Objective: Microalbuminuria is associated with increased risk of cardiovascular disease and mortality. The objective of the study was to evaluate if HIV infection was an independent risk factor for microalbuminuria.
Design: Cross sectional.
Methods: The relationship between HIV infection and microalbuminuria was assessed using subjects enrolled in the study of Fat Redistribution and Metabolic Change in HIV Infection, which consists of HIV-positive and control men and women. Participants with proteinuria (dipstick ≥ 1+) were excluded.
Results: Microalbuminuria (urinary albumin/creatinine ratio, ACR > 30 mg/g) was present in 11% of HIV infected, and 2% of control participants (P < 0.001); a fivefold odds after multivariate adjustment (odds ratio, 5.11; 95% confidence interval, 1.97–13.31; P=0.0008). Several cardiovascular risk factors were associated with higher ACR in HIV participants: insulin resistance (HOMA > 4; 32%, P < 0.0001), systolic blood pressure (21%, P = 0.01 for 120–140 versus < 120 mmHg, and 43%, P = 0.06 for > 140 versus < 120 mmHg), and family history of hypertension (17%, P = 0.03). Higher CD4 cell count was associated with lower albumin/creatinine ratio (−24%, P = 0.009 for 200–400 versus < 200 cells/ml and −26%, P = 0.005 for > 400 versus < 200 cells/ml).
Conclusion: HIV infection had a strong and independent association with microalbuminuria, the severity of which was predicted by markers of insulin resistance, hypertension, and advanced HIV infection. These associations warrant further investigation, as the increased prevalence of microalbuminuria in HIV infection may be a harbinger of future risk of cardiovascular and kidney diseases.
From the aDuke University Medical Center, Department of Medicine, Division of Nephrology, Durham, North Carolina, USA
bUniversity of California, San Francisco, California, USA
cSan Francisco Veterans Affairs Medical Center, San Francisco, California, USA
dCalifornia State University, East Bay, Department of Statistics, Hayward, California, USA
eof North Carolina, Department of Medicine, Division of Infectious Diseases, Chapel Hill, North Carolina, USA
fKaiser Permanente Northern California Division of Research, Oakland, California, USA.
Received 9 October, 2006
Revised 21 November, 2006
Accepted 29 November, 2006
Correspondence to C. Grunfeld, University of California, San Francisco, Veterans Affairs Medical Center, Metabolism Section 111F, 4150 Clement Street, San Francisco, CA 94121, USA. Tel: +1 415 750 2005; fax: +1 415 750 6927; e-mail: firstname.lastname@example.org