Masaki Hara1,2, Naoki Yanagisawa3,2, Akihito Ohta1, Kumiko Momoki1,2, Ken Tsuchiya2, Kosaku Nitta2, Minoru Ando4,5. 1. Division of Nephrology, Department of Medicine, Tokyo Metropolitan Komagome Hospital, Bunkyo-ku, Tokyo, Japan. 2. Department IV of Internal Medicine, Tokyo Women's Medical University, Shinjuku-ku, Tokyo, Japan. 3. Division of Infectious Diseases, Department of Medicine, Tokyo Metropolitan Komagome Hospital, Bunkyo-ku, Tokyo, Japan. 4. Division of Nephrology, Department of Medicine, Tokyo Metropolitan Komagome Hospital, Bunkyo-ku, Tokyo, Japan. myhtando@f3.dion.ne.jp. 5. Department of Medicine, Tokyo Metropolitan Fu-chu Medical and Welfare Center for the Disabled, 2-9-2, Musashidai, Fuchu, Tokyo, 183-8553, Japan. myhtando@f3.dion.ne.jp.
Abstract
BACKGROUND: The risk of developing CKD is increased in HIV-infected patients; however, the relationship between renal function decline and lipid abnormalities currently remains unclear in these patients. METHODS: A retrospective cohort study was conducted on 661 HIV-infected patients, whose estimated glomerular filtration rates (eGFRs) were consecutively measured over 6 years. The rate of declines in eGFR per year was calculated, with decreases being evaluated using a linear mixed effect model. The distribution of decreases in eGFR ≥ 30 % from baseline during the follow-up period was compared across quartiles of non-high-density lipoprotein cholesterol (HDL-C) levels using the Cochran-Armitage test. A multivariate logistic regression model was built to examine the relationship between dyslipidemia and decreases in eGFR. RESULTS: The prevalence of CKD increased from 8.5 to 21.2 % during the follow-up. The average of 6 annual eGFR decline rates was 2.01 ± 0.09 ml/min/1.73 m2/year, which was more than 6-fold higher than that of age-matched controls. The distribution of decreases in eGFR significantly increased across the quartiles of non-HDL-C (p value for trend = 0.0359). Non-HDL-C levels greater than the median value of the cohort were identified as a significant risk factor for decreased eGFR [odds ratio (95 % confidence interval), 1.77 (1.07-3.00)]. CONCLUSION: Increased non-HDL-C levels are a risk factor for renal function decline in HIV-infected patients.
BACKGROUND: The risk of developing CKD is increased in HIV-infectedpatients; however, the relationship between renal function decline and lipid abnormalities currently remains unclear in these patients. METHODS: A retrospective cohort study was conducted on 661 HIV-infectedpatients, whose estimated glomerular filtration rates (eGFRs) were consecutively measured over 6 years. The rate of declines in eGFR per year was calculated, with decreases being evaluated using a linear mixed effect model. The distribution of decreases in eGFR ≥ 30 % from baseline during the follow-up period was compared across quartiles of non-high-density lipoprotein cholesterol (HDL-C) levels using the Cochran-Armitage test. A multivariate logistic regression model was built to examine the relationship between dyslipidemia and decreases in eGFR. RESULTS: The prevalence of CKD increased from 8.5 to 21.2 % during the follow-up. The average of 6 annual eGFR decline rates was 2.01 ± 0.09 ml/min/1.73 m2/year, which was more than 6-fold higher than that of age-matched controls. The distribution of decreases in eGFR significantly increased across the quartiles of non-HDL-C (p value for trend = 0.0359). Non-HDL-C levels greater than the median value of the cohort were identified as a significant risk factor for decreased eGFR [odds ratio (95 % confidence interval), 1.77 (1.07-3.00)]. CONCLUSION: Increased non-HDL-C levels are a risk factor for renal function decline in HIV-infectedpatients.
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