HIV-associated nephropathy is manifested by heavy proteinuria and renal ins
ufficiency and characterized pathologically by the collapsing variant of fo
cal and segmental glomerulosclerosis with acute tubular necrosis and mild i
nterstitial inflammation. Untreated, it may result in endstage renal diseas
e in as little as 4 months. It may present in patients with any manifestati
on of HIV infection, and affects predominantly black individuals. Insights
into pathogenesis have come from a transgenic mouse model, renal cell cultu
res, and from study of human biopsy material. Although the pathogenesis is
not completely understood, current considerations revolve around the role o
f HIV or protein in renal epithelium and the effects of cytokines, includin
g transforming growth factor-p and basic fibroblast growth factor, on renal
structures. Therapy with zidovudine, corticosteroids, or angiotensin-conve
rting enzyme inhibitors has met with modest success; to date, protease inhi
bitors have not been assessed.