Objective: Cardiovascular events (CVEs) are a significant cause of mortality in HIV/AIDS patients. The objective is to determine the correlation between kidney function and the risk of CVEs in the HIV-infected population.
Design: Nested, matched, case–control study design was employed.
Methods: We performed a single-center study of 315 HIV-infected patients (63 patients who had CVEs and 252 controls). Estimated glomerular filtration rate (eGFR), calculated by the Chronic Kidney Disease Epidemiology Collaboration formula and the Modification of Diet in Renal Disease equation, and proteinuria were the primary exposures of interest.
Results: Mean eGFR was significantly lower in the patients compared with controls (68.4 vs. 103.2 ml/min per 1.73 m2, P < 0.001 by Chronic Kidney Disease Epidemiology Collaboration formula and 69.0 vs. 103.1 ml/min per 1.73 m2, P < 0.001 by Modification of Diet in Renal Disease equation). In univariate analysis, an eGFR of less than 60 ml/min per 1.73 m2 was associated with a 15.9-fold increased odds of a CVE compared with an eGFR of at least 60 ml/min per 1.73 m2 (P < 0.001). In multivariate analysis, a 10 ml/min per 1.73 m2 decrease in eGFR was associated with a 20% increased odds of a CVE (odds ratio 1.2, 95% confidence interval 1.1–1.4). The prevalence of proteinuria in the patients was approximately twice that of controls (51 vs. 25%, P < 0.001). Proteinuria was associated with CVEs both in univariate and multivariate analyses (odds ratio 3.6, 95% confidence interval 1.9–7.0 and odds ratio 2.2, 95% confidence interval 1.1–4.8, respectively). Traditional cardiovascular risk factors, such as history of previous CVEs, diabetes mellitus, and dyslipidemia, along with low CD4 cell counts were also found as significant predictors of risk of CVEs.
Conclusion: Our study shows a significant independent association between decreased kidney function and increased risk of CVE in HIV-1-infected patients.
aAll India Institute of Medical Sciences, New Delhi, India
bDepartment of Medicine, Division of Infectious Diseases, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA
cDepartment of Medicine, St. Luke's Roosevelt Hospital Center, New York, New York, USA
dDepartment of Medicine, Division of Nephrology, USA
eDepartment of Medicine, Division of General Internal Medicine, Johns Hopkins University School of Medicine, Baltimore, Maryland, USA.
Received 18 October, 2009
Revised 10 November, 2009
Accepted 20 November, 2009
Correspondence to Mohamed G. Atta, MD, MPH, 1830 E. Monument Street, Suite 416, Baltimore, MD 21205, USA. Tel: +1 410 955 5268; fax: +1 410 955 0485; e-mail: firstname.lastname@example.org