Human Immunodeficiency Virus

HIV-associated nephropathy is seen after an interval of approximately 2.5 years from discovery of HIV, and many patients have low CD4 counts. Most lesions on renal biopsy show FSGS followed by MPGN. Other less common renal lesions include DPGN, IgA nephropathy, MCD, and membranous or mesangioproliferative glomerulonephritis.

 The disease affects up to 10% of HIV-infected patients and is more commonly seen in African-American men than in Caucasians, and in intravenous drug users or homosexuals. The FSGS characteristically reveals collapse of the glomerular capillary tuft called collapsing glomerulopathy, visceral epithelial cell swelling, microcystic dilatation of renal tubules, and tubuloreticular inclusions. Renal epithelial cells express replicating HIV virus, but host immune responses also play a role in the pathogenesis. MPGN and DPGN have been reported more commonly in HIV-infected Caucasians and in patients co-infected with hepatitis B or C. HIV-associated TTP has also been reported.
HIV patients with FSGS typically present with nephrotic-range proteinuria and hypoalbuminemia, but unlike patients with other etiologies for nephrotic syndrome, they do not commonly have hypertension, edema, or hyperlipidemia. Renal ultrasound also reveals large, echogenic kidneys, and renal function in some patients declines rapidly.

 Treatment with inhibitors of the renin-angiotensin system decreases the proteinuria. Although evidence from large well-designed clinical trials is lacking, many feel that effective antiretroviral therapy benefits both the patient and the kidney. Dismal survival once renal failure is reached has improved, and many centers now offer renal allografts to select HIV patients.