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In view of inducing action of hyperlipidemia on progression of nephropathy and relationships between thrombogenesis, atherogenesis and sclerosis, the authors examined fluvastatin effects on platelet-rheological hemostasis. The 12-week course in a dose 20-40 mg/ day produced minimal side effects while its hypolipidemic action was noticeable: a 18, 21 and 20% fall in concentrations of total cholesterol, LDL cholesterol, triglycerides, respectively. The platelet rheology underwent the following changes: spontaneous platelet aggregation went down from 2.58 +/- 0.3 to 1.64 +/- 0.27 r.units, ADP-induced platelet aggregation rose from 6.5 +/- 0.66 to 8.08 +/- 0.77 r.units. No marked changes were registered in hematocrit, plasma and blood density, red cell aggregation and deformability. Thus, active lowering of blood lipids was not associated with evident inhibition of platelet activity. The absence of this feedback in lipid-platelet relations probably indicates an independent significance of hemostatic disturbances in ischemic heart disease and needs further study.

The incidence of podagric nephropathy in different age groups was studied on a large populational material (41,452 persons over 30 years). The number of patients suffering from podagra was shown to increase with each decade of life. In 122 patients with podagric nephropathy, deviations in urinalyses were recorded in 80 cases (65.5%). Of these, 53 patients (72.6%) were ot 60 years of age and older. In patients over 60, derangement of nitrogen-excretory renal function was seen more frequently (in 64.4%) than in other age groups. The greater incidence of podagra and podagric nephropathy over the recent decade may be related not to the changes in the nutrition pattern and hypodynamia but also, and possibly to a larger measure, with deterioration of the environmental conditions and alterations in radiation background.

DNA repair was explored in continuous cells withdrawn from gout patients.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.

As many as 8 families suffering from gout were examined with the use of four tests for the repair of DNA damages. The criteria applied for the assessment of the reparative activity made it possible to identify in total or in different combinations the inhibition of the repair in the lymphocytes of all the probands examined. The use of 1-3 procedures revealed the repair defects in all the families, namely in the lymphocytes of the probands' relatives. Based on this fact an attempt has been made to identify possible carriership of the "pathological" genes in the proband's relatives, which in future will make it possible to develop approaches to the identification of the genetic markers of the disease as well as to the disease prevention.

An analysis of a course of acute renal insufficiency (ARI) in middle-aged and old patients (aged over 60) is based on a follow-up of 123 patients. Attention is drawn to multifactorial development of ARI in middle-aged persons, to disturbances of water-electrolyte balance and the blood coagulation system. Various aspects of therapeutic tactics for middle-aged ARI patients are considered.