The role of androgenous deficiency in the development of urolitiasis in experimental ethylenglycol rat model

In spite of high incidence of urolitiasis there is still no integral concept explaining all its causing factors and conditions as well as mechanisms of its development. Judging by the clinical observations one may suppose the androgenous deficiency might boost the formation of stones in the kidneys however there are no decisive proofs of androgenous deficiency role in concrement formation in kidney. These proofs may be yielded by means of a crude experimental model. 60 albino male rats were studied in “ethylenglycol” rat model reproducing urolithiasis for the assessment of androgenous deficiency effect on the development of this disease. “Ethyleneglycol” model of urolithiasis consisted of adding 1 % ethylene glycol solution to drinking water for 4 weeks. Androgenous deficiency was reproduced by castration. The experimental model has successfully produced urolithiasis with considerable disturbances in the structure and function of kidneys including microconcrement formation. Androgenous deficiency (castration) was shown to considerably boost the development of urolitiasis caused by ethylene glycol. In spite of similar morphological signs of urolitiasis in both experimental groups the androgenous deficiency caused by castration has been demonstrated to speed up and worsen the development of the disease. The microconcrements by the papilla of kidney in castrated rats with androgenous deficiency formed earlier and were multitudinous and larger in size than in experimental animals receiving 1 % ethylene glycol solution to drinking water for 4 weeks but without castration.

urolithiasis, testosterone, rat urolithiasis experimental model, androgenous deficiency