Alison G Abraham1, Annie Darilay2, Heather McKay1, Joseph B Margolick3, Michelle M Estrella4, Frank J Palella5, Robert Bolan6, Charles R Rinaldo7, Lisa P Jacobson1. 1. Department of Epidemiology. 2. Astrazeneca, Gaithersburg, Maryland. 3. Department of Molecular Microbiology and Immunology, Johns Hopkins Bloomberg School of Public Health. 4. Division of Nephrology, Johns Hopkins School of Medical, Baltimore. 5. Division of Infectious Diseases, Northwestern University Feinberg School of Medicine, Chicago, Illinois. 6. Los Angeles LGBT Center, California. 7. Department of Infectious Diseases and Microbiology, University of Pittsburgh Graduate School of Public Health, Pennsylvania.
Abstract
BACKGROUND: Human immunodeficiency virus (HIV)-infected individuals are at higher risk for chronic kidney disease than HIV-uninfected individuals. We investigated whether the inflammation present in treated HIV infection contributes to kidney dysfunction among HIV-infected men receiving highly active antiretroviral therapy. METHODS: The glomerular filtration rate (GFR) was directly measured (using iohexol) along with 12 markers of inflammation in Multicenter AIDS Cohort Study participants. Exploratory factor analysis was used to identify inflammatory processes related to kidney dysfunction. The estimated levels of these inflammatory processes were used in adjusted logistic regression analyses evaluating cross-sectional associations with kidney function outcomes. RESULTS: There were 434 HIV-infected men receiving highly active antiretroviral therapy and 200 HIV-uninfected men. HIV-infected men were younger (median age, 51 vs 53 years) and had higher urine protein-creatinine ratios (median, 98 vs 66 mg/g) but comparable GFRs (median, 109 vs 106 mL/min|1.73 m(2)). We found an inflammatory process dominated by markers: soluble tumor necrosis factor receptor 2, soluble interleukin 2 receptor α, soluble gp130, soluble CD27, and soluble CD14. An increase of 1 standard deviation in that inflammatory process was associated with significantly greater odds of GFR ≤90 mL/min/1.73 m(2) (odds ratio, 2.0) and urine protein >200 mg/g (odds ratio, 2.3). CONCLUSIONS: Higher circulating levels of immune activation markers among treated HIV-infected men may partially explain their higher burden of kidney dysfunction compared with uninfected men.
BACKGROUND: Human immunodeficiency virus (HIV)-infected individuals are at higher risk for chronic kidney disease than HIV-uninfected individuals. We investigated whether the inflammation present in treated HIV infection contributes to kidney dysfunction among HIV-infectedmen receiving highly active antiretroviral therapy. METHODS: The glomerular filtration rate (GFR) was directly measured (using iohexol) along with 12 markers of inflammation in Multicenter AIDS Cohort Study participants. Exploratory factor analysis was used to identify inflammatory processes related to kidney dysfunction. The estimated levels of these inflammatory processes were used in adjusted logistic regression analyses evaluating cross-sectional associations with kidney function outcomes. RESULTS: There were 434 HIV-infectedmen receiving highly active antiretroviral therapy and 200 HIV-uninfectedmen. HIV-infectedmen were younger (median age, 51 vs 53 years) and had higher urine protein-creatinine ratios (median, 98 vs 66 mg/g) but comparable GFRs (median, 109 vs 106 mL/min|1.73 m(2)). We found an inflammatory process dominated by markers: soluble tumornecrosis factor receptor 2, soluble interleukin 2 receptor α, soluble gp130, soluble CD27, and soluble CD14. An increase of 1 standard deviation in that inflammatory process was associated with significantly greater odds of GFR ≤90 mL/min/1.73 m(2) (odds ratio, 2.0) and urine protein >200 mg/g (odds ratio, 2.3). CONCLUSIONS: Higher circulating levels of immune activation markers among treated HIV-infectedmen may partially explain their higher burden of kidney dysfunction compared with uninfected men.
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