A 60-year-old male had tested in 1986, at age;16, positive for human immuno
deficiency virus (HIV). In mid-1996 he was started on a protease inhibitor
regimen, which included indinavir, lamivudine and stavudine, and remained o
n this therapy until his death. In April 1999 he was hospitalized after a f
ainting episode. Although examination focusing on cardiac disease did not d
isclose any remarkable findings, he died suddenly one week after being disc
harged from hospital. At autopsy the kidneys were enlarged, with a total we
ight of 500 g, patchy pale gray and pinkish. Microscopy showed leukocytic c
ell casts in many of the tubules and collecting ducts. In many of these cas
ts there were clefts left by crystals. In the interstitium, both in the cor
tex and the medulla, there was focal inflammation and fibrosis. Death was a
ttributed to sudden cardiac dysfunction, probably ventricular fibrillation
as a consequence of severe nephropathy with electrolyte disturbances. It is
likely that kidney damage developed secondary to the indinavir treatment a
s indinavir can cause not only nephrolithiasis but also crystal-induced acu
te renal failure.