[The dynamics of the urinary glycosaminoglycan indices in the pathogenetic therapy of glomerulonephritis].

A positive dynamics of the course of glomerulonephritis under the effect of pathogenetic therapy evaluated in 140 patients was accompanied by a statistically valid reduction of glycoseaminoglycanes in the urine. This allows to use these indices as adjunctive criteria of treatment efficiency, especially in patients with chronic forms of the disease.

[Lipid metabolism in primary and combined lesions of the kidneys in pregnant women].

Urinary and blood lipid metabolism was examined during pregnancy complicated by different forms of nephropathies. The pregnant with primary nephropathy and with chronic pyelonephritis showed a significant increase of lipid peroxidation products in erythrocytes while the pregnant with chronic glomerulonephritis showed high-molecular lipoproteids in the urine. A relationship was found of metabolic disorders and indices characterizing the degree of renal lesions in the pregnant.

[Changes in the kallikrein-kinin system as a result of electrical-medicinal anesthesia].

The results of kallikrein-kinin system studies are analysed in 105 urological patients at different stages of surgical treatment. It has been established that changes in kallikrein-kinin system during combined electrical and drug anesthesia as well as during ataralgesia are unidirectional and reside in moderate system activation of compensatory nature. It is concluded that combined electrical and drug anesthesia is an adequate anesthetic technique to be used during urological surgery.

[Mechanisms of hypertension in patients with terminal kidney failure on programmed hemodialysis].

The state of some mechanisms involved in AP regulation was studied in 18 patients with terminal renal failure (TRF) on programmed hemodialysis for 7-9 mos. The imbalance of extra- and intracellular sodium, potassium and water causing hypertension, was noted in TRF patients. TRF patients revealed (against a background of the normal activity of plasma renin) a high activity of carboxycathepsin resulting in the creation of conditions for enhanced kinin degradation playing a depressor role and for intense angiotensin II formation, being an important mechanism of persistent hypertension.

[State of the blood prekallikrein-kallikrein system in patients with glomerulonephritis as affected by pathogenetic therapy].

A study was made of the effect of the treatment with glucocorticoids (GC), cyclophosphamide and indocide on the prekallikrein-kallikrein system (PKKS) of the blood in 108 patients with glomerulonephritis. It was revealed that in patients with acute and chronic GN, the PKKS was activated before treatment. The PKKS activation was marked by a decrease in the content of prekallikrein and elevation of the alpha 2-macroglobulin content, particularly in patients with the nephrotic syndrome.

Abnormalities of lipid metabolism and methods of their correction in patients with glomerulonephritis.

The results of integrated estimations of a complex of lipid indices are presented. Their abnormalities are considered to be atherosclerosis risk factors in the evolution of glomerulonephritis and its different variants, types and stages. The quantitative and qualitative peculiarities of the indicated abnormalities are revealed, in particular, their major expressiveness in chronic form, nephrotic variant and in the stage of renal failure.

[The effect of proteolytic inhibitors on tolerance to renal ischemia].

Proteolytic inhibitors like Contrykal are able to protect kidney tissue from ischemic injury and therefore recommended for cadaver donor preparation.

[Energy metabolism in subcellular fractions of normal and acute ischemic kidneys].

The level of oxidative phosphorylation, activity of phosphofructokinase, fructose-1,6-diphosphate aldolase, ketose-1-phosphate aldolase, glucose-6-phosphatase and lactate dehydrogenase are determined in subcellular fractions in the kidney cortex layer of rabbits which have suffered from acute ischemia (for 15, 30, 60, 120 min). Ischemia inhibits the oxidative processes in mitochondria which is proportional to the duration of the effect. An increase in the activity of glycolytic chain enzymes in microsomes and soluble fraction for 15-30 min of ischemia evidences for a compensation of the energy losses at the expense of glycolysis with short periods of ischemia.