Glomerular alterations in experimental oliguric and nonoliguric acute renal failure.

Studies were performed in oliguric and nonoliguric forms of uranyl acetate (UA)-induced and ischemic acute renal failure (ARF) to examine whether a reduction in GFR is correlated with glomerular morphologic alterations. UA-induced nonoliguric and oliguric ARF were induced in rabbits by i.v. injections of 0.9 and 2 mg/kg, respectively. A 60-min renal artery clamping produced nonoliguric ARF in previously uninephrectomized rats, but oliguric ARF in the clamped kidneys of sham-nephrectomized animals. A decline in the whole-kidney CIn rate was more marked in oliguric ARF kidneys of both models than in nonoliguric ARF kidneys. Also, tubular damage was more pronounced in oliguric kidneys when compared with nonoliguric kidneys. Scanning electron microscopic observations revealed glomerular alterations in oliguric and nonoliguric kidneys in both models, evidenced by a flattening and spreading of podocyte cell bodies associated with loss of epithelial foot processes and a reduction in the density and diameter of endothelial fenestrae. There was no significant difference in these glomerular changes between oliguric and nonoliguric kidneys. The findings suggest that less reduction in the whole-kidney GFR in nonoliguric ARF kidneys is ascribed largely to less pronounced tubular damage rather than to less severe glomerular morphologic alterations.