In the era of combined antiretroviral therapy, classic focal segmental glomerulosclerosis (FSGS) is the most common histopathological finding in African American HIV-positive patients with kidney disease. We sought to determine whether HIV suppression is associated with lower risk of progression to end-stage renal disease (ESRD) among HIV-positive African Americans with biopsy-confirmed classic FSGS.
HIV-positive African Americans who underwent kidney biopsies at a single tertiary hospital between January 1996 and June 2011 were confirmed as having classic FSGS by the presence of segmental glomerulosclerosis without features of HIV-associated nephropathy. Multivariable Cox proportional hazards models were used to examine the independent association of viral suppression (HIV-RNA < 400 copies per milliliter at biopsy) with time to progression to ESRD.
Of the 55 HIV-positive African Americans with classic FSGS, 26 had suppressed viral loads at the time of biopsy. Compared to viremic patients, those who were virally suppressed had a significantly higher mean CD4+ cell count (452 vs. 260 cell/mm3, respectively; P = 0.02) and median estimated glomerular filtration rate (53.5 vs 35.5 mL/min/1.73 m2, respectively; P = 0.002). Adjusting for sex and baseline CD4+ cell count, estimated glomerular filtration rate, and proteinuria, those with HIV-RNA levels <400 copies per milliliter at baseline had a 75% lower risk of progressing to ESRD (hazard ratio = 0.25; 95% CI: 0.07 to 0.88) during a median follow-up time of 2.70 years (interquartile range: 0.80–5.15 years).
HIV suppression is associated with significantly lower risk of progression to ESRD among HIV-infected African Americans with classic FSGS, supporting the potential role of combined antiretroviral therapy for this histopathology in addition to HIV-associated nephropathy among HIV-positive individuals.
*Division of Nephrology, Johns Hopkins University School of Medicine, Baltimore, MD;
†Division of Nephrology, Medical University of South Carolina, Charleston, SC;
‡Department of Internal Medicine in Baton Rouge, Louisiana State University Medical Center, New Orleans, LA;
§Division of Infectious Disease, Johns Hopkins University School of Medicine, Baltimore, MD; and
║Division of Nephrology, University of California, San Francisco, CA.
Correspondence to: Mohamad Hanouneh, MD, Division of Nephrology, Department of Medicine, Johns Hopkins University, 1830 E Monument Street, Room 416, Baltimore, MD 21287 (e-mail: Mhanoun1@jhmi.edu).
Supported by the NIDDK Grant K23DK081317.
The authors have no funding or conflicts of interest to disclose.
M.M.E. and M.G.A. are co-senior authors.
Received June 08, 2018
Accepted August 29, 2018