We developed a rat model of cadmium (Cd)-induced nephrotoxicity and tr
ied to prevent renal damage by treating the animals with pentoxifyllin
e (PTX). Sprague-Dawley (SD) rats given CdCl2 3.0 mg/kg sc, daily for
2 wk showed evidences of renal proximal tubular damage, including sign
ificant increases in urine volume, urinary excretion of N-acetyl-beta-
D-glucosaminidase (NAG), alanine aminopeptidase (AAP), and fractional
excretion of sodium (FENa), and a decrease in the percentage of tubula
r reabsorption of phosphate (%TRP). PTX significantly improved the uri
nary excretion of NAG and %TRP. Urine volume was increased threefold i
n the CdCl2-treated rats and fivefold in the Cd + PTX-treated rats, re
spectively, as compared with saline-treated control. Total protein, AA
P, and creatinine clearance, showed no change after PTX administration
. Concentration of Cd in the renal cortex was three times higher than
that in the renal medulla, but there were no differences in concentrat
ion between the Cd-treated rats and the Cd + PTX-treated rats. Our ani
mal model was useful in studying the renal tubular damage produced by
cadmium. PTX appears useful for improving the nephrotoxicity of Cd.