Annotation. The aim of our study was to explore the pathogenetical aspects of tubulointerstitial syndrome development in alloxan-induced experimental diabetes mellitus. The experiments were carried out on 20 white non-linear mature male rats, 10 with experimental diabetes mellitus (EDМ) induced by intraperitoneal administration of alloxan at a dose of 160 mg/kg of body weight, 10 intact rats served as the control group. 25 days after administration of the diabetogenic substance, the animals were withdrawn from the experiment. The concentration of sodium and potassium ions in urine and blood plasma samples was determined, followed by calculation (considering water-induced 2-hour diuresis and endogenous creatinine clearance) of glomerular filtration rate, electrolyte excretion, their filtration rate, absolute and relative reabsorption, clearance, their proximal and distal renal transport. Removed after decapitation rats’ kidneys were dissected to 3 parts – renal cortex, medulla and papilla, sodium and potassium content was determined in water-extract of the corresponding part of the renal parenchyma, and papillary-cortical, papillary-medullar and medullary-cortical concentration ion gradients were calculated. Significant suppression of papillary-medullar and papillary-cortical concentration sodium gradients, as well as a slight limitation of its medullary-cortical gradient were established. The concentration potassium gradients were significantly reduced. Statistical processing of the obtained data was carried out with the determination of the average value, standard deviations. To assess the probability of the difference between the study groups used non-parametric Mann-Whitney ranking criterion according to the algorithms implemented in the computer program “Statistica for Windows”, “Version 8.0”. There was a decrease of the sodium-potassium ratio in urine, enhanced urinary excretion of potassium and an increase of its content in urine, as well as intensification of absolute transtubular sodium transport due to equivalent augmentation of the filtration charge of this cation, increase of proximal sodium reabsorption and, to a lesser degree, – of distal one. The distal and proximal sodium reabsorption, reduced to a unit of active nephrons, was found to be decreased, and the relative reabsorption of the cation significantly exceeded the control values, contributing to the limitation of natriuresis. The results of the study suggest that in 26-day alloxan-induced experimental diabetes hemodynamic-hyperperfusion overload on the tubular apparatus of the kidney causes the development of relative insufficiency of the proximal and distal tubules, disorders of hormone-dependent reabsorption of cations, limitation of regulatory influence of aldosterone and ADH with further tubulointerstitial disturbances that unable adequate osmotic concentration of urine.
Streptozotocin model of stable diabetes mellitus
