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• W1997650038 endingPage "1990" @default.
• W1997650038 startingPage "1982" @default.
• W1997650038 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≥45 ml/min/1.73m2) 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. 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≥45 ml/min/1.73m2) 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. Epidemiological studies have repeatedly demonstrated an inverse relationship between the risk of atherosclerotic cardiovascular disease and plasma levels of high-density lipoprotein cholesterol (HDL-C), as well as of its major apolipoprotein (apo), apoA-I (1.Vega G.L. Grundy S.M. Hypoalphalipoproteinemia (low high density lipoprotein cholesterol) as a risk factor for coronary heart disease.Curr. Opin. Lipidol. 1996; 7: 209-216Crossref PubMed Scopus (78) Google Scholar, 2.Lewington S. Whitlock G. Clarke R. Sherliker P. Emberson J. Halsey J. Qizilbash N. Peto P. Collins R. Blood cholesterol and vascular mortality by age, sex, and blood pressure: a meta-analysis of individual data from 61 prospective studies with 55,000 vascular deaths.Lancet. 2007; 207: 1829-1839Google Scholar). Despite proven efficacy, primary and secondary prevention trials have shown that there remains a considerable residual cardiovascular risk during cholesterol-lowering treatment (3.Third Report of the National Cholesterol Education Program (NCEP). Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III): final report. 2002. Circulation. 106: 3143–3421.Google Scholar). In view of anti-atherogenic properties of HDL, this lipoprotein fraction has been identified as a therapeutic target (4.Borggreve S.E. de Vries R. Dullaart R.P.F. Alterations in high-density lipoprotein metabolism and reverse cholesterol transport in insulin resistance and type 2 diabetes mellitus: role of lipolytic enzymes, lecithin:cholesterol acyltransferase and lipid transfer proteins.Eur. J. Clin. Invest. 2003; 33: 1051-1069Crossref PubMed Scopus (222) Google Scholar, 5.Linsel-Nitschke P. Tall A.R. HDL as a target in the treatment of atherosclerotic cardiovascular disease.Nat. Rev. Drug Discov. 2005; 4: 193-205Crossref PubMed Scopus (417) Google Scholar, 6.Singh I.M. Shishehbor M.H. Ansell B.J. High-density lipoprotein as a therapeutic target: a systematic review.J. Am. Med. Assoc. 2007; 298: 786-798Crossref PubMed Scopus (384) Google Scholar, 7.Dullaart R.P.F. Dallinga-Thie G.M. Wolffenbuttel B.H.R. van Tol A. CETP inhibition in cardiovascular risk management: a critical appraisal.Eur. J. Clin. Invest. 2007; 37: 90-98Crossref PubMed Scopus (48) Google Scholar). Therefore, progress in our understanding of HDL metabolism and HDL function is expected to contribute to the development of novel strategies in order to reduce the burden of atherosclerotic disease in humans (5.Linsel-Nitschke P. Tall A.R. HDL as a target in the treatment of atherosclerotic cardiovascular disease.Nat. Rev. Drug Discov. 2005; 4: 193-205Crossref PubMed Scopus (417) Google Scholar, 6.Singh I.M. Shishehbor M.H. Ansell B.J. High-density lipoprotein as a therapeutic target: a systematic review.J. Am. Med. Assoc. 2007; 298: 786-798Crossref PubMed Scopus (384) Google Scholar, 8.Lewis G.F. Rader D.J. New insights into the regulation of HDL metabolism and reverse cholesterol transport.Circ. Res. 2005; 96: 1221-1232Crossref PubMed Scopus (832) Google Scholar). The metabolism of HDL particles, which comprise a heterogeneous group of lipoproteins, is in a complex way regulated by many factors, including lipases, lipid transfer proteins, and cellular receptors (4.Borggreve S.E. de Vries R. Dullaart R.P.F. Alterations in high-density lipoprotein metabolism and reverse cholesterol transport in insulin resistance and type 2 diabetes mellitus: role of lipolytic enzymes, lecithin:cholesterol acyltransferase and lipid transfer proteins.Eur. J. Clin. Invest. 2003; 33: 1051-1069Crossref PubMed Scopus (222) Google Scholar, 6.Singh I.M. Shishehbor M.H. Ansell B.J. High-density lipoprotein as a therapeutic target: a systematic review.J. Am. Med. Assoc. 2007; 298: 786-798Crossref PubMed Scopus (384) Google Scholar, 8.Lewis G.F. Rader D.J. New insights into the regulation of HDL metabolism and reverse cholesterol transport.Circ. Res. 2005; 96: 1221-1232Crossref PubMed Scopus (832) Google Scholar). The liver and intestine are major sites of apoA-I secretion and hence contribute to HDL particle generation (8.Lewis G.F. Rader D.J. New insights into the regulation of HDL metabolism and reverse cholesterol transport.Circ. Res. 2005; 96: 1221-1232Crossref PubMed Scopus (832) Google Scholar, 9.Moestrup S.K. Kozyraki R. Cubilin, a high-density lipoprotein receptor.Curr. Opin. Lipidol. 2000; 11: 133-140Crossref PubMed Scopus (55) Google Scholar, 10.Moestrup S.K. Nielsen L.B. The role of the kidney in lipid metabolism.Curr. Opin. Lipidol. 2005; 16: 301-306Crossref PubMed Scopus (72) Google Scholar). Importantly, studies in rats, rabbits, and hamsters have shown that a major fraction of radiolabeled apoA-I is being taken up by the kidney in vivo (11.Glass C.K. Pittman R.C. Keller G.A. Steinberg D. Tissue sites of degradation of apoprotein A-I in the rat.J. Biol. Chem. 1983; 258: 7161-7167Abstract Full Text PDF PubMed Google Scholar, 12.Braschi S. Neville T.A. Maugeais C. Ramsamy T.A. Seymour R. Sparks D.L. Role of the kidney in regulating the metabolism of HDL in rabbits: evidence that iodination alters the catabolism of apolipoprotein A-I by the kidney.Biochemistry. 2000; 39: 5441-5449Crossref PubMed Scopus (35) Google Scholar, 13.Woollett L.A. Spady D.K. Kinetic parameters for high density lipoprotein apoprotein AI and cholesteryl ester transport in the hamster.J. Clin. Invest. 1997; 99: 1704-1713Crossref PubMed Scopus (45) Google Scholar), with the proximal renal tubule representing a likely site for apoA-I uptake and degradation (14.Dallinga-Thie G.M. van 't Hooft F.M. van Tol A. Tissue sites of high density lipoprotein A-IV in rats.Arteriosclerosis. 1986; 6: 277-284Crossref PubMed Google Scholar). A plausible mechanism that may explain the role of the kidney in apoA-I catabolism includes filtration of apoA-I through the glomerular basement membrane and subsequent proximal tubular uptake via the cubilin-megalin-amnionless complex, which enables endocytosis of HDL-derived proteins (9.Moestrup S.K. Kozyraki R. Cubilin, a high-density lipoprotein receptor.Curr. Opin. Lipidol. 2000; 11: 133-140Crossref PubMed Scopus (55) Google Scholar, 10.Moestrup S.K. Nielsen L.B. The role of the kidney in lipid metabolism.Curr. Opin. Lipidol. 2005; 16: 301-306Crossref PubMed Scopus (72) Google Scholar, 15.Kozyraki R. Fyfe J. Kristiansen M. Gerdes C. Jacobsen C. Cui S. Christensen E.I. Aminoff M. de la Chapelle A. Krahe R. et al.The intrinsic factor-vitamin B12 receptor, cubilin, is a high-affinity apolipoprotein A-I receptor facilitating endocytosis of high-density lipoprotein.Nat. Med. 1999; 5: 656-661Crossref PubMed Scopus (229) Google Scholar, 16.Hammad S.M. Barth J.L. Knaak C. Argraves W.S. Megalin acts in concert with cubilin to mediate endocytosis of high density lipoproteins.J. Biol. Chem. 2000; 275: 12003-12008Abstract Full Text Full Text PDF PubMed Scopus (139) Google Scholar). Despite the prominent role of the kidney in apoA-I catabolism as inferred from animal experiments (9.Moestrup S.K. Kozyraki R. Cubilin, a high-density lipoprotein receptor.Curr. Opin. Lipidol. 2000; 11: 133-140Crossref PubMed Scopus (55) Google Scholar, 10.Moestrup S.K. Nielsen L.B. The role of the kidney in lipid metabolism.Curr. Opin. Lipidol. 2005; 16: 301-306Crossref PubMed Scopus (72) Google Scholar, 11.Glass C.K. Pittman R.C. Keller G.A. Steinberg D. Tissue sites of degradation of apoprotein A-I in the rat.J. Biol. Chem. 1983; 258: 7161-7167Abstract Full Text PDF PubMed Google Scholar, 12.Braschi S. Neville T.A. Maugeais C. Ramsamy T.A. Seymour R. Sparks D.L. Role of the kidney in regulating the metabolism of HDL in rabbits: evidence that iodination alters the catabolism of apolipoprotein A-I by the kidney.Biochemistry. 2000; 39: 5441-5449Crossref PubMed Scopus (35) Google Scholar, 13.Woollett L.A. Spady D.K. Kinetic parameters for high density lipoprotein apoprotein AI and cholesteryl ester transport in the hamster.J. Clin. Invest. 1997; 99: 1704-1713Crossref PubMed Scopus (45) Google Scholar, 14.Dallinga-Thie G.M. van 't Hooft F.M. van Tol A. Tissue sites of high density lipoprotein A-IV in rats.Arteriosclerosis. 1986; 6: 277-284Crossref PubMed Google Scholar) and the observation that increased catabolism of apoA-I is a predominant kinetic abnormality in humans with low HDL-C (17.Horowitz B.S. Goldberg I.J. Merab J. Vanni T.M. Ramakrishnan R. Ginsberg H.N. Increased plasma and renal clearance of an exchangeable pool of apolipoprotein A-I in subjects with low levels of high density lipoprotein cholesterol.J. Clin. Invest. 1993; 91: 1743-1752Crossref PubMed Scopus (192) Google Scholar), the relationship of HDL-C and apoA-I in subjects without severely compromised kidney function has received little attention. In fact, most studies have focused on low HDL-C and apoA-I levels in subjects with severe chronic kidney disease (18.Vaziri N.D. Dyslipidemia of chronic renal failure: the nature, mechanisms, and potential consequences.Am. J. Physiol. Renal Physiol. 2006; 290: F262-F272Crossref PubMed Scopus (394) Google Scholar, 19.Muntner P. Hamm L.L. Kusek J.W. Chen J. Whelton P.K. He J. The prevalence of nontraditional risk factors for coronary heart disease in patients with chronic kidney disease.Ann. Intern. Med. 2004; 140: 9-17Crossref PubMed Scopus (357) Google Scholar, 20.Chen J. Muntner P. Hamm L.L. Jones D.W. Batuman V. Fonseca V. Whelton P.K. He J. The metabolic syndrome and chronic kidney disease in US adults.Ann. Intern. Med. 2004; 140: 167-174Crossref PubMed Scopus (1139) Google Scholar, 21.Shlipak M.G. Fried L.F. Cushman M. Manolio T.A. Peterson D. Stehman-Breen C. Bleyer A. Newman A. Siscovick D. Psaty B. Cardiovascular mortality risk in chronic kidney disease: comparison of traditional and novel risk factors.JAMA. 2005; 13: 1737-1745Crossref Scopus (591) Google Scholar, 22.Parikh N.I. Hwang S.J. Larson M.G. Meigs J.B. Levy D. Fox C.S. Cardiovascular disease risk factors in chronic kidney disease: overall burden and rates of treatment and control.Arch. Intern. Med. 2006; 166: 1884-1891Crossref PubMed Scopus (178) Google Scholar). Few epidemiological studies have determined the relationship of HDL-C with estimates of glomerular filtration rate (GFR) in populations with low prevalence of severe chronic kidney disease (23.Lo J.C. Go A.S. Chandra M. Fan D. Kaysen G.A. GFR, body mass index, and low high-density lipoprotein concentration in adults with and without CKD.Am. J. Kidney Dis. 2007; 50: 552-558Abstract Full Text Full Text PDF PubMed Scopus (32) Google Scholar, 24.Verhave J.C. Hillege H.L. Burgerhof J.G. Gansevoort R.T. de Zeeuw D. de Jong P.E. PREVEND Study GroupThe association between atherosclerotic risk factors and renal function in the general population.Kidney Int. 2005; 67: 1967-1973Abstract Full Text Full Text PDF PubMed Scopus (91) Google Scholar, 25.de Boer I.H. Astor B.C. Kramer H. Palmas W. Seliger S.L. Shlipak M.G. Siscovick D.S. Tsai M.Y. Kestenbaum B. Lipoprotein abnormalities associated with mild impairment of kidney function in the multi-ethnic study of atherosclerosis.Clin. J. Am. Soc. Nephrol. 2008; 3: 125-132Crossref PubMed Scopus (55) Google Scholar). Using data from the Kaiser Permanente Renal Registry, it was found that the prevalence of low HDL-C was increased in subjects with an estimated GFR (e-GFR) ≤ 60 ml/min/1.73m2, irrespective of obesity (23.Lo J.C. Go A.S. Chandra M. Fan D. Kaysen G.A. GFR, body mass index, and low high-density lipoprotein concentration in adults with and without CKD.Am. J. Kidney Dis. 2007; 50: 552-558Abstract Full Text Full Text PDF PubMed Scopus (32) Google Scholar). An analysis from the population-based PREVEND (“Prevention of REnal and Vascular ENd stage Disease”) cohort demonstrated the lowest HDL-C in subjects with the highest compared with subjects with the lowest creatinine clearance (24.Verhave J.C. Hillege H.L. Burgerhof J.G. Gansevoort R.T. de Zeeuw D. de Jong P.E. PREVEND Study GroupThe association between atherosclerotic risk factors and renal function in the general population.Kidney Int. 2005; 67: 1967-1973Abstract Full Text Full Text PDF PubMed Scopus (91) Google Scholar). In apparent contrast, a report from the Multi-Ethnic Study of Atherosclerosis showed among subjects with e-GFR > 60 ml/min/1.73m2 that HDL-C and HDL particle concentrations were related inversely to serum cystatin-C levels, as a measure of renal function (25.de Boer I.H. Astor B.C. Kramer H. Palmas W. Seliger S.L. Shlipak M.G. Siscovick D.S. Tsai M.Y. Kestenbaum B. Lipoprotein abnormalities associated with mild impairment of kidney function in the multi-ethnic study of atherosclerosis.Clin. J. Am. Soc. Nephrol. 2008; 3: 125-132Crossref PubMed Scopus (55) Google Scholar). Of note, in these studies, the relationship of kidney function with apoA-I was not determined (23.Lo J.C. Go A.S. Chandra M. Fan D. Kaysen G.A. GFR, body mass index, and low high-density lipoprotein concentration in adults with and without CKD.Am. J. Kidney Dis. 2007; 50: 552-558Abstract Full Text Full Text PDF PubMed Scopus (32) Google Scholar, 24.Verhave J.C. Hillege H.L. Burgerhof J.G. Gansevoort R.T. de Zeeuw D. de Jong P.E. PREVEND Study GroupThe association between atherosclerotic risk factors and renal function in the general population.Kidney Int. 2005; 67: 1967-1973Abstract Full Text Full Text PDF PubMed Scopus (91) Google Scholar, 25.de Boer I.H. Astor B.C. Kramer H. Palmas W. Seliger S.L. Shlipak M.G. Siscovick D.S. Tsai M.Y. Kestenbaum B. Lipoprotein abnormalities associated with mild impairment of kidney function in the multi-ethnic study of atherosclerosis.Clin. J. Am. Soc. Nephrol. 2008; 3: 125-132Crossref PubMed Scopus (55) Google Scholar). Moreover, in several of these reports (24.Verhave J.C. Hillege H.L. Burgerhof J.G. Gansevoort R.T. de Zeeuw D. de Jong P.E. PREVEND Study GroupThe association between atherosclerotic risk factors and renal function in the general population.Kidney Int. 2005; 67: 1967-1973Abstract Full Text Full Text PDF PubMed Scopus (91) Google Scholar, 25.de Boer I.H. Astor B.C. Kramer H. Palmas W. Seliger S.L. Shlipak M.G. Siscovick D.S. Tsai M.Y. Kestenbaum B. Lipoprotein abnormalities associated with mild impairment of kidney function in the multi-ethnic study of atherosclerosis.Clin. J. Am. Soc. Nephrol. 2008; 3: 125-132Crossref PubMed Scopus (55) Google Scholar), associations of HDL-C with kidney function were not controlled for factors affecting both kidney function and HDL-C, such as obesity and insulin resistance (26.Dengel D.R. Goldberg A.P. Mayuga R.S. Kairis G.M. Weir M.R. Insulin resistance, elevated glomerular filtration fraction, and renal injury.Hypertension. 1996; 28: 127-132Crossref PubMed Scopus (129) Google Scholar, 27.Krikken J.A. Lely A.T. Bakker S.J. Navis G. The effect of a shift in sodium intake on renal hemodynamics is determined by body mass index in healthy young men.Kidney Int. 2007; 71: 260-265Abstract Full Text Full Text PDF PubMed Scopus (85) Google Scholar, 28.Borggreve S.E. Hillege H.L. Wolffenbuttel B.H. de Jong P.E. Bakker S.J. van der Steege G. van Tol A. Dullaart R.P. PREVEND Study GroupThe effect of cholesteryl ester transfer protein -629C->A promoter polymorphism on high-density lipoprotein cholesterol is dependent on serum triglycerides.J. Clin. Endocrinol. Metab. 2005; 90: 4198-4204Crossref PubMed Scopus (57) Google Scholar). The present study was initiated to test the hypothesis that HDL-C and apoA-I are inversely associated with GFR in subjects without severely compromised renal function. To this end, we carried out cross-sectional analyses in a random sample of the general population that makes part of the PREVEND cohort. Fasting subjects were included, and we took potential confounding due to obesity, insulin resistance, and serum triglycerides into account. This study was conducted among subjects who participate in the Prevention of REnal and Vascular End-stage Disease (PREVEND) study, which began in 1997. This prospective cohort study in the city of Groningen (The Netherlands) investigates the natural course of urinary albumin excretion and its relation to renal and cardiovascular disease. The study was approved by the local medical ethics committee. All participants gave written informed consent. Details of the study protocol have been published elsewhere (29.Hillege H.L. Janssen W.M. Bak A.A. Diercks G.F. Grobbee D.E. Crijns H.J. Van Gilst W.H. De Zeeuw D. De Jong P.E. Prevend Study GroupMicroalbuminuria is common, also in a nondiabetic, nonhypertensive population, and an independent indicator of cardiovascular risk factors and cardiovascular morbidity.J. Intern. Med. 2001; 249: 519-526Crossref PubMed Scopus (516) Google Scholar, 30.Pinto-Sietsma S.J. Janssen W.M.T. Hillege H.L. Navis G. de Jong P.E. Urinary albumin excretion is associated with renal functional abnormalities in a non-diabetic population.J. Am. Soc. Nephrol. 2000; 11: 1882-1888PubMed Google Scholar). In summary, all inhabitants of the city of Groningen aged 28–75 years were sent a questionnaire and a vial to collect a first-morning-void urine sample (prescreening). Of these subjects, 40,856 responded (47.8%) and returned a vial to a central laboratory for urinary albumin and urinary creatinine assessment. From these 40,856 subjects, the PREVEND cohort was selected with the aim to create a cohort enriched for the presence of high urinary albumin excretion. After exclusion of insulin-using diabetic patients and pregnant women (defined by self-report), all subjects with a urinary albumin concentration of ≥10 mg/L (n = 7,768) were invited, of whom 6,000 participated. Furthermore, a randomly selected control group with a urinary albumin concentration of <10 mg/L (n = 3,394) was invited, and 2,592 participated. These 8,592 subjects constitute the entire PREVEND cohort and were asked to collect two consecutive 24 h urine samples (baseline screening). In order to compose a “random sample” representative of the Groningen population, we considered a subcohort of the 8,592 subjects. For this purpose, we included all subjects with a urinary albumin concentration of <10 mg/L who completed the first screening (n = 2,592) and added a subset of the “oversampled” subjects whose urinary albumin concentration was >10 mg/L by proportionally taking a computer-generated, random subset (n = 840) (31.Gansevoort R.T. Verhave J.C. Hillege H.L. Burgerhof J.G. Bakker S.J. de Zeeuw D. de Jong P.E. for the PREVEND Study GroupThe validity of screening based on spot morning urine samples to detect subjects with microalbuminuria in the general population.Kidney Int. Suppl. 2005; 94: S28-S35Abstract Full Text Full Text PDF PubMed Google Scholar). After exclusion of 18 participants known to have proteinuria or renal disease, a cohort of 3,414 participants was created. As expected, the characteristics of this “random sample” were similar to that of the original population (n = 40,856) (32.Lambers Heerspink H.J. Brantsma A.H. de Zeeuw D. Bakker S.J. de Jong P.E. Gansevoort R.T. PREVEND Study GroupAlbuminuria assessed from first-morning-void urine samples versus 24-hour urine collections as a predictor of cardiovascular morbidity and mortality.Am. J. Epidemiol. 2008; 168: 897-905Crossref PubMed Scopus (189) Google Scholar). Because we aimed to test a physiological relationship of HDL-C and apoA-I with kidney function, we selected individuals without manifest disease. Therefore, we excluded subjects with an estimated glomerular filtration rate (e-GFR) ≤ 45 ml/min/1.73 m2 [assessed using the Modification of Diet in Renal Disease (MDRD) equation; see below] and urinary albumin excretion >300 mg/24 h. We also excluded subjects with prior history of cardiovascular disease or with diabetes mellitus (see definitions), as well as subjects using any anti-hypertensives or lipid-lowering agents (including diuretics, angiotensin converting enzyme inhibitors, angiotensin antagonists, statins, and fibrates) in order to avoid bias attributable to associations of prevalent cardiovascular disease with (apo)lipoproteins and interference due to HDL effects of lipid-lowering and anti-hypertensive drugs. Individuals who were nonfasting at the time of screening were not allowed to participate to be able to calculate insulin resistance. Finally, we excluded subjects with missing values for HDL-C, apoA-I and apoA-II, and triglycerides (n = 24), leaving a study population consisting of 2,484 subjects. Participants underwent two visits to the outpatient research unit for the baseline survey. All participants completed a questionnaire on demographics, cardiovascular disease history, and medication use prior to their first visit. Height and weight were measured on the first visit; body mass index (BMI) was calculated as the ratio between weight and height squared (in kg/m2). Waist circumference was measured on the bare skin between the 10th rib and iliac crest. During the first and second visit, blood pressure was measured in supine position every min for 10 min with an automatic device (Dinamap XL Model 9300, Johnson-Johnson Medical, Tampa, FL). Blood pressure values are given as the mean of the last two recordings of both visits. The participants collected two 24 h urine samples for measurement of creatinine and albumin excretion; microalbuminuria and macroalbuminuria were defined as mean urinary albumin excretion between 30 and 300 mg/24 h, and >300 mg/24 h, respectively (30.Pinto-Sietsma S.J. Janssen W.M.T. Hillege H.L. Navis G. de Jong P.E. Urinary albumin excretion is associated with renal functional abnormalities in a non-diabetic population.J. Am. Soc. Nephrol. 2000; 11: 1882-1888PubMed Google Scholar, 31.Gansevoort R.T. Verhave J.C. Hillege H.L. Burgerhof J.G. Bakker S.J. de Zeeuw D. de Jong P.E. for the PREVEND Study GroupThe validity of screening based on spot morning urine samples to detect subjects with microalbuminuria in the general population.Kidney Int. Suppl. 2005; 94: S28-S35Abstract Full Text Full Text PDF PubMed Google Scholar, 32.Lambers Heerspink H.J. Brantsma A.H. de Zeeuw D. Bakker S.J. de Jong P.E. Gansevoort R.T. PREVEND Study GroupAlbuminuria assessed from first-morning-void urine samples versus 24-hour urine collections as a predictor of cardiovascular morbidity and mortality.Am. J. Epidemiol. 2008; 168: 897-905Crossref PubMed Scopus (189) Google Scholar). Participants were instructed to remain fasting for at least 8 h before blood sampling, which was done at the second visit. Diabetes mellitus was diagnosed by fasting plasma glucose ≥7.0 mmol/l according to 1997 American Diabetes Association criteria (33.Expert Committee on the Diagnosis and Classification of Diabetes MellitusReport of the Expert Committee on the Diagnosis and Classification of diabetes mellitus.Diabetes Care. 1997; 20: 1183-1197Crossref PubMed Scopus (7576) Google Scholar) or use of glucose-lowering drugs. Furthermore, information on medication use was checked using pharmacy-dispensing data from all community pharmacies in the city of Groningen, which covers complete information on drug use in 80% of PREVEND participants. Insulin resistance was estimated using homeostasis model assessment (HOMAir), which was quantified as insulin · glucose/22.5 (34.Matthews D.R. Hosker J.P. Rudenski A.S. Naylor B.A. Treacher D.F. Turner R.C. Homeostasis model assessment: insulin resistance and beta-cell function from fasting plasma glucose and insulin concentrations in man.Diabetologia. 1985; 28: 412-419Crossref PubMed Scopus (25844) Google Scholar). Three estimates of kidney function were applied: e-GFR calculated with the MDRD equation (35.Levey A.S. Bosch J.P. Lewis J.B. Greene T. Rogers N. Roth D. A more accurate method to estimate glomerular filtration rate from serum creatinine: a new prediction equation. Modification of Diet in Renal Disease Study Group.Ann. Intern. Med. 1999; 130: 461-470Crossref PubMed Scopus (13129) Google Scholar), e-GFR calculated with the new Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation (36.Levey A.S. Stevens L.A. Schmid C.H. Zhang Y.L. Castro 3rd, A.F. Feldman H.I. Kusek J.W. Eggers P. Van Lente F. Greene T. et al.CKD-EPI (Chronic Kidney Disease Epidemiology Collaboration). A new equation to estimate glomerular filtration rate.Ann. Intern. Med. 2009; 150: 604-612Crossref PubMed Scopus (16589) Google Scholar) (supplementary Table I) and the mean of two 24 h creatinine clearance measurements. All estimates of kidney function were corrected for 1.73 m2 of body surface area, which was calculated as 0.007184 · (height in cm) 0.725 · (body weight) 0.425 (37.Dubois D. DuBois E.F. A formula to estimate the approximate surface area if height and weight be known.Arch. Intern. Med. 1916; 17: 863-871Crossref Scopus (4129) Google Scholar). Plasma glucose was measured shortly after blood collection. For other measurements, serum samples were stored at −80°C until analysis. Serum and urinary creatinine, serum total cholesterol, and plasma glucose were measured using Kodak Ektachem dry chemistry (Eastman Kodak, Rochester, NY) with intra- and inter-assay coefficients of variation (CVs) < 3%. HDL-C was measured with a homogeneous method (direct HDL, no. 7D67, AEROSETTM System, Abbott Laboratories, Abbott Park, IL). In this assay system, HDL and apoB-containing lipoproteins are complexed with one reagent, followed by solubilizing HDL particles by another reagens (38.Warnick G.R. Nauck M. Rifai N. Evolution of methods for measurement of HDL cholesterol: from ultracentrifugation to homogenous assays.Clin. Chem. 2001; 47: 1579-1596Crossref PubMed Scopus (166) Google Scholar). Serum triglycerides were measured enzymatically. Serum apoA-I and apoA-II were determined by nephelometry applying commercially available reagents for Dade Behring nephelometer systems [BN II, Dade Behring, Marburg, Germany; apoA-I test kit, code no. OUED; apoA-II test kit, code no. OQBA, apo B test kit, code no. OSAN (39.Steinmetz J. Tarallo P. Fournier B. Caces E. Siest G. Reference limits of apolipoprotein A-I and apolipoprotein B using an IFCC standardized immunonephelometric method.Eur. J. Clin. Chem. Clin. Biochem. 1995; 33: 337-342PubMed Google Scholar)]. Intra- and inter-assay CVs of apoA-I, apoA-II, and HDL-C were all <5%. Urinary albumin concentration was determined by nephelometry, with a threshold of 2.3 mg/l and intra- and inter-assay CVs <3% (BNII; Dade Behring). Data are given in mean ± SD for parametrically distributed variables and in median (interquartile range) for variables with a skewed distribution. Univariate correlations were calculated using Pearson's regression coefficients. We additionally estimated the continuous relationships between HDL-C, apoA-I and apoA-II, and eGFR (MDRD) with polynomial regression analysis. Associations of HDL-C, apoA-I, and apoA-II with kidney function were also determined by dividing GFR estimates and creatinine clearance into quintiles using one-way ANOVA. Multiple linear regr" @default.
• W1997650038 created "2016-06-24" @default.
• W1997650038 creator A5005549802 @default.
• W1997650038 creator A5025686747 @default.
• W1997650038 creator A5041851398 @default.
• W1997650038 date "2010-07-01" @default.
• W1997650038 modified "2023-10-15" @default.
• W1997650038 title "Lower HDL-C and apolipoprotein A-I are related to higher glomerular filtration rate in subjects without kidney disease" @default.
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