Etiology, pathogenesis. The most common causes of chronic renal failure are chronic glomerulonephritis, chronic pyelonephritis, nephritis in systemic connective tissue diseases (systemic lupus erythematosus, systemic scleroderma, polyarteritis nodosa, Wegener's granulomatosis, hemorrhagic vasculitis), metabolic diseases (diabetes mellitus, amyloidosis, gout, cystinosis, hyperoxaluria) , congenital kidney diseases (polycystic kidney disease, renal hypoplasia, Alport syndrome, Fanconi syndrome, etc.), arterial hypertension and nephroangiosclerosis, obstructive nephropathies (urolithiasis, hydronephrosis, tumors of the genitourinary system).
The main pathogenetic mechanism of chronic renal failure is a progressive decrease in the number of active nephrons, leading to a decrease in the efficiency of renal processes, and then to impaired renal function. The morphological picture of the kidney in chronic renal failure depends on the underlying disease, but most often there is replacement of the parenchyma with connective tissue and wrinkling of the kidney. Chronic kidney disease can last from 2 to 10 years or more before chronic kidney disease occurs.
They go through a number of stages, the conditional identification of which is necessary for proper planning of treatment for both kidney diseases and chronic renal failure. When glomerular filtration and tubular reabsorption are maintained at normal levels, the underlying disease is still at a stage that is not accompanied by disturbances in renal processes. Over time, glomerular filtration becomes lower than normal, and the ability of the kidneys to concentrate urine also decreases—the disease enters the stage of disruption of renal processes.
At this stage, homeostasis is still preserved (there is no renal failure yet). With a further decrease in the number of active nephrons and the glomerular filtration rate below 40 ml/min, the levels of creatinine and urea in the blood plasma increase. At this stage, conservative treatment of chronic renal failure is required.
When filtration is below 15-20 ml/min, azotemia and other homeostasis disorders are steadily increasing, despite conservative therapy, and the end stage of chronic renal failure occurs, in which the use of dialysis is necessary. With the gradual development of chronic renal failure, homeostasis slowly changes - the levels in the blood of not only creatinine, urea, but guanidine derivatives, sulfates, phosphates and other metabolites increase. When diuresis is maintained (polyuria is often observed), sufficient water is excreted, and the levels of sodium, chloride, magnesium and potassium in the plasma do not change.
Constantly observed hypocalcemia is associated with impaired vitamin D metabolism and calcium absorption in the intestine. Hypersecretion of parathyroid hormone (the body's reaction aimed at eliminating hypocalcemia) leads to the development of osteodystrophy, as well as anemia, polyneuropathy, cardiopathy, impotence and other complications of uremia.
Polyuria can lead to hypokalemia. Metabolic acidosis is very often detected. In the terminal stage (especially when oliguria occurs), azotemia rapidly increases, acidosis worsens, hyperhydration increases, hyponatremia, hypochloremia, hypermagnesemia and especially life-threatening hyperkalemia develop.
The combination of humoral disorders causes the symptoms of chronic uremia.
Symptoms, course. In the initial stage (decrease in glomerular filtration to 40-60 ml/min) in the absence of severe arterial hypertension, the course of the disease is latent.
In the presence of anemia, polyuria and nocturia, to identify the initial stage of chronic renal failure, an examination is performed that reveals a decrease in the maximum relative density of urine below 10-18 in the Zimnitsky test, a decrease in glomerular filtration below 60 ml/min (with a daily diuresis of at least 1.5 l). The conservative stage of chronic renal failure (glomerular filtration 15-40 ml/min) is characterized by polyuria and nocturia. Patients complain of fatigue, decreased performance, headache, and loss of appetite.
Sometimes they notice an unpleasant taste in the mouth, anorexia, nausea and