. When poisoning - from the body remove toxic substances by washing the stomach, intestines, the use of antidotes. In severe renal failure, hemodialysis or peritoneal dialysis sessions are performed.

Stages of treatment for patients with acute renal failure:

1. Eliminate all causes of decreased kidney function, amenable to specific therapy, including correction of prereal and postrenal factors;
2. Try to achieve a sustainable amount of urine output;
3. Conservative therapy:

• to reduce the amount of nitrogen, water and electrolytes entering the body to such an extent that they correspond to their withdrawable quantities;
• provide adequate nutrition to the patient;
• to change the nature of drug therapy;
• to ensure control over the clinical condition of the patient( the frequency of vital signs measurements is determined by the patient's condition, measuring the amounts of substances entering and leaving the body, body weight, inspection of wounds and places of intravenous infusion, physical examination should be carried out daily);
• to control biochemical parameters( the frequency of AMK, creatinine, electrolytes and blood count calculation will be dictated by the patient's condition, in oliguric and catabolized patients, these should be determined daily, the concentration of phosphorus, magnesium and uric acid less often)

4. Carry out a dialysistherapy

Hemodialysis

A number of manifestations of acute renal failure can be controlled with the help of conservative therapy. After any violations of the vascular fluid volume have been eliminated, the amount of fluid entering the body must exactly correspond to the sum of its measured withdrawal quantity and insignificant losses. The quantities of sodium and potassium introduced into the body should not exceed their measured deduced quantities. Daily monitoring of the balance of fluid and body weight makes it possible to establish whether the patient has a normal volume of intravascular fluid. In patients with acute renal failure receiving adequate treatment, body weight is reduced by 0.2-0.3 kg / day. A more significant decrease in body weight suggests hypercatabolism or a decrease in the volume of intravascular fluid, while a less significant one suggests that excess amounts of sodium and water enter the body. Since most drugs are excreted from the body, at least in part, by the kidneys, it is necessary to pay close attention to the use of medicines and their dosage. The concentration of sodium in serum serves as a guide for determining the required amount of water to be injected. Reducing the concentration of sodium indicates that there is an excess of water in the body, while an unusually high concentration indicates a lack of water in the body.

In order to reduce catabolism, it is necessary to ensure a daily intake of at least 100 g of carbohydrates into the body. In some of the recent studies, it is stated that when a mixture of amino acids and a hypertonic glucose solution is injected into the central veins, the condition of patients improves and the mortality in the group of patients suffering from acute renal insufficiency developed after surgery or trauma decreases. Since parenteral administration of excessively large amounts of nutrients can be associated with significant complications, this type of diet should be reserved for patients prone to catabolism, who can not obtain satisfactory results by the usual administration of nutrients through the mouth. Previously, anabolic androgens were used to reduce protein catabolism and reduce the rate of AMC increase. Currently, such treatment is not used. Additional measures that reduce the level of catabolism include the timely removal of necrotic tissues, control of hyperthermia and the early onset of specific antimicrobial therapy.

Patients with a low degree of metabolic acidosis associated with acute renal failure are not treated, except for those whose serum bicarbonate concentration does not decrease below 10 meq / l. The attempt to restore the acid-base state by the immediate introduction of alkalis can reduce the concentration of ionized calcium and provoke the development of tetany. Hypocalcemia usually occurs asymptomatically and rarely requires specific correction. Hyperphosphatemia should be monitored by oral administration of 30-60 ml of aluminum hydroxide 4-6 times a day, since calcification of calcium phosphorus over 70 develops calcification of soft tissues. Timely initiation of dialysis therapy will help to control the increased concentration of phosphorus in the blood serum of patients with severe form of hyperphosphataemia. If the patient does not have acute uric acid-induced nephropathy, then secondary hyperuricemia in acute renal failure most often does not require the use of allopurinol. The decrease in the glomerular filtration rate makes the fraction of filtered uric acid and, consequently, the deposition of uric acid within the tubules insignificant. In addition, for unknown reasons, acute renal failure, despite hyperuricemia, is rarely complicated by clinically manifested gout. For the timely detection of gastrointestinal bleeding, it is important to carefully monitor changes in the hematocrit number and the presence of latent blood in the feces. If the hematocrit number decreases rapidly and the rate of this decrease is inadequate to the degree of severity of renal failure, then alternative causes of anemia should be sought.

Congestive heart failure and hypertension serve as an indicator of the presence of excess fluid in the body and require appropriate measures. It should be remembered that many drugs, such as digoxin, are excreted mainly by the kidneys. As noted earlier, persistent hypertension is not always due to an increased volume of fluid in the body;in its development can contribute factors such as hyperenenemia. In some cases, in order to prevent gastrointestinal hemorrhage, selective blockade of histamine-2 receptors( cimetidine, ranitidine) was successfully performed in some seriously ill patients, but the expediency of such treatment in acute renal failure has not yet been investigated. To avoid infection and disrupt the integrity of anatomical barriers, prolonged catheterization of the bladder should be avoided, the oral cavity and skin should be sanitized, the intravenous infusion catheters inserted and the skin incision site should be treated with aseptic procedures and carefully monitored. When the body temperature rises, the patient should carefully examine it, paying special attention to the condition of the lungs, urinary tracts, wounds and places of introduction of a catheter for intravenous infusion.

In acute renal failure, hyperkalemia often develops. If the increase in potassium concentration in the serum is small( less than 6.0 mmol / l), then to correct it, it is sufficient to exclude from the diet all sources of potassium and to maintain constant careful laboratory monitoring of biochemical parameters. If the concentration of potassium in the blood serum increases to levels exceeding 6.5 mmol / and especially if there are any changes on the ECG, then you should begin active treatment of the patient. Treatment can be divided into emergency and routine forms. Emergency treatment includes intravenous calcium administration( 5-10 ml of 10% calcium chloride solution is administered intravenously for 2 min under ECG monitoring), bicarbonate( intravenously injected 44 mEq for 5 min) and glucose with insulin( 200-300 ml of 20% glucose solution containing 20-30 units of conventional insulin, is administered intravenously for 30 minutes).Routine treatment includes the administration of potassium-binding ion-exchange resins, such as sodium polystyrene sulfonate. They can be administered orally every 2-3 hours in a dose.25-50 g with 100 ml of 20% sorbitol for the prevention of constipation. On the other hand, a patient who can not take medicines through the mouth can be administered at intervals of 1 to 2 hours with 50 g of sodium polystyrene sulfonate and 50 g of sorbitol in 200 ml of water through a holding enema. In the case of development of refractory hyperkalemia, there may be a need for hemodialysis.

Some patients with acute renal failure, especially if they do not have oliguria and catabolism, can be successfully treated without dialysis therapy or with minimal use of it. There is an increasing tendency to use dialysis therapy in the early stages of acute renal failure to prevent possible complications. Early( preventive) dialysis often simplifies the management of the patient, creating the possibility of a more liberal approach to ensuring the intake of appropriate amounts of potassium and liquid in the body and allowing to improve the overall well-being of the patient. Absolute indications for dialysis are symptomatic uremia( usually manifested by symptoms from the central nervous system and / or gastrointestinal tract);development of resistant hyperkalemia, severe degree of acidemia, or accumulation in the body of excess fluid that can not be medicated, and pericarditis. In addition, many medical centers try to maintain pre-dialysis levels of AMK and creatinine in the blood serum, respectively, less than 1000 and 80 mg / l. To ensure adequate prevention of uremic symptoms for patients without oliguria and catabolism, dialysis may be required only in rare cases, and patients who are weighed down by catabolism and traumas may need daily dialysis. Often, peritoneal dialysis is an acceptable alternative to hemodialysis. Peritoneal dialysis can be particularly useful for a patient with non-catabolic renal failure who is shown to have frequent dialysis. To control the volume of extracellular fluid in patients with acute renal failure, slow continuous blood filtration can be used with high-permeability filters. The currently available filters that are connected to the circulatory system through the arteriovenous shunt allow the removal of 5 to 12 liters of ultrafiltrate of blood plasma per day without the use of a pump. Therefore, such devices appear to be especially useful for the treatment of patients suffering from oliguria and possessing an increased volume of extravascular fluid and unstable hemodynamics.

Eating such patients is very important.

Nutrition in acute renal failure

Hunger and thirst sharply worsen the condition of patients. Assign a low-protein diet( no more than 20 g of protein per day).The diet consists mainly of carbohydrates and fats( porridge on water, butter, kefir, bread, honey).When it is impossible to eat, intravenously inject nutrient mixtures, glucose.

Complications in acute renal failure

In the initiating and supporting phases of acute renal failure, excretion of the products of nitrogen metabolism, water, electrolytes and acids from the body with urine is disturbed. The severity of the changes occurring in this case in the chemical composition of the blood depends on the availability of oliguria, the state of catabolism in the patient. In non-oliguric patients, higher levels of glomerular filtration are noted than in patients with oliguria, and as a result, the first with urine excreted more products of nitrogen metabolism, water and electrolytes. Therefore, violations of the chemical composition of blood in acute renal failure in non-oliguric patients are usually less pronounced than those suffering from oliguria.

Patients suffering from acute renal failure, accompanied by oliguria, constitute a group at increased risk of developing salt and water overload, leading to hyponatremia, edema and stagnation of blood in the lungs. Hyponatremia is the result of excessive amounts of water entering the body, and swelling - excessive amounts and water, and sodium.

Acute renal failure is characterized by hyperkalemia due to reduced elimination of potassium by the kidneys with continued release of it from the tissues. The usual daily increase in potassium concentration in the serum of patients not suffering from oliguria and subject to catabolism of patients is 0.3-0.5 mmol / day. A larger daily increase in serum potassium concentration indicates a possible endogenous( tissue destruction, hemolysis) or exogenous( drugs, food ration, blood transfusion) potassium load or the release of potassium from cells due to acidemia. Usually, hyperkalemia occurs asymptomatically until the serum potassium concentration increases to values ​​exceeding 6.0-6.5 mmol / l. If this level is exceeded, changes are observed on the electrocardiogram( bradycardia, deviation of the electric axis of the heart to the left, pointed teeth T , enlargement of the ventricular complexes, increase in the P-R interval and a decrease in the amplitude of the P-wave) and eventually cardiac arrest may occur. Hyperkalemia can also lead to the development of muscle weakness and sluggish tetraparesis.

In acute renal failure, hyperphosphataemia, hypocalcemia and a weak degree of hypermagnesia are also observed.

Shortly after the development of significant azotemia, normocyte, normochromic anemia develops, and the hematocrit is stabilized at 20-30 volume percent. Anemia is caused by the weakening of erythropoiesis, and also by some decrease in the lifespan of erythrocytes.

Infectious diseases complicate the course of acute renal failure in 30-70% of patients and are considered as the leading cause of death. Gateways of infection are often used by the respiratory tract, surgical site and urinary tract. This often develops septicemia, caused by both gram-positive and gram-negative microorganisms.

Cardiovascular complications of acute renal failure include circulatory insufficiency, hypertension, arrhythmias and pericarditis.

Acute renal failure is often accompanied by neurologic impairment. Patients who are not on dialysis experience lethargy, drowsiness, clouding of consciousness, disorientation, "fluttering" trembling, anxious excitation, myoclonic twitching of the muscles and convulsive seizures. They are more typical for elderly patients and are amenable to correction in dialysis therapy.

Acute renal failure is often accompanied by complications from the gastrointestinal tract, including anorexia, nausea, vomiting, intestinal obstruction and vague complaints of abdominal discomfort.

Acute renal failure in pregnancy.

Most often, acute renal failure develops in the early or late stages of pregnancy. In the first trimester of pregnancy, acute renal failure usually develops in women after a criminal abortion in non-sterile conditions. In these cases, reduction in the volume of the intravascular fluid, sepsis and nephrotoxins contribute to the development of acute renal failure. The prevalence of this form of acute renal failure has decreased significantly now due to the widespread availability of abortion in a medical setting.

Acute renal failure may also develop as a result of extensive postpartum hemorrhage or pre-eclampsia in later stages of pregnancy. In most patients with this type of acute renal failure, a complete restoration of renal function usually occurs. However, in a small number of pregnant women suffering from acute renal failure, the kidney function is not restored, and in these cases, a histological examination reveals diffuse necrosis of the renal cortex. The presence of massive bleeding with placental abruption usually complicates this condition. Along with this, clinical and laboratory signs of intravascular coagulation of blood are detected.

A rare form of acute renal failure developed after 1-2 weeks after uncomplicated births, known as postpartum glomerulosclerosis, was described. This form of the disease is characterized by irreversible fast-progressive renal failure, although less severe cases have been described. Typically, patients suffer from concomitant microangiopathic hemolytic anemia. Histopathological changes in the kidneys with this form of renal failure are indistinguishable from similar changes that occur with malignant hypertension or scleroderma. Pathophysiology of this disease is not established. There are also no methods of treating patients that would ensure continued success, although it is considered advisable to use heparin.

Prevention of renal failure.

Preventive treatment deserves special attention due to high rates of morbidity and mortality among patients with acute renal failure. During the Vietnam War, military personnel experienced a five-fold decrease in mortality due to acute renal failure, compared to similar rates that occurred during the war in Korea. Such a reduction in mortality occurred in parallel with the provision of earlier evacuation of the wounded from the battlefield and an earlier increase in the volume of intravascular fluid. Therefore, it is very important to identify patients with a high incidence of acute renal failure in a timely manner, namely: patients with multiple injuries, burns, rhabdomyolysis and intracavitary hemolysis;patients receiving potential nephrotoxins;patients who underwent surgical operations, during which there was a need for temporary interruption of renal blood flow. Particular attention should be paid to the maintenance of optimal levels of intravascular fluid volume, minute heart volume and normal urine flow in such patients. Caution in the use of potentially nephrotoxic drugs, early treatment for cardiogenic shock, sepsis and eclampsia may also reduce the incidence of acute renal failure.

Doctor therapist Vostrenkova IN