06 Jan Black HIV Patients Have Greater Risk of Kidney Disease
Medical Research: What was the motivation for this study?
Dr. Abraham: HIV-infected individuals are at higher risk for kidney dysfunction compared to the general population. Prior to effective antiretroviral therapy, very aggressive forms of kidney disease were described primarily among black HIV-infected individuals. While effective therapy and increasing viral suppression rates have made HIV-associated nephropathy rare, some of these same drugs have nephrotoxic effects. In addition, the reduction in AIDS and mortality has led to HIV-infected individuals living long enough to experience age-related chronic diseases, which are also risk factors for kidney disease and end-stage renal disease. Thus we wanted to know how these competing forces were affecting end-stage renal disease risk in the well-treated HIV-infected North American population over time. Are we seeing more ESRD as a result of nephrotoxic drugs and chronic disease, or less ESRD as a result of better viral suppression and large reductions in HIV-associated nephropathy?
Medical Research: What are the main findings?
Dr. Abraham: We found that end stage renal disease rates have been steadily falling over the past 10 years coincident with notable improvements in viral suppression prevalence. However a large racial discrepancy in ESRD risk has persisted even though HIV-associated nephropathy cases are now rare. While ESRD cases among blacks in our study tended to have higher viral loads and lower CD4 counts compared to non-black ESRD cases, suggesting less effective HIV treatment, we found that the racial discrepancy in ESRD risk persisted even among the well-suppressed subset, i.e. those who had undetectable viral loads for 90% of their follow-up time.
Medical Research: What should clinicians and patients take away from your report?
Dr. Abraham: Lower ART utilization and delayed entry into care have been reported among HIV-infected black patients and longer exposure to HIV viremia may put this group at higher risk of ESRD, potentially as a result of increased or prolonged immune activation. We believe carriers of APOL1 high-risk alleles, who are predominantly black, may be susceptible to potentially damaging overexpression of APOL1 protein resulting from immune activation. Thus we need to work to achieve earlier entry into care, earlier ART initiation and long term viral suppression to attenuate immune activation among black HIV-infected patients to achieve renal protection in this group.
Medical Research: Do you have any plans for further research as a result of this study?
Dr. Abraham: We reported on many aspects of ESRD risk in the paper but could not include a full analysis of the risk resulting from nephrotoxic ARV drugs given the complexity of the topic. Thus we now want to examine the use and impact of these drugs; we are currently analyzing data from NA-ACCORD looking at clinical practice with regard to the use of potentially nephrotoxic ARVs in HIV-infected patients at risk for kidney disease. Additionally we are looking at the longitudinal kidney function trajectory of patients who initiate these drugs. We would like to understand the degree to which kidney disease risk factors influence the use of such ARVs and how much renal function recovery can occur after use is discontinued in an individual who experiences an acute kidney function decline as a result of these drugs and other unknown factors.
Alison G. Abraham, Keri N. Althoff, Yuezhou Jing, Michelle M. Estrella, Mari M. Kitahata, C. William Wester, Ronald J. Bosch, Heidi Crane, Joseph Eron, M. John Gill, Michael A. Horberg, Amy C. Justice, Marina Klein, Angel M. Mayor, Richard D. Moore, Frank J. Palella, Chirag R. Parikh, Michael J. Silverberg, Elizabeth T. Golub, Lisa P. Jacobson, Sonia Napravnik, and Gregory M. Lucas for the North American AIDS Cohort Collaboration on Research and Design (NA-ACCORD) of the International Epidemiologic Databases to Evaluate AIDS (IeDEA)
Clin Infect Dis. first published online November 18, 2014 doi:10.1093/cid/ciu919