The renal pathologic features of 120 consecutively autopsied patients affected by acquired immunodeficiency syndrome was investigated by light microscopic analysis. Variously associated renal changes were found in 82 patients (68.3%). Glomerular changes were present in 25. The following diagnoses were made: mesangial glomerulonephritis (16 patients), defined by the presence of deposits in the mesangium and/or mesangial cell proliferation; membranous glomerulonephritis (4 patients), cirrhotic glomerulosclerosis (2 patients); and lupuslike glomerulonephritis (3 patients). Glomerular diseases seemed to be significantly associated with chronic hepatitis or liver cirrhosis. Interstitial inflammation was present in 19 cases: chronic pyelonephritis (2 patients), focal nephritis (5 patients), multiple cortical abscesses (7 patients), granulomatous nephritis (5 patients). Cryptococci were found in one and undetermined microorganisms in two cases of multiple cortical abscesses. Atypical mycobacteria were found in two cases of granulomatous nephritis. Mycotic infections were identified in another 6 patients, in whom they did not elicit any inflammatory response. It is worth stressing that, although various generalized infections are common in patients with acquired immunodeficiency syndrome, only cryptococci and atypical mycobacteria also frequently involve the kidney. Focal tubular necrosis was observed in 15 patients. Benign nephrosclerosis was the most common vascular change (27 patients). Changes recalling hemolyticuremic and localized intravascular coagulation were found in three and six patients, respectively. Our data, dealing with a European Caucasian population, considerably differ from those reported in North American literature, in as much as we found no cases of human immunodeficiency virus nephropathy. Conversely, immune-mediated glomerular diseases were frequent, in agreement with recent studies on renal biopsy specimens from AIDS patients with acquired immunodeficiency syndrome. This type of infections, supplies multiple sources of antigens that may stimulate immune complex formation and, therefore, glomerular diseases.