Kogika M M, Hagiwara M K, Mirandola R M
Department of Internal Medicine, College of Veterinary Medicine, University of Sao Paulo, Brazil.
Vet Hum Toxicol. 1993 Apr;35(2):136-40.
To assess renal function changes in acute nephrotoxicosis in dogs, the development and evolution of renal damage during induced citrinin intoxication were studied. Six dogs (experimental group) were given 10 mg citrinin/kg/BW every 24 h during 2 d, and 5 dogs (control group) received exclusively the diluent (1 ml 1% sodium carbonate/kg/BW/d for 2 d). The dogs were daily submitted to physical examination, urinalysis and blood biochemistry analyses (blood urea, serum creatinine, potassium, sodium and glucose) during 2 w. The citrinin-induced renal lesions were mainly in the proximal convoluted tubule and characterized by proteinuria, glucosuria and the presence of numerous granular casts in the urine sediment; these could be detected before elevations in blood urea and creatinine. Glucosuria was the earliest abnormality found and lasted 5 d, while proteinuria and cylindruria were observed from days 1 to 5 and from days 1 to 15, respectively. The glomerular filtration rate was slightly affected as observed by blood urea and creatinine elevations from days 2 to 5. Urine analysis is a useful tool for the evaluation of nephrotoxicity since most nephrotoxins act primarily on the proximal convoluted tubule.
