[Tubulointerstitial nephritis and arterial hypertension--their clinical and population significance].
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Biomedical subjects
Publications and source records attributed to I M Balkarov.
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The examination of 30 patients with purin disbolism (mean age 23.8 years) has demonstrated that microalbuminuria higher than 20 mg/day may serve a diagnostic criterion of early damage to the kidneys. The level of microalbuminuria correlated with the degree of purin metabolism disorder.
The examination covered 125 elderly and senile subjects (106 females and 19 males) which made up 90.6% of those living in the boarding house. Their mean age was 81.3 years. Arterial hypertension was detected in 61.6% of the examinees. 18.5% of the examinees had hyperuricemia. Concentration function of the kidneys was affected in all the examinees. Half of them exhibited a moderate rise in the level of blood creatinine. The authors discuss the relationship between high prevalence of arterial hypertension, its tendency to crises and involutional processes in the kidneys in the onset and development of renoprival condition.
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Purine metabolism disturbances which may be responsible for urate nephropathy were revealed in 35% of the examinees with arterial hypertension. Gout manifestations occurred in many of the above patients. Purine metabolism disturbances contribute much to progression of renal disorders and arterial hypertension, require early diagnosis and treatment. Urate symptoms may serve a primary diagnostic indication.
After analysis of 1146 psoriasis patients, high incidence of asymptomatic hyperuricemia (18.8%) and elevated average levels of uric acid in these patients' blood were confirmed (346.8 +/- 2.4 mumol/l). More severe forms of uric acid disbolism lead to aggravated skin affections (psoriatic erythrodermia, exudative psoriasis), arthritis, occur in familial predisposition to psoriasis. Advanced psoriasis patients are at risk to develop apparent gout.
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DNA repair was explored in continuous cells withdrawn from gout patients. The data obtained were compared to those on primary cells (lymphocytes) from the same patients. Two continuous lines of fibroblasts obtained from the biopsy material of patients suffering from gout were examined for stability of reparation defects on long cell passage. The studies were made with 4 to 12 passages of patients' fibroblasts. The use of criteria reflecting certain stages of DNA repair (reparative synthesis of DNA, formation of induced DNA ruptures and their resynthesis during cell postincubation, reactivation and induced mutagenesis of measles vaccine virus in patients' cells) allowed confirmation of repair defect stability in gout patients' cells on their long passage. Based on the data on preservation of the repair defect on cell passage it is concluded that gout patients demonstrate the genetically determined impairment of the synthesis of DNA repair enzymes participating in the recovery of DNA impairments induced by UV radiation or UV mimetics.
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Based on studying the data obtained during examination of patients with psoriasis combined with the urinary syndrome possible varieties of psoriatic nephropathy, namely chronic glomerulonephritis (CGN) and amyloidosis were distinguished. CGN combined with psoriasis was mainly represented by latent glomerulonephritis (GN) and morphologically, it was mostly represented by the mesangio-proliferative variant, with IgA and C3 being fixed on the basal membrane of the capillaries and in the mesangium. The clinicomorphological feature of that form of psoriatic GN is combination of the signs of both associated CGN and hyperuricemia and IgA-nephritis. Special emphasis is laid on the diagnosis of rapid-progressing GN which is of paramount importance for institution of early etiopathogenetic therapy. Amyloidosis associated with psoriasis is characterized by the signs of acquired disease (AA-amyloidosis) and does not differ in its course from amyloidosis coupled with other diseases.