Renal insufficiency

Renal insufficiency. The main functions of the kidneys (excretion of metabolic products, maintenance of constancy of water-electrolyte composition and acid-base state) are carried out by the following processes: renal blood flow, glomerular filtration and tubules (reabsorbia, secretion, concentration ability). Not every change in these renal processes leads to severe disruption of renal functions and can be called renal failure. Renal insufficiency is a syndrome that develops as a result of severe disorders of kidney processes, leading to a disorder of homeostasis, and characterized by azotemia, a violation of the water-electrolyte composition and acid-base state of the organism. Acute renal failure may occur suddenly due to acute, most commonly reversible kidney disease. Chronic renal failure develops gradually as a result of the progressive irreversible loss of the functioning parenchyma.

Acute kidney failure (ARF). Etiology, pathogenesis. The causes of acute renal failure are manifold: 1) impairment of renal hemodynamics (shock, collapse, etc.); 2) exogenous intoxications (poisons used in the national economy and everyday life, bites of poisonous snakes and insects, medicines); 3) infectious diseases (hemorrhagic fever with renal syndrome and leptospirosis); 4) acute kidney disease (acute glomerulonephritis and acute pyelonephritis); 5) obstruction of the urinary tract; 6) Arena condition (trauma or removal of a single kidney).

Disturbances of renal hemodynamics and exogenous intoxications cause 90% of all cases of arthritis. The main mechanism of kidney damage in these two forms of OPN is the anoxia of the renal tubules. In these forms of OPN, necrosis of the tubular epithelium develops, edema and cellular infiltration of the interstitial tissue, damage to the capillaries of the kidneys, ie, necrotic nephrosis develops. In most cases, these lesions are reversible.

Symptoms, course. In the initial period of acute renal failure, symptoms caused by shock (pain, anaphylactic or bacterial), hemolysis, acute poisoning, an infectious disease come to the forefront, but already in the first day there is a drop in diuresis (less than 500 ml / day), ie a period Oliguria-anuria, and the homeostasis is already disturbed. In plasma, along with an increase in the levels of creatinine, urea, residual nitrogen, sulfates, phosphates, magnesium, potassium, the levels of sodium, chlorine and calcium decrease. The combination of humoral disorders causes the growing symptoms of acute uremia. Adynamia, loss of appetite, nausea, vomiting are already observed in the first days of oliguria-anuria. As the growth of azotemia (usually the level of urea increases by 0.5 g / l daily), acidosis, hyperhydration and electrolyte disorders, there are muscle twitchings, drowsiness, confusion of consciousness, dyspnea due to acidosis and pulmonary edema, the early stage of which is determined radiologically. Characteristic tachycardia, widening the boundaries of the heart, deaf tones, systolic noise at the top, sometimes noise pericardium friction. Part of the patients have arterial hypertension. Disorders of rhythm are often associated with hyperkalemia: it is especially dangerous and can be the cause of sudden death. With hyperkalemia more than 6.5 mmol / l on the ECG, the T wave is high, acute, the QRS complex is enlarged, the tooth of R. can decline. Blockages of the heart or ventricular fibrillation can result in cardiac arrest. Anemia persists in all periods of acute renal failure, leukocytosis is characteristic of the oliguria-anuria period. Pain in the abdomen, enlarged liver - frequent symptoms of acute uraemia. Death in OPN most often comes from uremic coma, hemodynamic disorders and sepsis. With OPN, hypoisostenuria is detected from the very beginning.

The protein content in the urine and the nature of the urinary sediment depend on the cause of the arthritis. An increase in diuresis more than 500 ml / day means the recovery period of diuresis. Clinical improvement becomes evident, even after the onset of polyuria, not immediately, but gradually, as the level of azotemia decreases and homeostasis is restored. During the polyuria period, hypokalemia (less than 3.8 mmol / L) with ECG change (low voltage of the T wave, U wave, S7 segment decrease) and extrasystole is possible. By the time of normalization of the residual nitrogen content in the blood, the homeostasis is basically restored - the period of recovery. In this period, renal processes are restored. It lasts for up to a year or more. However, the decrease in glomerular filtration and the concentration ability of the kidneys remains, however, and in some patients renal failure assumes a chronic course, an important role is played by the attached pyelonephritis.

The diagnosis is based on a sudden drop in diuresis as a result of one of the above reasons, the growth of azotemia and other typical homeostatic disorders. To differentiate from an exacerbation of a chronic renal failure or its terminal stage the data of the anamnesis, reduction of the sizes of kidneys at a chronic glomerulonephritis and a pyelonephritis help, revealing of a chronic urological disease. With acute glomeruponephritis, high proteinuria is observed.

Treatment. From the first hours of the disease, pathogenetic therapy is indicated, the nature of which is determined by the cause that caused the OPN. First of all, it is necessary to conduct plasmapheresis, the volume of which is determined by the severity of the patient's condition, the degree of intoxication. Replace the removed plasma with freshly frozen plasma, albumin solution. In hemodynamic disorders, anti-shock measures are shown (replenishment of blood loss by transfusion of blood components, blood substitutes, intravenous drip injection of 100-200 to 400 mg of prednisolone). With continued hypotension (after replenishment of blood loss), intravenous drip injection of 1 ml of 0.2% noradrenaline solution in 200 ml of isotonic sodium chloride solution is expedient. In acute poisoning, along with anti-shock therapy, measures are taken to remove the poison from the body (see Poisoning). With massive intravascular hemopisis, if the hematocrit is below 20%, a replacement blood transfusion (or plasma) is produced. If the cause of OPN is a bacterial shock, then in addition to anti-shock measures, antibiotics are prescribed. At the very beginning of the disease, an 10% solution of mannitol is administered iv at a dose of 1 g per kg of body weight of the patient. With continued 2-3 days of anuria treatment with mannitol is inappropriate. In the initial period of opiguria-anurii diuresis is stimulated with furosemide (IV iv 160 mg 4 times a day). If diuresis increases, then the use of furosemide continues. Further therapy is aimed at regulating homeostasis. Diet, limiting the intake of protein and potassium, should be high in calories due to a sufficient number of carbohydrates and fats. The amount of liquid administered should exceed the diuresis, and also the amount of water lost with vomiting and diarrhea, not more than 500 ml. This volume includes 400 ml of 20% glucose solution with 20 units of insulin. In addition, with hyperkalemia IV, 10-20 ml of a 10% solution of calcium gluconate are administered and 200 ml of a 5% solution of sodium hydrogencarbonate are added dropwise. Large quantities of sodium bicarbonate solution can be administered only after establishing the degree of acidosis and under the control of blood pH.

Intramuscularly injected testosterone propionate 50 mg / day or 100 mg retabolil once a week. The appointment of antibiotics is often necessary, but their dose is reduced by 2-3 times due to the restriction of allocation by packs. Streptomycin, monomycin, neomycin under anuric conditions have a very pronounced ototoxic property, and they should not be used with ARF. The continuing oliguria and the increase in the symptoms of uremia serve as an indication for the transfer of the patient to the hemodialysis department, where he can undergo extracorporeal cleansing with artificial kidney or peritoneal dialysis.

Indications for hemodialysis or peritoneal dialysis are the level of urea in the plasma more than 2 g / l, potassium - 6.5 mmol / l; Decompensated metabolic acidosis and clinical picture of acute uremia. Contraindications to hemodialysis: hemorrhages in the brain, gastric and intestinal bleeding, severe hemodynamic disorders with a fall in blood pressure. Contraindications to peritoneal dialysis are the newly performed surgery on the abdominal organs and adhesions in the abdominal cavity.

Forecast. With the timely and correct use of adequate treatment methods, most patients with acute arterial hypertension recuperate and return to normal life.

Chronic renal failure (CRF). Etiology, pathogenesis. The most common causes of chronic renal failure are chronic glomerulonephritis, chronic pyelonephritis, nephritis in systemic diseases, hereditary nephritis, polycystic kidney disease, nephroangiosclerosis, diabetic glomerulosclerosis, renal amyloidosis, and urological diseases (bilateral or single kidney). The main pathogenetic mechanism of CRF is a progressive decrease in the number of active nephrons, leading to a decrease in the effectiveness of renal processes, and then to impaired renal function. The morphological picture of the kidney in CRF depends on the underlying disease, but most often there is a substitution of the parenchyma with a connective tissue and wrinkling of the kidney.

Before the onset of chronic renal failure, chronic kidney disease can last from 2 to 10 years or more. They undergo a number of stages, the conditional release of which is necessary for the proper planning of treatment for both kidney disease and chronic renal failure. When the glomerular filtration and tubular reabsorption are maintained at a normal level, the underlying disease is still in the stage not accompanied by impaired renal processes. With the passage of time, glomerular filtration becomes below normal, the ability of the kidneys to concentrate urine is also reduced, and the kidneys become involved in the stage of renal failure. At this stage, the homeostasis is still preserved (there is still no renal insufficiency). With a further decrease in the number of active nephrons and a glomerular filtration rate below 50 ml / min, plasma levels of creatinine increase more than 0.02 g / l and urea levels more than 0.5 g / l. At this stage, conservative treatment of chronic renal failure is required. At a filtration below 10 ml / min, azotemia and other homeostatic disorders progress steadily, despite conservative therapy, the terminal stage of CRF occurs, in which dialysis is necessary.

With the gradual development of chronic renal failure, homeostasis also slowly changes - the blood levels of not only creatinine, urea, but derivatives of guanidine, sulfates, phosphates and other metabolites increase. When diuresis is saved (polyuria is often observed), water is removed enough, and the level of sodium, chlorine, magnesium and potassium in the plasma does not change. Constantly observed hypocalcemia is associated with impaired metabolism of vitamin D and calcium absorption in the intestine. Polyuria can lead to hypokalemia. Very often, metabolic acidosis is detected. In the terminal stage (especially when there is an oliguria) rapidly increases azotemia, aggravated acidosis, hyperhydration increases, hyponatremia, hypochloremia, hypermagnesia and especially life-threatening hyperkalemia develop. The aggregate of humoral disorders determines the symptoms of chronic uraemia.

Symptoms, course. Patients complain of rapid fatigue, decreased performance, headache, decreased appetite. Sometimes they notice an unpleasant taste in the mouth, nausea and vomiting appear. The patient is pale, the skin is dry, flabby. Muscles lose tonus, there are minor twitching of muscles, tremors of fingers and hands. Sometimes there are pains in the bones and joints. Anemia develops, leukocytosis and bleeding occur. Often there is arterial hypertension, which is usually caused by the underlying kidney disease. The boundaries of the heart are expanded, its tones are muffled, changes in the ECG are determined (sometimes they are associated with diokalemia). This stage can last several years. Conservative therapy makes it possible to regulate homeostasis, and the general condition of the patient often allows him to work, but increased physical activity, mental stress, dietary errors, drinking restriction, infection, surgery can lead to impaired renal function and aggravation of uremic symptoms.

At a glomerular filtration below 10 ml / min conservative correction of a homeostasis is impossible. For this terminal stage of CRF, emotional lability is characteristic (apathy is replaced by excitation), disturbance of night sleep, drowsiness during the day, inhibition and inadequacy of behavior. The face is puffy, gray-yellow, itchy, there are combs on the skin, hair is dull, brittle. Dystrophy develops, hypothermia is characteristic. Appetite is not present. The voice is hoarse. From his mouth there is an ammonia smell. There is aphthous stomatitis. The tongue is laid, the stomach is swollen, vomiting, regurgitation is often repeated. Often, diarrhea, stool stinking, dark color. Anemia and hemorrhagic, syndrome, muscle twitchings become frequent and painful. With a prolonged course of uremia, pain in the arms and legs, fragility of the bones are observed, which is explained by uremic neuropathy and renal osteodystrophy. Noisy breathing often depends on acidosis, pulmonary edema or pneumonia. Ureemic intoxication is complicated by fibrinous pericarditis, pleurisy, ascites, encephalopathy and uremic coma.

The diagnosis is based on the history of chronic kidney disease, characteristic symptoms of uremia, laboratory data on azotemia and other typical disorders of homeostasis. Differential diagnosis with acute renal failure is assisted by anamnestic data and symptoms that characterize chronic uremia (anemia, dystrophy, etc.).

Encephalopathy in CRF differs from an attack of encephalopathy in acute glomerulonephritis by gradual development, not always deep coma, minor convulsive twitching of certain muscle groups, noisy breathing, whereas renal eclampsia has an acute onset and is accompanied by complete loss of consciousness, pupil dilating, large convulsions and asphyxia.

Treatment of CRF is inseparable from the treatment of kidney disease, which led to kidney failure. In a stage not accompanied by disorders of renal processes, etiological and pathogenetic therapy is performed that can heal the patient and prevent the development of renal failure or lead to remission and a slower course of the disease. In the stage of disturbance of renal processes, pathogenetic therapy does not lose its significance, but the role of symptomatic methods of treatment increases (hypotensive drugs, antibacterial agents, protein restriction in the daily ration - no more than 1 g per 1 kg of body weight, sanatorium treatment, etc.). The combination of these measures allows delaying the onset of CRF, and periodic monitoring of the level of glomerular filtration, renal blood flow and the concentration ability of the kidneys for the level of creatinine and urea in plasma makes it possible to predict the course of the disease.

Conservative treatment of CRF: therapeutic measures are mainly aimed at restoring homeostasis, reducing azotemia and reducing uremia symptoms.

The protein content of the daily diet depends on the degree of impaired renal function. With glomerular filtration below 50 ml / min and a creatinine level in the blood above 0.02 g / l, it is advisable to reduce the amount of protein consumed to 30-40 g / day, and with a glomerular filtration below 20 ml / min, a diet with a protein content of not more than 20 -24 g / day. The diet should be high-calorie (about 3000 kcal) and contain essential amino acids (potato-egg diet without meat and fish). Food is prepared with a limited (up to 2-3 g) amount of table salt, and patients with high hypertension - without salt. In the absence of edema and the presence of moderate hypertension, the patient is given an additional 2-3 g of salt for dosing food. Violation of calcium metabolism and the development of osteodystrophy require a long-term use of calcium gluconate and vitamin D to 100,000 IU per day, but the administration of vitamin D in high doses with hyperphosphataemia can lead to calcification of the internal organs. To reduce the level of phosphate in the blood, use Almagel for 1-2 teaspoons 4 times a day; Treatment requires regular monitoring of the level of calcium and phosphorus in the blood.

In acidosis, depending on its degree, 100% to 200 ml of a 5% sodium hydrogencarbonate solution is injected into /. With a decrease in diuresis, furosemide (lasix) is shown in doses (up to 1 g / day) providing polyuria. To reduce blood pressure, use usual antihypertensive drugs (see Hypertension) in combination with furosemide. Treatment of anemia is complex and involves the appointment of testosterone propionate to enhance erythropoiesis in 1 ml of a 5% oily solution in the / m daily, iron preparations. With a hematocrit of 25% or less, transfusions of erythrocyte mass with fractional doses are shown. Antibiotics and chemotherapeutic drugs for CRF should be used cautiously: doses of penicillin, ampicillin, methicillin, chain and sulfonamides are reduced by 2-3 times. Streptomycin, monomycin, neomycin, polymyxin in chronic renal failure even in reduced doses can cause auditory nerve neuritis and other complications. The derivatives of nitrofurans in CRF are contraindicated.

With heart failure in patients with CRF, glycosides are used with caution, in reduced doses, especially with hypokalemia. In the treatment of pericarditis, small doses of prednisolone are prescribed, but hemodialysis is more effective. Hemodialysis can be indicated with exacerbation of renal failure, and after improving the patient's condition, it is possible to conduct conservative therapy again more or less continuously.

A good effect in chronic renal failure is given by repeated courses of plasmapheresis. In the terminal stage, if conservative therapy does not have an effect and if there are no contraindications, the patient is transferred to treatment with regular (2-3 times per week) hemodialysis. Regular hemodialysis is usually used when the creatinine clearance is below 10 ml / min, and its plasma level is above 0.1 g / l. Experience shows that a prolonged state of uremia, deep dystrophy, encephalopathy and other complications of CRF significantly worsen the results of hemodialysis and do not allow the kidney transplant operation, therefore, decisions on hemodialysis and kidney transplantation should be made in a timely manner.

Forecast. Hemodialysis and kidney transplantation change the fate of patients with CRF, allow them to prolong their life and achieve rehabilitation for years. Selection of patients for these types of treatment is carried out by specialists of hemodialysis centers and organ transplantation.