Internal illnesses. Chronic renal failure (most important)

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Internal illnesses. Chronic renal failure (most important)

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48. CHRONIC RENAL INSUFFICIENCY

Gradually emerging and steadily progressive impairment of kidney function, leading to uremic intoxication.

Etiology. Chronic glomerulonephritis, chronic pyelonephritis, diabetic glomerulonephritis, amyloidosis, polycystic kidney disease, kidney stones, adenoma, prostate cancer.

Pathogenesis. Pathogenetic mechanisms of the disease: lack of parenchyma regeneration, inevitable structural changes in the parenchyma, reduction in the number of functioning nephrons, their atrophy and shrinkage, disruption of excretory, blood purification and homeostatic functions, retention of nitrogenous metabolic products in the blood: urea, uric acid, ammonia, amino acids, creatinine, guanidine, phosphate retention, increased plasma and extracellular fluid potassium levels, hypocalcemia.

Clinic. In the subclinical form, an increase in the volume of fluid you drink (up to 3 liters per day), nocturia (up to 3 times per night), dryness, skin laxity, peeling, daytime sleepiness, weakness, fatigue, tinnitus, hearing loss.

In the clinical form, signs of pulmonary heart failure, severe anemia, changes in the liver, gastrointestinal tract without dysfunction.

In the terminal form: apathy, puffy face, dry skin, painful itching, muscle weakness, muscle twitching, large cramps, deep noisy breathing, chest pain, development of secondary pneumonia, moist rales, in the terminal stage - uremic pulmonary edema. Uremic pericarditis, hypertensive cardiovascular syndrome, uremic vasculitis, visceritis, and hypothermia develop. Anorexia, aversion to food, nausea, vomiting, heaviness, fullness in the epigastrium after eating, and thirst appear. Anemia, toxic leukocytosis with a neutrophil shift to the left, thrombocytopenia, and blood clotting disorders develop. Bone damage occurs, changes in the skeleton, secondary gout, change from polyuria to oligo- and anuria, urinary syndrome is slightly expressed.

Diagnostic research. Conduct a study of blood serum creatinine, nitrogenous metabolic products, the state of electrolyte and mineral metabolism, acid-base state, ultrasound of the kidneys, ECG study.

Treatment. A diet is shown to prevent the breakdown of one's own protein.

Hyperkalemia is being eliminated: the introduction of large amounts of glucose, hyponatremia: intravenous administration of a 10% sodium chloride solution, hypernatremia: the administration of natridiuretics (10% calcium gluconate solution), tachystin (0,125 mg), acidosis: diet, soda enemas, intravenous administration alkaline solutions, alkalosis: ammonium or 200 ml of a 2% potassium chloride solution, anemia: testosterone 300 mg per week for 3-6 months; iron supplements only when they are deficient.

Carry out hemodialysis, peritoneal dialysis.

Antihypertensive diuretics are used.

Forecast. The prognosis is determined by the phase of renal failure, the rate of its development.

Prevention. Active treatment of major diseases, systematic planned secondary prevention of chronic renal failure, clinical examination.

Author: Myshkina A.K.

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