[Acute renal insufficiency in rats in compensatory renal hypertrophy]. / Ostraia pochechnaia nedostatochnost' u krys pri kompensatornoi gipertrofii pochek.

Sodium bichromate and glycerol were administered to compare the course of acute renal failure in uninephrectomized rats and rats with two kidneys. The blood serum levels of creatinine, urea, sodium, potassium and osmotically active agents were found to be rather similar in the rats with one and two rats two days after the administration of nephrotic compounds. The concentration of electrolytes in the renal cortex and papilla of these animal groups. It is concluded that acute renal failure caused by glycerol and bichromate runs virtually similarly both in animals with one and two kidneys. Thus, in emergency, such as acute renal failure, the compensatorily hypertrophied kidney ensures the same elimination of nitrogen metabolic-waste products and maintains the electrolytic composition of the internal environment as in the animals with two working kidneys.

Renal failure and nephrotoxic drug-induced disturbances in rat kidney tissue.

The injection to rats of glycerol, cisplatin, uranyl acetate, sodium dichromate, and mercuric chloride is followed on the third day by acute renal failure. A new approach for quantitative estimation of disturbance of excretory renal function is presented. The decrease in renal function due to uranyl acetate was 77%; sodium dichromate, 71%; mercuric chloride, 52%; cisplatin, 25%; and glycerol, 10%. The kidneys still maintained serum ion concentration close to normal values. Injection of nephrotoxic drugs increased kidney wet weight by 24-57%. This was caused by swelling of renal tissue and increases in dry weight of the kidneys. The sodium content increased in the renal cortex and decreased in the papilla. The potassium content of the renal cortex is increased. The effect of some nephrotoxic drugs is suggested to depend on an increased number of cells in the renal cortex (probably due to hemostasis and inflammation) and a decrease of renal medulla function. The above drugs induce disturbance of kidney tissue but have no effect on the ion and water content in liver and m. gastrocnemius.

[The use of prednisolone for the attenuation of the nephrotoxic effect of cisplatin]. / Ispol'zovanie prednizolona dlia oslableniia nefrotoksicheskogo éffekta tsisplatina.

Rats experiments have indicated that prednisolone significantly decreases the nephrotoxic effect of the antitumor drug cisplatin. A single injection of the agent in a dose of 5 mg/kg body weight was followed by acute renal failure, which led to an increase in serum levels of creatinine and urea, to a rise in kidney weight, changes in renal water and ion content. The injection of prednisolone (5 mg/kg body weight) 3 hours prior to cisplatin administration resulted in a two-fold decrease in the concentration of nitrogen metabolic end products, without any effects on renal tissue. The protective effect of the hormone is not related to the decrease in renal cisplatin accumulation.