EFFECT OF POLYASPARTIC ACID ON CDCL2- INDUCED NEPHROTOXICITY IN THE RAT

We produced an animal model of CdCl2 nephrotoxicity in rats, and treat ed them with polyaspartic acid (PAA) to prevent renal damage. Male Spr ague-Dawley (SD) rats (190-200 g) were used to induce proximal renal t ubular damage by daily injection of CdCl2 3.0 mg/1,000 g body wt for 2 wk. CdCl2-exposed SD rats exhibited significant increases in urine vo lume, urinary excretion of N-acetyl-beta-D-glucosaminidase (NAG), alan ine aminopeptidase (AAP), and fractional excretion of sodium (FENa) an d a decrease in the percentage of tubular reabsorption of phosphate (% TRP). Of these indicators of proximal tubular function, AAP and %TRP a re more sensitive than NAG or FENa. No glycosuria or aminoaciduria, ho wever, were observed. PAA markedly improved these indicators of proxim al tubular function. Daily urinary protein excretion and creatinine cl earance, on the other hand, did not change after administration of PAA . Cd concentrations in the cortex were 3 times higher than in the medu lla, however, there were no differences between Cd-treated rats and PA A-treated rats. Our animal model is an excellent one for determining t he effect of cadmium on renal proximal tubule damage. PAA appears to b e useful in the treatment of CdCl2 nephrotoxicity.