Metabolic nephropathy (hyperuricemia): causes, symptoms, diagnosis, treatment

Dismetabolic nephropathy with violation of purine metabolism.

Over the past decades, the spread of uricosuria and uricosemia in both children and adults has increased. The pathology of the kidneys, caused by impaired purine metabolism, can be diagnosed in 2.4% of the child population. According to screening studies in adults, increased uricosuria occurs in 19.2%. Such an increase in the disturbances in the metabolism of purine bases is explained by ecological reasons: the products of the work of gasoline engines, which saturate the air of large cities, significantly affect the purine metabolism. The term "eco-nephropathy" arose. It is practically important to consider that maternal hyperuricemia is dangerous for the fetus because of its teratogenic influence and the possibility of forming congenital nephropathies - anatomical and histological. Uric acid and its salts have a direct nephrotoxic effect.

In the pathogenesis of hyperuricemia it is important to determine its type: metabolic, renal or mixed. Metabolic type suggests an increased synthesis of uric acid, a high level of uricosuria with normal or elevated uric acid clearance. Kidney type is diagnosed with a violation of uric acid excretion and, respectively, with a decrease in these parameters. The combination of metabolic and renal, or mixed type, is a condition in which the uraturia does not exceed the norm or is lowered, and the uric acid clearance is not changed.

Since violations of purine metabolism are inherently deterministic, in most patients with this pathology it is possible to find the main markers of hereditary nephropathies: the presence in the pedigree of persons with kidney diseases; often recurrent abdominal syndrome; a large number of small stigmas of disembryogenesis; propensity to arterial hypo- or hypertension. The range of diseases in the pedigree of the proband with dysmetabolic nephropathy by the type of violations of purine metabolism is wide: the pathology of the digestive tract, joints, endocrine disorders. In the development of the pathology of uric acid metabolism, the staging is traced . Metabolic disorders without clinical manifestations exert a toxic effect on the tubulointerstitial structures of the kidneys, resulting in the development of interstitial nephritis of dismetabolic origin. With the attachment of bacterial infection, secondary pyelonephritis occurs. When starting the mechanisms of lithogenesis, the formation of urolithiasis is possible. The participation of uric acid and its salts in the immunological reconstruction of the body is allowed. In children with impaired purine metabolism, a hypoimmune condition is often diagnosed. The development of glomerulonephritis is not ruled out.

Intestinal manifestations of uncomplicated form of violation of purine metabolism are nonspecific. In younger children (1-8 years), the most frequent abdominal pains, constipation, dysuria, myalgia and arthralgia, increased sweating, nocturnal enuresis, tics, logoneurosis. The most frequent manifestations in older children and adolescents are overweight, itching in the urethra, dyskinesia of the biliary tract, and low back pain. Moderate signs of intoxication and asthenia are possible. In children with impaired purine metabolism, it is usually possible to find a large number of external stigmas of demembriogenesis (up to 12) and an anomaly of the structure of internal organs ("small" heart defects, that is, prolapse of valves, additional chords, abnormalities in the structure of the kidneys and gallbladder). In 90% of cases, chronic pathology of the digestive tract is diagnosed. Signs of metabolic disturbances in the myocardium occur almost as often - in 80-82%. More than half of these children have arterial hypotension, one-fourth of patients have a tendency to arterial hypertension, which increases with the age of the child. Most children drink little and have low diuresis ("opyuria"). Urinary syndrome is typical for tubulointerstitial disorders: crystalluria, hematuria, less often - leukocyturia (predominantly lymphocyturia) and cylindruria, unstable proteinuria. Obviously, there is a close relationship between purine metabolism and oxalate metabolism. Crystalluria can be of mixed composition. In 80% of cases, disturbances in the circadian rhythm of urination can be detected - the predominance of nocturnal diuresis over daytime diuresis. With the progression of interstitial nephritis, the daily excretion of ammonium ions decreases.

Forecast of dismetabolic nephropathy with violation of purine metabolism. In rare cases, extreme situations are possible, when hyperuricemia leads to an acute occlusion of the tubular system of the kidneys and urinary tracts with the development of acute renal failure ("acute uric acid crisis"). Glomerulonephritis against a background of purine metabolism disorders usually flows through the hematuric variant with episodes of reversible decline in renal function with the prospect of developing chronic renal failure within 5-15 years. Secondary pyelonephritis, as a rule, proceeds latently. The doctor's task is to diagnose abnormalities of purine metabolism at the preclinical stage, that is, to isolate patients at risk and to make recommendations regarding lifestyle and nutrition that will help slow the development of pathology and prevent complications.

Treatment of patients with impaired purine metabolism is based on dietary restrictions on products rich in purine bases or provoking increased synthesis (strong tea, coffee, fatty fish, dishes containing gelatin), and increased fluid intake. Mineral waters of alkaline reaction (Borjomi) are recommended, a citrated mixture is prescribed for courses of 10-14 days or magurlite. In the metabolic type of violation of purine metabolism, uricosodepressor agents are shown: allopurinol at a dose of 150 mg / day for children under 6 years, 300 mg / day at the age of 6 to 10 years and up to 600 mg / day for older students. The drug is given in a full dose for 2-3 weeks after a meal with the transition to a half-maintenance dose for a long course up to 6 months. In addition, orotic acid is prescribed (potassium orotate in a dose of 10-20 mg / kg per day for 2-3 doses). With renal type, drugs of uricosuric action are prescribed: aspirin, etamid, urodan, anturan, - oppressive reabsorption of uric acid by the canaliculus of the kidneys. In a mixed type, a combination of uricosodepressors with uricosuric drugs is applicable. Both drugs are prescribed in a half dose each. It is necessary to monitor the reaction of urine with its obligatory alkalinization. For long-term use in outpatient settings, the allomarone preparation containing 50 mg of allopurinol and 20 mg of benzobromarone is recommended. Senior students and adults are assigned 1 tablet a day.

[1], [2], [3], [4], [5], [6], [7], [8], [9], [10]