Female Wistar rats were given 1% or 0.1% lead acetate in drinking wate
r for 2 or 4 months, respectively. Urinary beta(2)-microglobulin, N-ac
etyl-beta-D-glucosaminidase, lactate dehydrogenase and lysozyme were u
sed as markers of tubular dysfunction. Excretion of albumin and glomer
ular filtration rate were used as indicators of glomerular impairment.
Kidney and body weights and morphological changes in the kidney were
also studied. Exposure to 1% lead acetate induced a mean blood Lead le
vel of 1730 mu g l(-1) and caused only an increase of beta(2)-microglo
bulin excretion and relative kidney weight. Light microscopy of kidney
revealed morphological changes mainly in the epithelial cells of the
proximal tubules. The role of acetate or reduced water intake on kidne
y function was excluded because 1% sodium acetate or the restriction o
f water intake to the volume consumed by the rats of the lead-exposed
group was ineffective. Exposure to 0.1% lead acetate induced a blood l
ead level of 376 mu g l(-1), corresponding to the current level in ind
ustry workers, without any sign of nephrotoxicity, Comparison of this
study with the results of a previous study on male rats indicates no s
ex difference in the nephrotoxicity of lead.