Abstract
Animal experiments show that the kidney contributes to apolipoprotein (apo)A-I catabolism. We tested relationships of HDL cholesterol (HDL-C) and apo-I with kidney function in subjects without severe chronic kidney disease. Included was a random sample of the general population (part of the PREVEND cohort). Kidney function [estimated glomerular filtration rate (e-GFR) by two well-established equations and creatinine clearance], HDL-C, triglycerides, apoA-I and insulin resistance (HOMAir) were measured in 2,484 fasting subjects (e-GFR>or=45 ml/min/1.73 m2) without macroalbuminuria, cardiovascular disease, diabetes, or the use of anti-hypertensives and/or lipid-lowering agents. HDL-C (r=-0.056 to -0.102, P<0.01 to <0.001) and apo A-I (r=-0.096 to -0.126, P<0.001) were correlated inversely with both GFR estimates and creatinine clearance in univariate analyses. Multiple linear regression analyses also demonstrated inverse relationships of HDL-C and apoA-I with all measures of kidney function even after adjustment for age, sex, waist circumference, HOMAir, triglycerides, and urinary albumin excretion (P=0.053 to 0.004). In conclusion, HDL-C and apoA-I are inversely related to e-GFR and creatinine clearance in subjects without severely compromised kidney function, which fits the concept that the kidney contributes to apoA-I regulation in humans. High glomerular filtration rate may be an independent determinant of a pro-atherogenic lipoprotein profile.
Highlights
Animal experiments show that the kidney contributes to apolipoproteinA-I catabolism
E-glomerular filtration rate (GFR) calculated using the Modification of Diet in Renal Disease (MDRD) equation was strongly correlated with estimated glomerular filtration rate (e-GFR) calculated using the CKD-EPI equation (r = 0.963, P < 0.001). e-GFR calculated using the MDRD equation and e-GFR calculated using the CKD-EPI equation were correlated with creatinine clearance, expressed
Similar relationships were found with creatinine clearance, which underscores the robustness of our findings
Summary
Animal experiments show that the kidney contributes to apolipoprotein (apo)A-I catabolism. Kidney function [estimated glomerular filtration rate (e-GFR) by two wellestablished equations and creatinine clearance], HDL-C, triglycerides, apoA-I and insulin resistance (HOMAir) were measured in 2,484 fasting subjects (e-GFRу45 ml/ min/1.73m2) without macroalbuminuria, cardiovascular disease, diabetes, or the use of anti-hypertensives and/or lipidlowering agents. HDL-C (r = ؊0.056 to ؊0.102, P < 0.01 to < 0.001) and apo A-I (r = ؊0.096 to ؊0.126, P < 0.001) were correlated inversely with both GFR estimates and creatinine clearance in univariate analyses. HDL-C and apoA-I are inversely related to e-GFR and creatinine clearance in subjects without severely compromised kidney function, which fits the concept that the kidney contributes to apoA-I regulation in humans. Lower HDL-C and apolipoprotein A-I are related to higher glomerular filtration rate in subjects without kidney disease.
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