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1. Age and Association of Kidney Measures With Mortality and End-stage Renal Disease

Author: Wright, Jt, Appel, Lj, Greene, T, Astor, Bc, Chalmers, J, Macmahon, S, Woodward, M, Arima, H, Yatsuya, H, Yamashita, K, Toyoshima, H, Tamakoshi, K, Tonelli, M, Hemmelgarn, Br, Bello, A, James, Mt, Coresh, J, Matsushita, K, Sang, Y, Atkins, Rc, Polkinghorne, Kr, Chadban, S, Shankar, A, Klein, R, Klein, Be, Lee, Ke, Wang, H, Wang, F, Zhang, L, Zuo, L, Levin, A, Djurdjev, O, Sacks, Fm, Curhan, Gc, Shlipak, M, Peralta, C, Katz, R, Fried, Lf, Iso, H, Kitamura, A, Ohira, T, Yamagishi, K, Jafar, Th, Islam, M, Hatcher, J, Poulter, N, Chaturvedi, N, Landray, Mj, Emberson, J, Townend, Jn, Wheeler, Dc, Rothenbacher, D, Brenner, H, Müller, H, Schöttker, B, Fox, Cs, Hwang, Sj, Meigs, Jb, Perkins, Rm, Fluck, N, Clark, Le, Prescott, Gj, Marks, A, Black, C, Cirillo, Massimo, Hallan, S, Aasarød, K, Øien, Cm, Radtke, M, Irie, F, Sairenchi, T, Smith, Dh, Weiss, Jw, Johnson, Es, Thorp, Ml, Collins, Aj, Vassalotti, Ja, Li, S, Chen, Sc, Lee, Bj, Wetzels, Jf, Blankestijn, Pj, Van, Zuilen, Sarnak, M, Levey, As, Inker, La, Menon, V, Kramer, Hj, Kronenberg, F, Kollerits, B, Ritz, E, Roderick, P, Nitsch, D, Fletcher, A, Bulpitt, C, Ishani, A, Neaton, Jd, Froissart, M, Stengel, B, Metzger, M, Haymann, Jp, Houillier, P, Flamant, M, Ohkubo, T, Metoki, H, Nakayama, M, Kikuya, M, Imai, Y, Iseki, K, Nelson, Rg, Knowler, Wc, Gansevoort, Rt, Jong, De, Mahmoodi, Bk, Heerspink, Hj, Jassal, Sk, Barrett Connor, E, Bergstrom, J, Brenner, Be, Zeeuw, De, D, Warnock, Dg, Muntner, P, Judd, S, Mcclellan, W, Jee, Sh, Kimm, H, Jo, J, Mok, Y, Lim, Je, Rossing, P, Parving, Hh, Tangri, N, Naimark, D, Wen, Cp, Wen, Sf, Tsao, Ck, Tsai, Mk, Ärnlöv, J, Lannfelt, L, Larsson, A, Bilo, Hj, Joosten, H, Kleefstra, N, Groenier, Kh, Drion, I, Ballew, Sh, Grams, M, Camarata, L, Hui, X, Seltzer, J, Winegrad, H., Cardiovascular Centre (CVC), Groningen Kidney Center (GKC), Wright JT Jr, Appel, Lj, Greene, T, Astor, Bc, Chalmers, J, Macmahon, S, Woodward, M, Arima, H, Yatsuya, H, Yamashita, K, Toyoshima, H, Tamakoshi, K, Tonelli, M, Hemmelgarn, Br, Bello, A, James, Mt, Coresh, J, Matsushita, K, Sang, Y, Atkins, Rc, Polkinghorne, Kr, Chadban, S, Shankar, A, Klein, R, Klein, Be, Lee, Ke, Wang, H, Wang, F, Zhang, L, Zuo, L, Levin, A, Djurdjev, O, Sacks, Fm, Curhan, Gc, Shlipak, M, Peralta, C, Katz, R, Fried, Lf, Iso, H, Kitamura, A, Ohira, T, Yamagishi, K, Jafar, Th, Islam, M, Hatcher, J, Poulter, N, Chaturvedi, N, Landray, Mj, Emberson, J, Townend, Jn, Wheeler, Dc, Rothenbacher, D, Brenner, H, Müller, H, Schöttker, B, Fox, C, Hwang, Sj, Meigs, Jb, Perkins, Rm, Fluck, N, Clark, Le, Prescott, Gj, Marks, A, Black, C, Cirillo, Massimo, Hallan, S, Aasarød, K, Øien, Cm, Radtke, M, Irie, F, Sairenchi, T, Smith, Dh, Weiss, Jw, Johnson, E, Thorp, Ml, Collins, Aj, Vassalotti, Ja, Li, S, Chen, Sc, Lee, Bj, Wetzels, Jf, Blankestijn, Pj, van Zuilen AD, Sarnak, M, Levey, A, Inker, La, Menon, V, Kramer, Hj, Kronenberg, F, Kollerits, B, Ritz, E, Roderick, P, Nitsch, D, Fletcher, A, Bulpitt, C, Ishani, A, Neaton, Jd, Froissart, M, Stengel, B, Metzger, M, Haymann, Jp, Houillier, P, Flamant, M, Ohkubo, T, Metoki, H, Nakayama, M, Kikuya, M, Imai, Y, Iseki, K, Nelson, Rg, Knowler, Wc, Gansevoort, Rt, de Jong PE, Mahmoodi, Bk, Heerspink, Hj, Jassal, Sk, Barrett-Connor, E, Bergstrom, J, Brenner, Be, de Zeeuw, D, Warnock, Dg, Muntner, P, Judd, S, Mcclellan, W, Jee, Sh, Kimm, H, Jo, J, Mok, Y, Lim, Je, Rossing, P, Parving, Hh, Tangri, N, Naimark, D, Wen, Cp, Wen, Sf, Tsao, Ck, Tsai, Mk, Ärnlöv, J, Lannfelt, L, Larsson, A, Bilo, Hj, Joosten, H, Kleefstra, N, Groenier, Kh, Drion, I, Ballew, Sh, Grams, M, Camarata, L, Hui, X, Seltzer, J, and Winegrad, H.
Subjects: Male, BLOOD-PRESSURE, urologic and male genital diseases, Kidney, età, GLOMERULAR-FILTRATION-RATE, Cohort Studies, eGFR, Young adult, Renal disorder [IGMD 9], ALL-CAUSE MORTALITY, GENERAL-POPULATION, insufficienza renale, biology, CYSTATIN C, CARDIOVASCULAR RISK, Age Factors, General Medicine, Middle Aged, female genital diseases and pregnancy complications, RISK POPULATION COHORTS, medicine.anatomical_structure, Female, medicine.symptom, Glomerular Filtration Rate, albuminuria, rischio, mortalità, Adult, Risk, medicine.medical_specialty, Adolescent, Renal function, Context (language use), End stage renal disease, Young Adult, Internal medicine, medicine, Albuminuria, Humans, OLDER-ADULTS, Aged, urogenital system, business.industry, URINARY ALBUMIN EXCRETION, medicine.disease, Endocrinology, Cystatin C, COLLABORATIVE METAANALYSIS, biology.protein, Kidney Failure, Chronic, business, Kidney disease
Abstract: Context Chronic kidney disease (CKD) is prevalent in older individuals, but the risk implications of low estimated glomerular filtration rate (eGFR) and high albuminuria across the full age range are controversial.Objective To evaluate possible effect modification (interaction) by age of the association of eGFR and albuminuria with clinical risk, examining both relative and absolute risks.Design, Setting, and Participants Individual-level meta-analysis including 2 051 244 participants from 33 general population or high-risk (of vascular disease) cohorts and 13 CKD cohorts from Asia, Australasia, Europe, and North/South America, conducted in 1972-2011 with a mean follow-up time of 5.8 years (range, 0-31 years).Main Outcome Measures Hazard ratios (HRs) of mortality and end-stage renal disease (ESRD) according to eGFR and albuminuria were meta-analyzed across age categories after adjusting for sex, race, cardiovascular disease, diabetes, systolic blood pressure, cholesterol, body mass index, and smoking. Absolute risks were estimated using HRs and average incidence rates.Results Mortality (112 325 deaths) and ESRD (8411 events) risks were higher at lower eGFR and higher albuminuria in every age category. In general and high-risk cohorts, relative mortality risk for reduced eGFR decreased with increasing age; eg, adjusted HRs at an eGFR of 45 mL/min/1.73 m(2) vs 80 mL/min/1.73 m(2) were 3.50 (95% CI, 2.55-4.81), 2.21 (95% CI, 2.02-2.41), 1.59 (95% CI, 1.42-1.77), and 1.35 (95% CI, 1.23-1.48) in age categories 18-54, 55-64, 65-74, and >= 75 years, respectively (P Conclusions Both low eGFR and high albuminuria were independently associated with mortality and ESRD regardless of age across a wide range of populations. Mortality showed lower relative risk but higher absolute risk differences at older age.
Published: 2012

2. Associations of kidney disease measures with mortality and end-stage renal disease in individuals with and without diabetes: a meta-analysis

Author: Fox, Cs, Matsushita, K, Woodward, M, Bilo, Hj, Chalmers, J, Heerspink, Hj, Lee, Bj, Perkins, Rm, Rossing, P, Sairenchi, T, Tonelli, M, Vassalotti, Ja, Yamagishi, K, Coresh, J, Jong, De, Wen, Cp, Nelson, Rg, Chronic, Kidney, Disease, Prognosis, Consortium, Investigators/collaborators:, Wright, J, Appel, L, Greene, T, Astor, Bc, Macmahon, S, Arima, H, Yatsuya, H, Yamashita, K, Toyoshima, H, Tamakoshi, K, Sang, Y, Atkins, Rc, Polkinghorne, Kr, Chadban, S, Shankar, A, Klein, R, Klein, Be, Lee, Ke, Wang, H, Wang, F, Zhang, L, Zuo, L, Levin, A, Djurdjev, O, Sacks, Fm, Curhan, Gc, Shlipak, M, Peralta, C, Katz, R, Fried, L, Iso, H, Kitamura, A, Ohira, T, Jafar, Th, Islam, M, Hatcher, J, Poulter, N, Chaturvedi, N, Landray, Mj, Emberson, Jr, Townend, Jn, Wheeler, Dc, Rothenbacher, D, Brenner, H, Müller, H, Schöttker, B, Hwang, Sj, Meigs, Jb, Fluck, N, Clark, Le, Prescott, Gj, Marks, A, Black, C, Cirillo, Massimo, Hallan, S, Aasarød, K, Øien, Cm, Radtke, M, Irie, F, Smith, Dh, Weiss, Jw, Johnson, Es, Thorp, Ml, Collins, Aj, Li, S, Chen, Sc, Wetzels, Jf, Blankestijn, Pj, Van, Zuilen, Sarnak, M, Levey, As, Menon, V, Kramer, Hj, Boer, De, Kronenberg, F, Kollerits, B, Ritz, E, Roderick, P, Nitsch, D, Fletcher, A, Bulpitt, C, Ishani, A, Neaton, Jd, Froissart, M, Stengel, B, Metzger, M, Haymann, Jp, Houillier, P, Flamant, M, Ohkubo, T, Metoki, H, Nakayama, M, Kikuya, M, Imai, Y, Knowler, Wc, Gansevoort, Rt, Mahmoodi, Bk, Bakker, Sj, Jassal, Sk, Barrett Connor, E, Bergstrom, J, Lambers, Heerspink, Brenner, Be, Zeeuw, D, Warnock, Dg, Muntner, P, Judd, S, Mcclellan, W, Jee, Sh, Kimm, H, Jo, J, Mok, Y, Lim, Je, Parving, Hh, Tangri, N, Naimark, D, Wen, Sf, Tsao, Ck, Tsai, Mk, Ärnlöv, J, Lannfelt, L, Larsson, A, Joosten, H, Kleefstra, N, Groenier, Kh, Drion, I, Hemmelgarn, B, Ballew, Sh, Grams, M, Camarata, L, Hui, X, Seltzer, J, Winegrad, H., Groningen Kidney Center (GKC), Methods in Medicines evaluation & Outcomes research (M2O), Lifestyle Medicine (LM), Fox, C, Matsushita, K, Woodward, M, Bilo, Hj, Chalmers, J, Heerspink, Hj, Lee, Bj, Perkins, Rm, Rossing, P, Sairenchi, T, Tonelli, M, Vassalotti, Ja, Yamagishi, K, Coresh, J, de Jong PE, Wen, Cp, Nelson, Rg, Investigators/Collaborators: Wright J, Chronic Kidney Disease Prognosis Consortium, Appel, L, Greene, T, Astor, Bc, Macmahon, S, Arima, H, Yatsuya, H, Yamashita, K, Toyoshima, H, Tamakoshi, K, Sang, Y, Atkins, Rc, Polkinghorne, Kr, Chadban, S, Shankar, A, Klein, R, Klein, Be, Lee, Ke, Wang, H, Wang, F, Zhang, L, Zuo, L, Levin, A, Djurdjev, O, Sacks, Fm, Curhan, Gc, Shlipak, M, Peralta, C, Katz, R, Fried, L, Iso, H, Kitamura, A, Ohira, T, Jafar, Th, Islam, M, Hatcher, J, Poulter, N, Chaturvedi, N, Landray, Mj, Emberson, Jr, Townend, Jn, Wheeler, Dc, Rothenbacher, D, Brenner, H, Müller, H, Schöttker, B, Hwang, Sj, Meigs, Jb, Fluck, N, Clark, Le, Prescott, Gj, Marks, A, Black, C, Cirillo, Massimo, Hallan, S, Aasarød, K, Øien, Cm, Radtke, M, Irie, F, Smith, Dh, Weiss, Jw, Johnson, E, Thorp, Ml, Collins, Aj, Li, S, Chen, Sc, Wetzels, Jf, Blankestijn, Pj, van Zuilen AD, Sarnak, M, Levey, A, Menon, V, Kramer, Hj, de Boer IH, Kronenberg, F, Kollerits, B, Ritz, E, Roderick, P, Nitsch, D, Fletcher, A, Bulpitt, C, Ishani, A, Neaton, Jd, Froissart, M, Stengel, B, Metzger, M, Haymann, Jp, Houillier, P, Flamant, M, Ohkubo, T, Metoki, H, Nakayama, M, Kikuya, M, Imai, Y, Knowler, Wc, Gansevoort, Rt, Mahmoodi, Bk, Bakker, Sj, Jassal, Sk, Barrett-Connor, E, Bergstrom, J, Lambers Heerspink HJ, Brenner, Be, Zeeuw, D, Warnock, Dg, Muntner, P, Judd, S, Mcclellan, W, Jee, Sh, Kimm, H, Jo, J, Mok, Y, Lim, Je, Parving, Hh, Tangri, N, Naimark, D, Wen, Sf, Tsao, Ck, Tsai, Mk, Ärnlöv, J, Lannfelt, L, Larsson, A, Joosten, H, Kleefstra, N, Groenier, Kh, Drion, I, Hemmelgarn, B, Ballew, Sh, Grams, M, Camarata, L, Hui, X, Seltzer, J, and Winegrad, H.
Subjects: medicine.medical_specialty, Population, UNITED-STATES, Renal function, ALL-CAUSE, GLOMERULAR-FILTRATION-RATE, albuminuria, End stage renal disease, Diabetic nephropathy, CKD-PC Consortium, Diabetes mellitus, Internal medicine, eGFR, Medicine, ESTIMATED GFR, education, Intensive care medicine, Renal disorder [IGMD 9], OUTCOMES, education.field_of_study, end-stage renal disease, diabetes, business.industry, Hazard ratio, PROTEINURIA, General Medicine, mortality, medicine.disease, RISK POPULATION COHORTS, PREVALENCE, diabete, COLLABORATIVE METAANALYSIS, Albuminuria, medicine.symptom, HIGHER ALBUMINURIA, business, Kidney disease
Abstract: Item does not contain fulltext BACKGROUND: Chronic kidney disease is characterised by low estimated glomerular filtration rate (eGFR) and high albuminuria, and is associated with adverse outcomes. Whether these risks are modified by diabetes is unknown. METHODS: We did a meta-analysis of studies selected according to Chronic Kidney Disease Prognosis Consortium criteria. Data transfer and analyses were done between March, 2011, and June, 2012. We used Cox proportional hazards models to estimate the hazard ratios (HR) of mortality and end-stage renal disease (ESRD) associated with eGFR and albuminuria in individuals with and without diabetes. FINDINGS: We analysed data for 1,024,977 participants (128,505 with diabetes) from 30 general population and high-risk cardiovascular cohorts and 13 chronic kidney disease cohorts. In the combined general population and high-risk cohorts with data for all-cause mortality, 75,306 deaths occurred during a mean follow-up of 8.5 years (SD 5.0). In the 23 studies with data for cardiovascular mortality, 21,237 deaths occurred from cardiovascular disease during a mean follow-up of 9.2 years (SD 4.9). In the general and high-risk cohorts, mortality risks were 1.2-1.9 times higher for participants with diabetes than for those without diabetes across the ranges of eGFR and albumin-to-creatinine ratio (ACR). With fixed eGFR and ACR reference points in the diabetes and no diabetes groups, HR of mortality outcomes according to lower eGFR and higher ACR were much the same in participants with and without diabetes (eg, for all-cause mortality at eGFR 45 mL/min per 1.73 m(2) [vs 95 mL/min per 1.73 m(2)], HR 1.35; 95% CI 1.18-1.55; vs 1.33; 1.19-1.48 and at ACR 30 mg/g [vs 5 mg/g], 1.50; 1.35-1.65 vs 1.52; 1.38-1.67). The overall interactions were not significant. We identified much the same findings for ESRD in the chronic kidney disease cohorts. INTERPRETATION: Despite higher risks for mortality and ESRD in diabetes, the relative risks of these outcomes by eGFR and ACR are much the same irrespective of the presence or absence of diabetes, emphasising the importance of kidney disease as a predictor of clinical outcomes. FUNDING: US National Kidney Foundation.
Published: 2012

3. Past Decline Versus Current eGFR and Subsequent Mortality Risk

Author: Naimark DMJ, Grams ME, Matsushita K, Black C, Drion I, Fox CS, Inker LA, Ishani A, Jee SA, Kitamura A, Lea JP, Nally J, Peralta CA, Rothenbacher D, Ryu S, Tonelli M, Yatsuya H, Coresh J, Gansevoort RT, Warnock DG, Woodward M, de Jong PE, the CKD Prognosis Consortium, Wright JTJr, Appel LJ, Greene T, MacMahon S, Chalmers J, Arima H, Yamashita K, Toyoshima H, Tamakoshi K, Hemmelgarn B, James M, Sang Y, Atkins RC, Polkinghorne KR, Chadban S, Shankar A, Klein R, Klein BEK, Lee KE, Levin A, Djurdjev O, Sacks FM, Curhan GC, Zawada AM, Rogacev KS, Seiler S, Heine GH, Navaneethan SD, Schold JD, Shlipak M, Sarnak MJ, Katz R, Imano H, Yamagishi K, Wheeler DC, Emberson J, Townend JN, Landray MJ, Brenner H, Müller H, Schöttker B, Hwang S-J, Meigs JB, Uphadhay A, Green J, Kirchner HL, Perkins R, Chang AR, Fluck N, Prescott GJ, Cirillo M, Hallan S, Aasarød K, Øien CM, Radtke M, Irie F, Iso H, Sairenchi T, Smith DH, Thorp ML, Johnson ES, Lee BJ, Guallar E, Chang SY, Cho J, Shin H, Chodick G, Shalev V, Birnbaum YC, Shainberg B, Wetzels JFM, Blankestijn PJ, van Zuilen AD, Levey AS, Neaton JD, Froissart M, Stengel B, Metzger M, Haymann J-P, Houillier P, Flamant M, Elley CR, Kenealy T, Moyes SA, Collins JF, Drury PL, Ohkubo T, Metoki H, Nakayama M, Imai Y, Iseki K, Nelson RG, Knowler WC, Bakker SJL, LHillege H, Jassal SK, Bergstrom J, Ix JH, Barrett-Connor E, Heerspink HJL, Brenner BE, de Zeeuw D, Kimm H, Mok Y, Tangri N, Wen C-P, Wen S-F, Tsao C-K, Tsai M-K, Ärnlöv J, Lannfelt L, Larsson A, Kovesdy CP, Kalantar-Zadeh K, Bilo HJ, Kleefstra N, Groenier KH, Joosten H, Ballew SH, Naimark, Dmj, Grams, Me, Matsushita, K, Black, C, Drion, I, Fox, C, Inker, La, Ishani, A, Jee, Sa, Kitamura, A, Lea, Jp, Nally, J, Peralta, Ca, Rothenbacher, D, Ryu, S, Tonelli, M, Yatsuya, H, Coresh, J, Gansevoort, Rt, Warnock, Dg, Woodward, M, de Jong, Pe, the CKD Prognosis, Consortium, Wright, Jtjr, Appel, Lj, Greene, T, Macmahon, S, Chalmers, J, Arima, H, Yamashita, K, Toyoshima, H, Tamakoshi, K, Hemmelgarn, B, James, M, Sang, Y, Atkins, Rc, Polkinghorne, Kr, Chadban, S, Shankar, A, Klein, R, Klein, Bek, Lee, Ke, Levin, A, Djurdjev, O, Sacks, Fm, Curhan, Gc, Zawada, Am, Rogacev, K, Seiler, S, Heine, Gh, Navaneethan, Sd, Schold, Jd, Shlipak, M, Sarnak, Mj, Katz, R, Imano, H, Yamagishi, K, Wheeler, Dc, Emberson, J, Townend, Jn, Landray, Mj, Brenner, H, Müller, H, Schöttker, B, Hwang, S-J, Meigs, Jb, Uphadhay, A, Green, J, Kirchner, Hl, Perkins, R, Chang, Ar, Fluck, N, Prescott, Gj, Cirillo, M, Hallan, S, Aasarød, K, Øien, Cm, Radtke, M, Irie, F, Iso, H, Sairenchi, T, Smith, Dh, Thorp, Ml, Johnson, E, Lee, Bj, Guallar, E, Chang, Sy, Cho, J, Shin, H, Chodick, G, Shalev, V, Birnbaum, Yc, Shainberg, B, Wetzels, Jfm, Blankestijn, Pj, van Zuilen, Ad, Levey, A, Neaton, Jd, Froissart, M, Stengel, B, Metzger, M, Haymann, J-P, Houillier, P, Flamant, M, Elley, Cr, Kenealy, T, Moyes, Sa, Collins, Jf, Drury, Pl, Ohkubo, T, Metoki, H, Nakayama, M, Imai, Y, Iseki, K, Nelson, Rg, Knowler, Wc, Bakker, Sjl, Lhillege, H, Jassal, Sk, Bergstrom, J, Ix, Jh, Barrett-Connor, E, Heerspink, Hjl, Brenner, Be, de Zeeuw, D, Kimm, H, Mok, Y, Tangri, N, Wen, C-P, Wen, S-F, Tsao, C-K, Tsai, M-K, Ärnlöv, J, Lannfelt, L, Larsson, A, Kovesdy, Cp, Kalantar-Zadeh, K, Bilo, Hj, Kleefstra, N, Groenier, Kh, Joosten, H, Ballew, Sh, Cardiovascular Centre (CVC), and Groningen Kidney Center (GKC)
Subjects: Gerontology, Male, CHRONIC KIDNEY-DISEASE, medicine.medical_specialty, Time Factors, 030232 urology & nephrology, Renal function, 030204 cardiovascular system & hematology, ALL-CAUSE, GLOMERULAR-FILTRATION-RATE, 03 medical and health sciences, 0302 clinical medicine, Risk Factors, Internal medicine, Cause of Death, Epidemiology, Risk of mortality, medicine, EQUATION, Humans, Clinical Epidemiology, Renal Insufficiency, Chronic, Aged, Proportional Hazards Models, business.industry, Hazard ratio, STAGE RENAL-DISEASE, DEATH, General Medicine, Middle Aged, POPULATION COHORTS, Confidence interval, Increased risk, Nephrology, CARDIOVASCULAR-DISEASE, COLLABORATIVE METAANALYSIS, Female, business, HIGHER ALBUMINURIA, All cause mortality, Glomerular Filtration Rate
Abstract: A single determination of eGFR associates with subsequent mortality risk. Prior decline in eGFR indicates loss of kidney function, but the relationship to mortality risk is uncertain. We conducted an individual-level meta-analysis of the risk of mortality associated with antecedent eGFR slope, adjusting for established risk factors, including last eGFR, among 1.2 million subjects from 12 CKD and 22 other cohorts within the CKD Prognosis Consortium. Over a 3-year antecedent period, 12% of participants in the CKD cohorts and 11% in the other cohorts had an eGFR slope-5 ml/min per 1.73 m(2) per year, whereas 7% and 4% had a slope5 ml/min per 1.73 m(2) per year, respectively. Compared with a slope of 0 ml/min per 1.73 m(2) per year, a slope of -6 ml/min per 1.73 m(2) per year associated with adjusted hazard ratios for all-cause mortality of 1.25 (95% confidence interval [95% CI], 1.09 to 1.44) among CKD cohorts and 1.15 (95% CI, 1.01 to 1.31) among other cohorts during a follow-up of 3.2 years. A slope of +6 ml/min per 1.73 m(2) per year also associated with higher all-cause mortality risk, with adjusted hazard ratios of 1.58 (95% CI, 1.29 to 1.95) among CKD cohorts and 1.43 (95% CI, 1.11 to 1.84) among other cohorts. Results were similar for cardiovascular and noncardiovascular causes of death and stronger for longer antecedent periods (3 versus3 years). We conclude that prior decline or rise in eGFR associates with an increased risk of mortality, independent of current eGFR.
Published: 2016

4. Comparison of risk prediction using the CKD-EPI equation and the MDRD study equation for estimated glomerular filtration rate

Author: Matsushita, K, Mahmoodi, Bk, Woodward, M, Emberson, Jr, Jafar, Th, Jee, Sh, Polkinghorne, Kr, Shankar, A, Smith, Dh, Tonelli, M, Warnock, Dg, Wen, Cp, Coresh, J, Gansevoort, Rt, Hemmelgarn, Br, Levey, As, Chronic, Kidney, Disease, Prognosis, Consortium, Wright, J, Appel, Lj, Greene, T, Astor, Bc, Chalmers, J, Macmahon, S, Yatsuya, H, Yamashita, K, Toyoshima, H, Tamakoshi, K, Sang, Y, Atkins, Rc, Chadban, S, Klein, R, Klein, Be, Lee, Ke, Wang, H, Wang, F, Zhang, L, Zuo, L, Levin, A, Djurdjev, O, Sacks, Fm, Curhan, Gc, Shlipak, M, Peralta, C, Katz, R, Fried, Lf, Iso, H, Ohira, T, Kitamura, A, Yamagishi, K, Islam, M, Hatcher, J, Poulter, N, Chaturvedi, N, Landray, Mj, Townend, Jn, Wheeler, Dc, Rothenbacher, D, Brenner, H, Müller, H, Schöttker, B, Fox, Cs, Hwang, Sj, Meigs, Jb, Perkins, Rm, Fluck, N, Clark, Le, Prescott, Gj, Marks, A, Black, C, Cirillo, Massimo, Hallan, S, Aasarød, K, Øien, Cm, Radtke, M, Irie, F, Sairenchi, T, Johnson, Es, Thorp, Ml, Weiss, Jw, Collins, Aj, Li, S, Chen, Sc, Vassalotti, Ja, Lee, Bj, Wetzels, Jf, Blankestijn, Pj, Van, Zuilen, Sarnak, M, Menon, V, Boer, De, Kramer, Hj, Kronenberg, F, Kollerits, B, Ritz, E, Roderick, P, Nitsch, D, Fletcher, A, Bulpitt, C, Ishani, A, Neaton, Jd, Froissart, M, Stengel, B, Metzger, M, Haymann, Jp, Houillier, P, Flamant, M, Ohkubo, T, Nakayama, M, Metoki, H, Kikuya, M, Imai, Y, Iseki, K, Nelson, Rg, Knowler, Wc, Jong, De, Bakker, Sj, Jassal, Sk, Barrett-Connor, E, Bergstrom, J, Heerspink, Hj, Zeeuw, De, D, Brenner, Be, Muntner, P, Judd, S, Mcclellan, W, Kimm, H, Jo, J, Mok, Y, Choi, E, Rossing, P, Parving, Hh, Tangri, N, Naimark, D, Wen, Sf, Tsao, Ck, Tsai, Mk, Ärnlöv, J, Larsson, A, Lannfelt, L, Bilo, Hj, Kleefstra, N, Groenier, Kh, Drion, I, Joosten, H, Ballew, Sh, Grams, M, Camarata, L, Hui, X, Seltzer, J, Winegrad, H., Matsushita, K, Mahmoodi, Bk, Woodward, M, Emberson, Jr, Jafar, Th, Jee, Sh, Polkinghorne, Kr, Shankar, A, Smith, Dh, Tonelli, M, Warnock, Dg, Wen, Cp, Coresh, J, Gansevoort, Rt, Hemmelgarn, Br, Levey, A, Chronic, Kidney, Disease, Prognosi, Consortium, Wright, J, Appel, Lj, Greene, T, Astor, Bc, Chalmers, J, Macmahon, S, Yatsuya, H, Yamashita, K, Toyoshima, H, Tamakoshi, K, Sang, Y, Atkins, Rc, Chadban, S, Klein, R, Klein, Be, Lee, Ke, Wang, H, Wang, F, Zhang, L, Zuo, L, Levin, A, Djurdjev, O, Sacks, Fm, Curhan, Gc, Shlipak, M, Peralta, C, Katz, R, Fried, Lf, Iso, H, Ohira, T, Kitamura, A, Yamagishi, K, Islam, M, Hatcher, J, Poulter, N, Chaturvedi, N, Landray, Mj, Townend, Jn, Wheeler, Dc, Rothenbacher, D, Brenner, H, Müller, H, Schöttker, B, Fox, C, Hwang, Sj, Meigs, Jb, Perkins, Rm, Fluck, N, Clark, Le, Prescott, Gj, Marks, A, Black, C, Cirillo, Massimo, Hallan, S, Aasarød, K, Øien, Cm, Radtke, M, Irie, F, Sairenchi, T, Johnson, E, Thorp, Ml, Weiss, Jw, Collins, Aj, Li, S, Chen, Sc, Vassalotti, Ja, Lee, Bj, Wetzels, Jf, Blankestijn, Pj, Van, Zuilen, Ad, Sarnak, M, Menon, V, De, Boer, Ih, Kramer, Hj, Kronenberg, F, Kollerits, B, Ritz, E, Roderick, P, Nitsch, D, Fletcher, A, Bulpitt, C, Ishani, A, Neaton, Jd, Froissart, M, Stengel, B, Metzger, M, Haymann, Jp, Houillier, P, Flamant, M, Ohkubo, T, Nakayama, M, Metoki, H, Kikuya, M, Imai, Y, Iseki, K, Nelson, Rg, Knowler, Wc, De, Jong, Pe, Bakker, Sj, Jassal, Sk, Barrett-Connor, E, Bergstrom, J, Heerspink, Hj, De, Zeeuw, D, Brenner, Be, Muntner, P, Judd, S, Mcclellan, W, Kimm, H, Jo, J, Mok, Y, Choi, E, Rossing, P, Parving, Hh, Tangri, N, Naimark, D, Wen, Sf, Tsao, Ck, Tsai, Mk, Ärnlöv, J, Larsson, A, Lannfelt, L, Bilo, Hj, Kleefstra, N, Groenier, Kh, Drion, I, Joosten, H, Ballew, Sh, Grams, M, Camarata, L, Hui, X, Seltzer, J, Winegrad, H., Cardiovascular Centre (CVC), and Groningen Kidney Center (GKC)
Subjects: CHRONIC KIDNEY-DISEASE, Gerontology, Male, EVALUATION PROGRAM KEEP, Population, Renal function, Black People, Ckd epi equation, urologic and male genital diseases, Risk Assessment, White People, Article, Decision Support Techniques, Cohort Studies, Sex Factors, Asian People, EPIDEMIOLOGY COLLABORATION EQUATION, Diabetes mellitus, CYSTATIN-C, Medicine, Humans, education, ALL-CAUSE MORTALITY, Cardiovascular mortality, Aged, Renal disorder [IGMD 9], GENERAL-POPULATION, education.field_of_study, business.industry, CARDIOVASCULAR RISK, Hazard ratio, STAGE RENAL-DISEASE, General Medicine, POPULATION COHORTS, Middle Aged, Models, Theoretical, medicine.disease, female genital diseases and pregnancy complications, Net reclassification improvement, SERUM CREATININE VALUES, Cardiovascular Diseases, Kidney Failure, Chronic, Female, business, Algorithms, Demography, Glomerular Filtration Rate
Abstract: Contains fulltext : 110640.pdf (Publisher’s version ) (Closed access) CONTEXT: The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) equation more accurately estimates glomerular filtration rate (GFR) than the Modification of Diet in Renal Disease (MDRD) Study equation using the same variables, especially at higher GFR, but definitive evidence of its risk implications in diverse settings is lacking. OBJECTIVE: To evaluate risk implications of estimated GFR using the CKD-EPI equation compared with the MDRD Study equation in populations with a broad range of demographic and clinical characteristics. DESIGN, SETTING, AND PARTICIPANTS: A meta-analysis of data from 1.1 million adults (aged >/= 18 years) from 25 general population cohorts, 7 high-risk cohorts (of vascular disease), and 13 CKD cohorts. Data transfer and analyses were conducted between March 2011 and March 2012. MAIN OUTCOME MEASURES: All-cause mortality (84,482 deaths from 40 cohorts), cardiovascular mortality (22,176 events from 28 cohorts), and end-stage renal disease (ESRD) (7644 events from 21 cohorts) during 9.4 million person-years of follow-up; the median of mean follow-up time across cohorts was 7.4 years (interquartile range, 4.2-10.5 years). RESULTS: Estimated GFR was classified into 6 categories (>/=90, 60-89, 45-59, 30-44, 15-29, and /=65 years), sex, race/ethnicity (white, Asian, and black), and presence or absence of diabetes and hypertension. The results in the high-risk and CKD cohorts were largely consistent with the general population cohorts. CONCLUSION: The CKD-EPI equation classified fewer individuals as having CKD and more accurately categorized the risk for mortality and ESRD than did the MDRD Study equation across a broad range of populations.
Published: 2012

5. Estimated glomerular filtration rate and albuminuria for prediction of cardiovascular outcomes: a collaborative meta-analysis of individual participant data

Author: Matsushita, K, Coresh, J, Sang, Y, Chalmers, J, Fox, C, Guallar, E, Jafar, T, Jassal, Sk, Landman, Gw, Muntner, P, Roderick, P, Sairenchi, T, Schöttker, B, Shankar, A, Shlipak, M, Tonelli, M, Townend, J, van Zuilen, A, Yamagishi, K, Yamashita, K, Gansevoort, R, Sarnak, M, Warnock, Dg, Woodward, M, Ärnlöv J, CKD Prognosis Consortium, Macmahon, S, Arima, H, Yatsuya, H, Toyoshima, H, Tamakoshi, K, Atkins, Rc, Polkinghorne, Kr, Chadban, S, Klein, R, Klein, Be, Lee, Ke, Sacks, Fm, Curhan, Gc, Sarnak, Mj, Katz, R, Iso, H, Kitamura, A, Imano, H, Jafar, Th, Islam, M, Hatcher, J, Poulter, N, Chaturvedi, N, Wheeler, Dc, Emberson, J, Townend, Jn, Landray, Mj, Brenner, H, Rothenbacher, D, Müller, H, Fox, Cs, Hwang, Sj, Meigs, Jb, Upadhyay, A, Perkins, R, Chang, Ar, Cirillo, Massimo, Hallan, S, Aasarød, K, Øien, Cm, Romundstad, S, Ryu, S, Chang, Y, Cho, J, Shin, H, Chodick, G, Shalev, V, Ash, N, Shainberg, B, Wetzels, Jf, Blankestijn, Pj, Van, Zuilen, Levey, As, Inker, La, Menon, V, Peralta, C, Nitsch, D, Fletcher, A, Bulpitt, C, Elley, Cr, Kenealy, T, Moyes, Sa, Collins, Jf, Drury, P, Ohkubo, T, Metoki, H, Nakayama, M, Kikuya, M, Imai, Y, Gansevoort, Rt, Bakker, Sj, Hillege, Hl, Heerspink, Hj, Bergstrom, J, Jh, Ix, Barrett Connor, E, Judd, S, Mcclellan, W, Jee, Sh, Kimm, H, Mok, Y, Tangri, N, Sud, M, Naimark, D, Wen, Cp, Wen, Sf, Tsao, Ck, Tsai, Mk, Ärnlöv, J, Lannfelt, L, Larsson, A, Bilo, Hj, Kleefstra, N, Groenier, Kh, Joosten, H, Drion, I, Jong, De, Iseki, K, Stengel, B, Warnock, D, Ballew, Sh, Woodward, M., Matsushita, K, Coresh, J, Sang, Y, Chalmers, J, Fox, C, Guallar, E, Jafar, T, Jassal, Sk, Landman, Gw, Muntner, P, Roderick, P, Sairenchi, T, Schöttker, B, Shankar, A, Shlipak, M, Tonelli, M, Townend, J, van Zuilen, A, Yamagishi, K, Yamashita, K, Gansevoort, R, Sarnak, M, Warnock, Dg, Woodward, M, Ärnlöv, J, CKD Prognosis, Consortium, Macmahon, S, Arima, H, Yatsuya, H, Toyoshima, H, Tamakoshi, K, Atkins, Rc, Polkinghorne, Kr, Chadban, S, Klein, R, Klein, Be, Lee, Ke, Sacks, Fm, Curhan, Gc, Sarnak, Mj, Katz, R, Iso, H, Kitamura, A, Imano, H, Jafar, Th, Islam, M, Hatcher, J, Poulter, N, Chaturvedi, N, Wheeler, Dc, Emberson, J, Townend, Jn, Landray, Mj, Brenner, H, Rothenbacher, D, Müller, H, Hwang, Sj, Meigs, Jb, Upadhyay, A, Perkins, R, Chang, Ar, Cirillo, Massimo, Hallan, S, Aasarød, K, Øien, Cm, Romundstad, S, Ryu, S, Chang, Y, Cho, J, Shin, H, Chodick, G, Shalev, V, Ash, N, Shainberg, B, Wetzels, Jf, Blankestijn, Pj, Van, Zuilen, Ad, Levey, A, Inker, La, Menon, V, Peralta, C, Nitsch, D, Fletcher, A, Bulpitt, C, Elley, Cr, Kenealy, T, Moyes, Sa, Collins, Jf, Drury, P, Ohkubo, T, Metoki, H, Nakayama, M, Kikuya, M, Imai, Y, Gansevoort, Rt, Bakker, Sj, Hillege, Hl, Heerspink, Hj, Bergstrom, J, Ix, Jh, Barrett Connor, E, Judd, S, Mcclellan, W, Jee, Sh, Kimm, H, Mok, Y, Tangri, N, Sud, M, Naimark, D, Wen, Cp, Wen, Sf, Tsao, Ck, Tsai, Mk, Lannfelt, L, Larsson, A, Bilo, Hj, Kleefstra, N, Groenier, Kh, Joosten, H, Drion, I, De, Jong, Pe, Iseki, K, Stengel, B, Warnock, D, Ballew, Sh, Woodward, M., Cardiovascular Centre (CVC), and Groningen Kidney Center (GKC)
Subjects: CHRONIC KIDNEY-DISEASE, Male, Endocrinology, Diabetes and Metabolism, Coronary Disease, 030204 cardiovascular system & hematology, chemistry.chemical_compound, 0302 clinical medicine, Endocrinology, cardiovascular disease, Risk Factors, eGFR, EQUATION, ARTERY-DISEASE, EPIDEMIOLOGY, 030212 general & internal medicine, RISK, education.field_of_study, CYSTATIN C, biology, ASSOCIATION, Middle Aged, 3. Good health, Stroke, 1101 Medical Biochemistry and Metabolomics, Cardiovascular Diseases, Creatinine, eGFR, albuminuria, cardiovascular disease, HEART, Female, medicine.symptom, Life Sciences & Biomedicine, Glomerular Filtration Rate, Adult, medicine.medical_specialty, Population, Renal function, 1117 Public Health and Health Services, Endocrinology & Metabolism, 03 medical and health sciences, Diabetes mellitus, Internal medicine, CKD, Internal Medicine, medicine, Albuminuria, Humans, education, CKD Prognosis Consortium, Heart Failure, Science & Technology, business.industry, MORTALITY, 1103 Clinical Sciences, medicine.disease, chemistry, Cystatin C, Heart failure, biology.protein, Renal disorders Radboud Institute for Health Sciences [Radboudumc 11], business, Follow-Up Studies, Kidney disease
Abstract: Item does not contain fulltext BACKGROUND: The usefulness of estimated glomerular filtration rate (eGFR) and albuminuria for prediction of cardiovascular outcomes is controversial. We aimed to assess the addition of creatinine-based eGFR and albuminuria to traditional risk factors for prediction of cardiovascular risk with a meta-analytic approach. METHODS: We meta-analysed individual-level data for 637 315 individuals without a history of cardiovascular disease from 24 cohorts (median follow-up 4.2-19.0 years) included in the Chronic Kidney Disease Prognosis Consortium. We assessed C statistic difference and reclassification improvement for cardiovascular mortality and fatal and non-fatal cases of coronary heart disease, stroke, and heart failure in a 5 year timeframe, contrasting prediction models for traditional risk factors with and without creatinine-based eGFR, albuminuria (either albumin-to-creatinine ratio [ACR] or semi-quantitative dipstick proteinuria), or both. FINDINGS: The addition of eGFR and ACR significantly improved the discrimination of cardiovascular outcomes beyond traditional risk factors in general populations, but the improvement was greater with ACR than with eGFR, and more evident for cardiovascular mortality (C statistic difference 0.0139 [95% CI 0.0105-0.0174] for ACR and 0.0065 [0.0042-0.0088] for eGFR) and heart failure (0.0196 [0.0108-0.0284] and 0.0109 [0.0059-0.0159]) than for coronary disease (0.0048 [0.0029-0.0067] and 0.0036 [0.0019-0.0054]) and stroke (0.0105 [0.0058-0.0151] and 0.0036 [0.0004-0.0069]). Dipstick proteinuria showed smaller improvement than ACR. The discrimination improvement with eGFR or ACR was especially evident in individuals with diabetes or hypertension, but remained significant with ACR for cardiovascular mortality and heart failure in those without either of these disorders. In individuals with chronic kidney disease, the combination of eGFR and ACR for risk discrimination outperformed most single traditional predictors; the C statistic for cardiovascular mortality fell by 0.0227 (0.0158-0.0296) after omission of eGFR and ACR compared with less than 0.007 for any single modifiable traditional predictor. INTERPRETATION: Creatinine-based eGFR and albuminuria should be taken into account for cardiovascular prediction, especially when these measures are already assessed for clinical purpose or if cardiovascular mortality and heart failure are outcomes of interest. ACR could have particularly broad implications for cardiovascular prediction. In populations with chronic kidney disease, the simultaneous assessment of eGFR and ACR could facilitate improved classification of cardiovascular risk, supporting current guidelines for chronic kidney disease. Our results lend some support to also incorporating eGFR and ACR into assessments of cardiovascular risk in the general population. FUNDING: US National Kidney Foundation, National Institute of Diabetes and Digestive and Kidney Diseases.
Published: 2015

6. Associations of kidney disease measures with mortality and end-stage renal disease in individuals with and without hypertension: a meta-analysis

Author: Mahmoodi, Bk, Matsushita, K., Woodward, M., Blankestijn, Pj, Cirillo, Massimo, Ohkubo, T., Rossing, P., Sarnak, Mj, Stengel, B., Yamagishi, K., Yamashita, K., Zhang, L., Coresh, J., PE de Jong, Wright, BC Astor for the Chronic Kidney Disease Prognosis C. o. n. s. o. r. t. i. u. m. Investigators/Collaborators: J., Appel, L., Greene, T., Astor, Bc, Chalmers, J., Macmahon, S., Arima, H., Yatsuya, H., Toyoshima, H., Tamakoshi, K., Sang, Y., Atkins, R. C., Polkinghorne, Kr, Chadban, S., Shankar, A., Klein, R., Bek, Klein, Lee, Ke, Wang, H., Wang, F., Zuo, L., Levin, A., Djurdjev, O., Tonelli, M., Sacks, Fm, Curhan, Gc, Shlipak, M., Peralta, C., Katz, R., Fried, L., Iso, H., Kitamura, A., Ohira, T., Jafar, Th, Islam, M., Hatcher, J., Poulter, N., Chaturvedi, N., Landray, M. J., Emberson, Jr, Townend, Jn, Wheeler, Dc, Rothenbacher, D., Brenner, H., Muller, H., Schottker, B., Fox, Cs, Hwang, S. J., Meigs, Jb, Perkins, Rm, Fluck, N., Clark, Le, Prescott, Gj, Marks, A., Black, C., Hallan, S., Aasarod, K., Oien, Cm, Radtke, M., Irie, F., Sairenchi, T., Smith, Dh, Weiss, Jw, Johnson, Es, Thorp, Ml, Collins, Aj, Vassalotti, Ja, Li, S., Chen, S. C., Lee, Bj, Wetzels, Jf, AD van Zuilen, Sarnak, M., Levey, As, Menon, V., Kramer, Hj, IH de Boer, Kronenberg, F., Kollerits, B., Roderick, E. R. i. t. z. P., Nitsch, D., Fletcher, A., Bulpitt, C., Ishani, A., Neaton, Jd, Froissart, M., Metzger, M., Haymann, J. P., Houillier, P., Flamant, M., Metoki, H., Nakayama, M., Kikuya, M., Imai, Y., Iseki, K., Nelson, Rg, Knowler, Wc, Gansevoort, Rt, Hillege, H., Jassal, Sk, Barrett Connor, E., Bergstrom, J., HJ Lambers Heerspink, Brenner, Be, de Zeeuw, D., Warnock, Dg, Muntner, P., Judd, S., Mcclellan, W., Jee, Sh, Kimm, H., Jo, J., Mok, Y., Parving, H. H., Tangri, N., Naimark, D., Wen, C. P., Wen, S. F., Tsao, C. K., Tsai, M. K., Arnlov, J., Lannfelt, L., Larsson, A., Bilo, Hj, Joosten, H., Kleefstra, N., Groenier, Kh, Steering Committee: BC Astor, I. D. r. i. o. n., Hemmelgarn, Br, Data Coordinating Center: SH Ballew, M. W. o. o. d. w. a. r. d., Grams, M., Camarata, L., Hui, X., Seltzer, J., Winegrad, H., Mahmoodi, Bk, Matsushita, K, Woodward, M, Blankestijn, Pj, Cirillo, M, Ohkubo, T, Rossing, P, Sarnak, Mj, Stengel, B, Yamagishi, K, Yamashita, K, Zhang, L, Coresh, J, de Jong, Pe, Investigators/Collaborators: J Wright, BC Astor for the Chronic Kidney Disease Prognosis Consortium., Appel, L, Greene, T, Astor, Bc, Chalmers, J, Macmahon, S, Arima, H, Yatsuya, H, Toyoshima, H, Tamakoshi, K, Sang, Y, C Atkins, R, Polkinghorne, Kr, Chadban, S, Shankar, A, Klein, R, Klein, Bek, Lee, Ke, Wang, H, Wang, F, Zuo, L, Levin, A, Djurdjev, O, Tonelli, M, Sacks, Fm, Curhan, Gc, Shlipak, M, Peralta, C, Katz, R, Fried, L, Iso, H, Kitamura, A, Ohira, T, Jafar, Th, Islam, M, Hatcher, J, Poulter, N, Chaturvedi, N, J Landray, M, Emberson, Jr, Townend, Jn, Wheeler, Dc, Rothenbacher, D, Brenner, H, Muller, H, Schottker, B, Fox, C, Hwang, S-J, Meigs, Jb, Perkins, Rm, Fluck, N, Clark, Le, Prescott, Gj, Marks, A, Black, C, Hallan, S, Aasarod, K, Oien, Cm, Radtke, M, Irie, F, Sairenchi, T, Smith, Dh, Weiss, Jw, Johnson, E, Thorp, Ml, Collins, Aj, Vassalotti, Ja, Li, S, Chen, S-C, Lee, Bj, Wetzels, Jf, van Zuilen, Ad, Sarnak, M, Levey, A, Menon, V, Kramer, Hj, de Boer, Ih, Kronenberg, F, Kollerits, B, P Roderick, E Ritz., Nitsch, D, Fletcher, A, Bulpitt, C, Ishani, A, Neaton, Jd, Froissart, M, Metzger, M, Haymann, J-P, Houillier, P, Flamant, M, Metoki, H, Nakayama, M, Kikuya, M, Imai, Y, Iseki, K, Nelson, Rg, Knowler, Wc, Gansevoort, Rt, Hillege, H, Jassal, Sk, Barrett-Connor, E, Bergstrom, J, Lambers Heerspink, Hj, Brenner, Be, de Zeeuw, D, Warnock, Dg, Muntner, P, Judd, S, Mcclellan, W, Jee, Sh, Kimm, H, Jo, J, Mok, Y, Parving, H-H, Tangri, N, Naimark, D, Wen, C-P, Wen, S-F, Tsao, C-K, Tsai, M-K, Arnlov, J, Lannfelt, L, Larsson, A, Bilo, Hj, Joosten, H, Kleefstra, N, Groenier, Kh, Steering Committee: BC Astor, I Drion., Hemmelgarn, Br, Data Coordinating Center: SH Ballew, M Woodward., Grams, M, Camarata, L, Hui, X, Seltzer, J, and Winegrad., H
Subjects: Male, medicine.medical_specialty, hypertension, Blood Pressure, BLOOD-PRESSURE, GLOMERULAR-FILTRATION-RATE, Article, albuminuria, DIABETIC-NEPHROPATHY, End stage renal disease, CKD-PC Consortium, Risk Factors, Cause of Death, Internal medicine, REVERSE EPIDEMIOLOGY, eGFR, EQUATION, medicine, Humans, Intensive care medicine, Aged, Proportional Hazards Models, ALL-CAUSE MORTALITY, Renal disorder [IGMD 9], Aged, 80 and over, end-stage renal disease, business.industry, General Medicine, Middle Aged, medicine.disease, mortality, RISK POPULATION COHORTS, PREVALENCE, Chronic Disease, COLLABORATIVE METAANALYSIS, Kidney Failure, Chronic, Female, HIGHER ALBUMINURIA, business, Glomerular Filtration Rate, Kidney disease
Abstract: Item does not contain fulltext BACKGROUND: Hypertension is the most prevalent comorbidity in individuals with chronic kidney disease. However, whether the association of the kidney disease measures, estimated glomerular filtration rate (eGFR) and albuminuria, with mortality or end-stage renal disease (ESRD) differs by hypertensive status is unknown. METHODS: We did a meta-analysis of studies selected according to Chronic Kidney Disease Prognosis Consortium criteria. Data transfer and analyses were done between March, 2011, and June, 2012. We used Cox proportional hazards models to estimate the hazard ratios (HR) of mortality and ESRD associated with eGFR and albuminuria in individuals with and without hypertension. FINDINGS: We analysed data for 45 cohorts (25 general population, seven high-risk, and 13 chronic kidney disease) with 1,127,656 participants, 364,344 of whom had hypertension. Low eGFR and high albuminuria were associated with mortality irrespective of hypertensive status in the general population and high-risk cohorts. All-cause mortality risk was 1.1-1.2 times higher in individuals with hypertension than in those without hypertension at preserved eGFR. A steeper relative risk gradient in individuals without hypertension than in those with hypertension at eGFR range 45-75 mL/min per 1.73 m(2) led to much the same mortality risk at lower eGFR. With a reference eGFR of 95 mL/min per 1.73 m(2) in each group to explicitly assess interaction, adjusted HR for all-cause mortality at eGFR 45 mL/min per 1.73 m(2) was 1.77 (95% CI 1.57-1.99) in individuals without hypertension versus 1.24 (1.11-1.39) in those with hypertension (p for overall interaction=0.0003). Similarly, for albumin-creatinine ratio of 300 mg/g (vs 5 mg/g), HR was 2.30 (1.98-2.68) in individuals without hypertension versus 2.08 (1.84-2.35) in those with hypertension (p for overall interaction=0.019). We recorded much the same results for cardiovascular mortality. The associations of eGFR and albuminuria with ESRD, however, did not differ by hypertensive status. Results for chronic kidney disease cohorts were similar to those for general and high-risk population cohorts. INTERPRETATION: Chronic kidney disease should be regarded as at least an equally relevant risk factor for mortality and ESRD in individuals without hypertension as it is in those with hypertension. FUNDING: US National Kidney Foundation.
Published: 2012

7. Association between plasma triglycerides and HDL-cholesterol and microvascular kidney disease and retinopathy in type 2 diabetes: a global case-control study in 13 countries

Author: Sacks, Fm, Hermans, Mp, Fioretto, P, Valensi, P, Davis, T, Horton, E, Wanner, C, Al Rubeaan, K, Aronson, R, Barzon, I, Bishop, L, Bonora, Enzo, Bunnag, P, Chuang, Lm, Deerochanawong, C, Goldenberg, R, Harshfield, B, Hernández, C, Herzlinger Botein, S, Itoh, H, Jia, W, Jiang, Yd, Kadowaki, T, Laranjo, N, Leiter, L, Miwa, T, Odawara, M, Ohashi, K, Ohno, A, Pan, C, Pan, J, Pedro Botet, J, Reiner, Z, Rotella, Cm, Simo, R, Tanaka, M, Tedeschi Reiner, E, Twum Barima, D, Zoppini, Giacomo, and Carey, Vj
Subjects: diabetes (kidney), epidemiology, lipids, renal function, retinopathy, risk prediction
Published: 2014

8. The Residual Risk Reduction Initiative: a call to action to reduce residual vascular risk in dyslipidaemic patient

Author: Fruchart, Jc, Sacks, Fm, Hermans, Mp, Assmann, G, Brown, Wv, Ceska, R, Chapman, Mj, Dodson, Pm, Fioretto, Paola, Ginsberg, Hn, Kadowaki, T, Lablanche, Jm, Marx, N, Plutzky, J, Reiner, Z, Rosenson, Rs, Staels, B, Stock, Jk, Sy, R, Wanner, C, Zambon, Alberto, Zimmet, P, and Residual Risk Reduction Initiative
Subjects: medicine.medical_specialty, Health Knowledge, Attitudes, Practice, medicine.drug_class, Endocrinology, Diabetes and Metabolism, Fibrate, Type 2 diabetes, Health Promotion, chemistry.chemical_compound, Pharmacotherapy, Diabetes mellitus, Internal medicine, Internal Medicine, medicine, Humans, Intensive care medicine, Dyslipidemias, Hypolipidemic Agents, Evidence-Based Medicine, business.industry, Cholesterol, Microcirculation, nutritional and metabolic diseases, medicine.disease, Atherosclerosis, Combined Modality Therapy, Residual risk, Endocrinology, Treatment Outcome, chemistry, Cardiovascular Diseases, Practice Guidelines as Topic, lipids (amino acids, peptides, and proteins), Metabolic syndrome, Cardiology and Cardiovascular Medicine, business, Risk Reduction Behavior, Niacin
Abstract: Despite current standards of care aimed at achieving targets for low-density lipoprotein (LDL) cholesterol, blood pressure and glycaemia, dyslipidaemic patients remain at high residual risk of vascular events. Atherogenic dyslipidaemia, specifically elevated triglycerides and low levels of high-density lipoprotein (HDL) cholesterol, often with elevated apolipoprotein B and non-HDL cholesterol, is common in patients with established cardiovascular disease, type 2 diabetes, obesity or metabolic syndrome and is associated with macrovascular and microvascular residual risk. The Residual Risk Reduction Initiative (R3I) was established to address this important issue. This position paper aims to highlight evidence that atherogenic dyslipidaemia contributes to residual macrovascular risk and microvascular complications despite current standards of care for dyslipidaemia and diabetes, and to recommend therapeutic intervention for reducing this, supported by evidence and expert consensus. Lifestyle modification is an important first step. Additionally, pharmacotherapy is often required. Adding niacin, a fibrate or omega-3 fatty acids to statin therapy improves achievement of all lipid risk factors. Outcomes studies are evaluating whether these strategies translate to greater clinical benefit than statin therapy alone. In conclusion, the R3i highlights the need to address with lifestyle and/or pharmacotherapy the high level of residual vascular risk among dyslipidaemic patients who are treated in accordance with current standards of care.
Published: 2008

9. The cholesterol ester transfer protein (CETP) TaqIB variant, HDL cholesterol levels, cardiovascular risk and the efficacy of pravastatin treatment – an individual patient meta-analisis of 13,677 subjects

Author: Boekholdt, Sm, Sacks, Fm, Jukema, Jw, Freeman, Dj, Mcmahon, Ad, Cambien, F, Nicaud, V, DE GROOTH GJ, Talmud, Pj, Humphries, Se, Eiriksdottir, G, Gudnason, V, Kauma, H, Kakko, S, Savolainen, Mj, Arca, Marcello, Montali, Anna, Liu, S, Lanz, Hj, Zwinderman, Ah, Kuivenhoven, Ja, and Kastelein, Jjp
Published: 2005

10. FTO genotype and 2-year change in body composition and fat distribution in response to weight-loss diets: the POUNDS LOST trial. Diabetes 2012;61:3005–3011

Author: Zhang, X, primary, Qi, Q, additional, Zhang, C, additional, Hu, FB, additional, Sacks, FM, additional, and Qi, L, additional
Published: 2013
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11. Effects of 4 weight-loss diets differing in fat, protein, and carbohydrate on fat mass, lean mass, visceral adipose tissue, and hepatic fat: results from the POUNDS LOST trial.

Author: Souza, RJ, primary, Bray, GA, additional, Carey, VJ, additional, Hall, KD, additional, Leboff, MS, additional, Loria, CM, additional, Laranjo, NM, additional, Sacks, FM, additional, and Smith, SR, additional
Published: 2012
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12. PRAVASTATIN REDUCES CARDIOVASCULAR EVENTS IN OLDER PATIENTS AFTER A MYOCARDIAL INFARCTION

Author: Lewise, SJ, primary, Moye, LA, additional, and Sacks, FM, additional
Published: 1999
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13. The relation between dietary intake and adipose tissue composition of selected fatty acids in US women

Author: Garland, M, primary, Sacks, FM, additional, Colditz, GA, additional, Rimm, EB, additional, Sampson, LA, additional, Willett, WC, additional, and Hunter, DJ, additional
Published: 1998
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14. Effects of shrimp consumption on plasma lipoproteins

Author: De Oliveira e Silva, ER, primary, Seidman, CE, additional, Tian, JJ, additional, Hudgins, LC, additional, Sacks, FM, additional, and Breslow, JL, additional
Published: 1996
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15. Effects of inherent responsiveness to diet and day-to-day diet variation on plasma lipoprotein concentrations

Author: O’Hanesian, MA, primary, Rosner, B, additional, Bishop, LM, additional, and Sacks, FM, additional
Published: 1996
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16. Neuropeptide Y promoter polymorphism modifies effects of a weight-loss diet on 2-year changes of blood pressure: the preventing overweight using novel dietary strategies trial.

Author: Zhang X, Qi Q, Liang J, Hu FB, Sacks FM, Qi L, Zhang, Xiaomin, Qi, Qibin, Liang, Jun, Hu, Frank B, Sacks, Frank M, and Qi, Lu
Abstract: Neuropeptide Y (NPY) is implicated in the regulation of blood pressure (BP), and NPY pathways in the hypothalamus are sensitive to dietary fat. We evaluated the potential effect of a functional variant rs16147 located in the NPY gene promoter region on the association between 2-year diet intervention and change in multiple BP measures in the randomized Preventing Overweight Using Novel Dietary Strategies Trial. The NPY rs16147 was genotyped in 723 obese adults who were randomly assigned to 1 of 4 diets differing in the target percentages of energy derived from fat, protein, and carbohydrate. The changes of 4 BP phenotypes, including systolic BP, diastolic BP, pulse pressure, and mean arterial pressure, during 2-year diet intervention were analyzed. In the total participants and participants with hypertension, we observed significant and consistent interactions between rs16147 genotype and dietary fat intake on changes in multiple BP phenotypes at 2 years (all P for interactions <0.05). The risk allele (C allele) was associated with a greater reduction of BP phenotypes in response to low-fat diet, whereas an opposite genetic effect was observed in response to high-fat diet. In addition, the C allele was related to greater changes in 4 BP phenotypes in hypertensive compared with nonhypertensive participants. Our data suggest that NPY rs16147 may modulate the association between dietary fat intake and changes in BP phenotypes, and the C allele exerts a long-term beneficial effect on lowering BP in response to low-fat diet in obese and hypertensive subjects. [ABSTRACT FROM AUTHOR]
Published: 2012
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17. FTO genotype and 2-year change in body composition and fat distribution in response to weight-loss diets: the POUNDS LOST Trial.

Author: Zhang X, Qi Q, Zhang C, Hu FB, Sacks FM, Qi L, Zhang, Xiaomin, Qi, Qibin, Zhang, Cuilin, Smith, Steven R, Hu, Frank B, Sacks, Frank M, Bray, George A, and Qi, Lu
Abstract: Recent evidence suggests that the fat mass and obesity-associated gene (FTO) genotype may interact with dietary intakes in relation to adiposity. We tested the effect of FTO variant on weight loss in response to 2-year diet interventions. FTO rs1558902 was genotyped in 742 obese adults who were randomly assigned to one of four diets differing in the proportions of fat, protein, and carbohydrate. Body composition and fat distribution were measured by dual-energy x-ray absorptiometry and computed tomography. We found significant modification effects for intervention varying in dietary protein on 2-year changes in fat-free mass, whole body total percentage of fat mass, total adipose tissue mass, visceral adipose tissue mass, and superficial adipose tissue mass (for all interactions, P < 0.05). Carriers of the risk allele had a greater reduction in weight, body composition, and fat distribution in response to a high-protein diet, whereas an opposite genetic effect was observed on changes in fat distribution in response to a low-protein diet. Likewise, significant interaction patterns also were observed at 6 months. Our data suggest that a high-protein diet may be beneficial for weight loss and improvement of body composition and fat distribution in individuals with the risk allele of the FTO variant rs1558902. [ABSTRACT FROM AUTHOR]
Published: 2012
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18. The effect of fish oil on blood pressure in mild hypertensive subjects: a randomized crossover trial

Author: Morris, MC, primary, Taylor, JO, additional, Stampfer, MJ, additional, Rosner, B, additional, and Sacks, FM, additional
Published: 1993
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19. Association of plasma phospholipid long-chain ω-3 fatty acids with incident atrial fibrillation in older adults: the cardiovascular health study.

Author: Wu JH, Lemaitre RN, King IB, Song X, Sacks FM, Rimm EB, Heckbert SR, Siscovick DS, Mozaffarian D, Wu, Jason H Y, Lemaitre, Rozenn N, King, Irena B, Song, Xiaoling, Sacks, Frank M, Rimm, Eric B, Heckbert, Susan R, Siscovick, David S, and Mozaffarian, Dariush
Published: 2012
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20. Low-density lipoproteins containing apolipoprotein C-III and the risk of coronary heart disease.

Author: Mendivil CO, Rimm EB, Furtado J, Chiuve SE, Sacks FM, Mendivil, Carlos O, Rimm, Eric B, Furtado, Jeremy, Chiuve, Stephanie E, and Sacks, Frank M
Published: 2011
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21. Circulating long-chain ω-3 fatty acids and incidence of congestive heart failure in older adults: the cardiovascular health study: a cohort study.

Author: Mozaffarian D, Lemaitre RN, King IB, Song X, Spiegelman D, Sacks FM, Rimm EB, Siscovick DS, Mozaffarian, Dariush, Lemaitre, Rozenn N, King, Irena B, Song, Xiaoling, Spiegelman, Donna, Sacks, Frank M, Rimm, Eric B, and Siscovick, David S
Abstract: Background: Few previous studies have evaluated associations between long-chain ω-3 fatty acids and incidence of congestive heart failure (CHF), and those that have are typically based on diet questionnaires and yield conflicting results. Circulating fatty acid concentrations provide objective biomarkers of exposure.Objective: To determine whether plasma phospholipid concentrations of long-chain ω-3 fatty acids, including eicosapentaenoic acid (EPA), docosapentaenoic acid (DPA), and docosahexaenoic acid (DHA), were associated with incident CHF.Design: Prospective cohort study.Setting: 4 U.S. communities.Patients: 2735 U.S. adults without prevalent heart disease who were enrolled in the Cardiovascular Health Study from 1992 to 2006.Measurements: Plasma phospholipid fatty acid concentrations and other cardiovascular risk factors were measured in 1992 by using standardized methods. Relationships with incident CHF (555 cases during 26 490 person-years, adjudicated by using medical records) were assessed by using Cox proportional hazards models.Results: After multivariate adjustment, plasma phospholipid EPA concentration was inversely associated with incident CHF; risk was approximately 50% lower in the highest versus the lowest quartile (hazard ratio [HR], 0.52 [95% CI, 0.38 to 0.72]; P for trend = 0.001). In similar analyses, trends toward lower risk were seen for DPA (HR, 0.76 [CI, 0.56 to 1.04]; P for trend = 0.057) and total long-chain ω-3 fatty acids (HR, 0.70 [CI, 0.49 to 0.99]; P for trend = 0.062) but not for DHA (HR, 0.84 [CI, 0.58 to 1.21]; P for trend = 0.38). In analyses censored to the middle of follow-up (7 years) to minimize exposure misclassification over time, multivariate-adjusted HRs were 0.48 for EPA (CI, 0.32 to 0.71; P for trend = 0.005), 0.61 for DPA (CI, 0.39 to 0.95; P for trend = 0.033), 0.64 for DHA (CI, 0.40 to 1.04; P for trend = 0.057), and 0.51 for total ω-3 fatty acids (CI, 0.32 to 0.80; P for trend = 0.003).Limitations: Temporal changes in fatty acid concentrations over time may have caused underestimation of associations. Unmeasured or imperfectly measured covariates may have caused residual confounding.Conclusion: Circulating individual and total ω-3 fatty acid concentrations are associated with lower incidence of CHF in older adults.Primary Funding Source: National Institutes of Health. [ABSTRACT FROM AUTHOR]
Published: 2011
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22. Insulin receptor substrate 1 gene variation modifies insulin resistance response to weight-loss diets in a 2-year randomized trial: the Preventing Overweight Using Novel Dietary Strategies (POUNDS LOST) trial.

Author: Qi Q, Bray GA, Smith SR, Hu FB, Sacks FM, Qi L, Qi, Qibin, Bray, George A, Smith, Steven R, Hu, Frank B, Sacks, Frank M, and Qi, Lu
Published: 2011
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23. Combination lipid therapy in type 2 diabetes.

Author: Sacks FM, Carey VJ, Fruchart JC, Sacks, Frank M, Carey, Vincent J, and Fruchart, Jean-Charles
Published: 2010
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24. Early behavioral adherence predicts short and long-term weight loss in the POUNDS LOST study.

Author: Williamson DA, Anton SD, Han H, Champagne CM, Allen R, LeBlanc E, Ryan DH, Rood J, McManus K, Laranjo N, Carey VJ, Loria CM, Bray GA, and Sacks FM
Subjects: WEIGHT loss, OBESITY, REGULATION of body weight, CARDIOVASCULAR diseases risk factors, REDUCING diets, HUMAN behavior research, ANTHROPOMETRY, WAIST-hip ratio
Abstract: The primary aim of this study was to test the association of early (first 6 months) adherence related to diet, self-monitoring, and attendance with changes in adiposity and cardiovascular risk factors. This study used data from the 24-month POUNDS LOST trial that tested the efficacy of four dietary macronutrient compositions for short-and long-term weight loss. A computer tracking system was used to record data on eight indicator variables related to adherence. Using canonical correlations at the 6 and 24 month measurement periods, early behavioral adherence was associated with changes in percent weight loss and waist circumference at 6 months ( R = 0.52) and 24 months ( R = 0.37), but was not associated with cardiovascular disease risk factor levels. Early dietary adherence was associated with changes in insulin at 6 months ( R = 0.19), but not at 24 months ( R = 0.08, ns). Early dietary adherence was not associated with changes in adiposity. [ABSTRACT FROM AUTHOR]
Published: 2010
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25. Adherence is a multi-dimensional construct in the POUNDS LOST trial.

Author: Williamson DA, Anton SD, Han H, Champagne CM, Allen R, LeBlanc E, Ryan DH, McManus K, Laranjo N, Carey VJ, Loria CM, Bray GA, and Sacks FM
Subjects: PATIENT compliance, OBESITY treatment, WEIGHT loss, OVERWEIGHT persons, DIET therapy, BEHAVIORAL medicine
Abstract: Research on the conceptualization of adherence to treatment has not addressed a key question: Is adherence best defined as being a uni-dimensional or multi-dimensional behavioral construct? The primary aim of this study was to test which of these conceptual models best described adherence to a weight management program. This ancillary study was conducted as a part of the POUNDS LOST trial that tested the efficacy of four dietary macronutrient compositions for promoting weight loss. A sample of 811 overweight/obese adults was recruited across two clinical sites, and each participant was randomly assigned to one of four macronutrient prescriptions: (1) Low fat (20% of energy), average protein (15% of energy); (2) High fat (40%), average protein (15%); (3) Low fat (20%), high protein (25%); (4) High fat (40%), high protein (25%). Throughout the first 6 months of the study, a computer tracking system collected data on eight indicators of adherence. Computer tracking data from the initial 6 months of the intervention were analyzed using exploratory and confirmatory analyses. Two factors (accounting for 66% of the variance) were identified and confirmed: (1) behavioral adherence and (2) dietary adherence. Behavioral adherence did not differ across the four interventions, but prescription of a high fat diet (vs. a low fat diet) was found to be associated with higher levels of dietary adherence. The findings of this study indicated that adherence to a weight management program was best conceptualized as being multi-dimensional, with two dimensions: behavioral and dietary adherence. [ABSTRACT FROM AUTHOR]
Published: 2010
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26. Fatty acid composition of subcutaneous adipose tissue and diet in postmenopausal US women

Author: London, SJ, primary, Sacks, FM, additional, Caesar, J, additional, Stampfer, MJ, additional, Siguel, E, additional, and Willett, WC, additional
Published: 1991
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27. Comparison of the absorption and effect on platelet function of a single dose of n—3 fatty acids given as fish or fish oil

Author: Silverman, DI, primary, Ware, JA, additional, Sacks, FM, additional, and Pasternak, RC, additional
Published: 1991
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28. Leapfrogging data: no shortcuts for safety or efficacy information.

Author: Pfeffer MA and Sacks FM
Published: 2008

29. Apolipoprotein CIII links hyperlipidemia with vascular endothelial cell dysfunction.

Author: Kawakami A, Osaka M, Tani M, Azuma H, Sacks FM, Shimokado K, Yoshida M, Kawakami, Akio, Osaka, Mizuko, Tani, Mariko, Azuma, Hiroshi, Sacks, Frank M, Shimokado, Kentaro, and Yoshida, Masayuki
Published: 2008
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30. Effect of protein, unsaturated fat, and carbohydrate intakes on plasma apolipoprotein B and VLDL and LDL containing apolipoprotein C-III: results from the OmniHeart Trial.

Author: Furtado JD, Campos H, Appel LJ, Miller ER, Laranjo N, Carey VJ, and Sacks FM
Abstract: BACKGROUND: Plasma apolipoprotein B (apo B) and VLDL and LDL with apolipoprotein C-III (apo C-III) are independent risk factors for cardiovascular disease (CVD). Dietary intake affects lipoprotein concentration and composition related to those apolipoproteins. OBJECTIVE: We studied differences in apo B lipoproteins with and without apo C-III after 3 healthy diets based on the Dietary Approaches to Stop Hypertension Trial diet. DESIGN: Healthy participants (n = 162) were fed each of 3 healthy diets for 6 wk in a crossover design. Diets differed by emphasis of either carbohydrate (Carb), unsaturated fat (Unsat), or protein (Prot). Blood was collected at baseline and after diets for analysis. RESULTS: Compared with the Carb diet, the Prot diet reduced plasma apo B and triglycerides in VLDL with apo C-III (16%, P = 0.07; 11%, P = 0.05, respectively) and apo B in LDL with apo C-III (16%, P = 0.04). Compared with the Unsat diet, the Prot diet reduced triglycerides in VLDL with apo C-III (16%, P = 0.02). Compared with baseline (subjects' usual diet was higher in saturated fat), the Prot diet reduced apo B in LDL with apo C-III (11%, P = 0.05), and all 3 diets reduced plasma total apo B (6-10%, P < 0.05) and apo B in the major type of LDL, LDL without apo C-III (8-10%, P < 0.01). All 3 diets reduced the ratio of apo C-III to apo E in VLDL. CONCLUSIONS: Substituting protein for carbohydrate in the context of a healthy dietary pattern reduced atherogenic apo C-III-containing LDL and its precursor, apo C-III-containing VLDL, resulting in the most favorable profile of apo B lipoproteins. In addition, compared with a typical high-saturated fat diet, healthy diets that emphasize carbohydrate, protein, or unsaturated fat reduce plasma total and LDL apo B and produce a lower more metabolically favorable ratio of apo C-III to apo E. Copyright © 2008 American Society for Nutrition [ABSTRACT FROM AUTHOR]
Published: 2008
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31. Apolipoprotein CIII induces expression of vascular cell adhesion molecule-1 in vascular endothelial cells and increases adhesion of monocytic cells.

Author: Kawakami A, Aikawa M, Alcaide P, Luscinskas FW, Libby P, Sacks FM, Kawakami, Akio, Aikawa, Masanori, Alcaide, Pilar, Luscinskas, Francis W, Libby, Peter, and Sacks, Frank M
Published: 2006

32. Healthy lifestyle factors in the primary prevention of coronary heart disease among men: benefits among users and nonusers of lipid-lowering and antihypertensive medications.

Author: Chiuve SE, McCullough ML, Sacks FM, and Rimm EB
Published: 2006

33. Soy protein, isoflavones, and cardiovascular health: an American Heart Association Science Advisory for professionals from the Nutrition Committee.

Author: Sacks FM, Lichtenstein A, Van Horn L, Harris W, Kris-Etherton P, Winston M, and American Heart Association. Nutrition Committee
Published: 2006

34. Apolipoprotein CIII in apolipoprotein B lipoproteins enhances the adhesion of human monocytic cells to endothelial cells.

Author: Kawakami A, Aikawa M, Libby P, Alcaide P, Luscinskas FW, and Sacks FM
Published: 2006

35. Non-high-density lipoprotein cholesterol and apolipoprotein B in the prediction of coronary heart disease in men.

Author: Pischon T, Girman CJ, Sacks FM, Rifai N, Stampfer MJ, and Rimm EB
Published: 2005

36. Evaluation of the paraoxonases as candidate genes for stroke: Gln192Arg polymorphism in the paraoxonase 1 gene is associated with increased risk of stroke.

Author: Ranade K, Kirchgessner TG, Iakoubova OA, Devlin JJ, DelMonte T, Vishnupad P, Hui L, Tsuchihashi Z, Sacks FM, Sabatine MS, Braunwald E, White TJ, Shaw PM, Dracopoli NC, Ranade, Koustubh, Kirchgessner, Todd G, Iakoubova, Olga A, Devlin, James J, DelMonte, Terrye, and Vishnupad, Priya
Published: 2005
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37. Effect of pravastatin on rate of kidney function loss in people with or at risk for coronary disease.

Author: Tonelli M, Isles C, Craven T, Tonkin A, Pfeffer MA, Shepherd J, Sacks FM, Furberg C, Cobbe SM, Simes J, West M, Packard C, and Curhan GC
Published: 2005

38. Cholesteryl ester transfer protein TaqIB variant, high-density lipoprotein cholesterol levels, cardiovascular risk, and efficacy of pravastatin treatment: individual patient meta-analysis of 13 677 subjects.

Author: Boekholdt SM, Sacks FM, Jukema JW, Shepherd J, Freeman DJ, McMahon AD, Cambien F, Nicaud V, de Grooth GJ, Eiriksdottir G, Gudnason V, Kauma H, Kakko S, Savolainen MJ, Arca M, Montali A, Liu S, Lanz HJ, Zwinderman AH, and Kuivenhoven JA
Published: 2005

39. Effect of pravastatin on cardiovascular events in people with chronic kidney disease.

Author: Tonelli M, Isles C, Curhan GC, Tonkin A, Pfeffer MA, Shepherd J, Sacks FM, Furberg C, Cobbe SM, Simes J, Craven T, and West M
Published: 2004

40. Effect of pravastatin on intermediate-density and low-density lipoproteins containing apolipoprotein CIII in patients with diabetes mellitus.

Author: Lee S, Sacks FM, Lee, Sung-Joon, and Sacks, Frank M
Abstract: The apolipoprotein (apo) B lipoproteins, intermediate-density lipoproteins (IDL) and low-density lipoproteins (LDL) that contain apo-CIII are associated with coronary heart disease in patients with diabetes mellitus. Apo-CIII is prominent in diabetic dyslipidemia. We studied whether these apo-B lipoprotein types containing apo-CIII in diabetics are reduced by 1 year of pravastatin treatment. We randomly selected 45 age- and gender-matched placebo/pravastatin pairs from diabetic patients in the Cholesterol and Recurrent Events trial, a randomized, double-blinded trial of pravastatin 40 mg monotherapy. Very-low-density lipoproteins (VLDL) and IDL + LDL particles were subdivided based on the presence of apo-E and apo-CIII to yield 3 particle types: E+CIII+, E-CIII+, and E-CIII-. Compared with placebo, pravastatin reduced IDL + LDL apo-B concentrations for E+CIII+, E-CIII+, and E-CIII- by 42% (p = 0.02), 17% (p = 0.7), and 29% (p = 0.002), respectively, commensurate with IDL + LDL cholesterol concentration reductions in the particle types of 29% (p = 0.002), 25% (p = 0.2), and 36% (p <0.0001), respectively. These IDL + LDL CIII+ particles are rich in triglycerides and cholesterol and are likely to be remnant particles of VLDL. Thus, pravastatin reduced potentially atherogenic remnant particles, a prominent component of diabetic dyslipidemia associated with coronary events; these results may contribute to its demonstrated effectiveness in reducing coronary heart disease in diabetics. [ABSTRACT FROM AUTHOR]
Published: 2003
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41. Pravastatin for secondary prevention of cardiovascular events in persons with mild chronic renal insufficiency.

Author: Tonelli M, Moyé L, Sacks FM, Kiberd B, Curhan G, Cholesterol and Recurrent Events (CARE) Trial Investigators, Tonelli, Marcello, Moyé, Lemuel, Sacks, Frank M, Kiberd, Bryce, and Curhan, Gary
Abstract: Background: Cardiovascular disease is a common cause of morbidity and death in persons with renal insufficiency. Although 3-hydroxy-3methylglutaryl coenzyme A reductase inhibitors (statins) are effective for secondary prevention of cardiovascular events in the general population, they have not been specifically studied in chronic renal insufficiency.Objective: To determine whether pravastatin is effective and safe for secondary prevention of cardiovascular events in persons with chronic renal insufficiency.Design: Post hoc subgroup analysis of a randomized, double-blind, placebo-controlled trial.Setting: The Cholesterol and Recurrent Events (CARE) study, a randomized trial of pravastatin versus placebo in 4159 participants with previous myocardial infarction and total plasma cholesterol levels less than 6.21 mmol/L (<240 mg/dL).Participants: 1711 participants with chronic renal insufficiency defined by creatinine clearance less than or equal to 75 mL/min, using the Cockcroft-Gault equation.Measurements: The primary outcome was death from coronary disease or symptomatic nonfatal myocardial infarction.Results: After a median follow-up of 58.9 months, the incidence of the primary end point was lower in participants receiving pravastatin than in those receiving placebo (adjusted hazard ratio, 0.72 [95% CI, 0.55 to 0.95]; P = 0.02). Pravastatin was associated with lower adjusted hazard ratios for major coronary events (0.72 [CI, 0.59 to 0.88]; P = 0.001) and coronary revascularization (0.65 [CI, 0.50 to 0.83]; P = 0.001), but not total mortality (0.81 [CI, 0.61 to 1.08]; P = 0.14) or stroke (0.62 [CI, 0.39 to 1.00]; P = 0.051). Tests for interaction suggested that the observed benefit was independent of the presence and severity of renal insufficiency. Incidence of side effects was similar in persons receiving pravastatin and those receiving placebo.Conclusions: These data suggest that pravastatin is effective and appears safe for secondary prevention of cardiovascular events in persons with mild chronic renal insufficiency. Since statins may be underused in this setting, physicians should consider prescribing them for patients with chronic renal insufficiency and known coronary disease. [ABSTRACT FROM AUTHOR]
Published: 2003
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42. The role of high-density lipoprotein (HDL) cholesterol in the prevention and treatment of coronary heart disease: expert group recommendations.

Author: Sacks FM, Expert Group on HDL Cholesterol, and Sacks, Frank M
Published: 2002
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43. Coronary heart disease in patients with low LDL-cholesterol: benefit of pravastatin in diabetics and enhanced role for HDL-cholesterol and triglycerides as risk factors.

Author: Sacks FM, Tonkin AM, Craven T, Pfeffer MA, Shepherd J, Keech A, Furberg CD, Braunwald E, Sacks, Frank M, Tonkin, Andrew M, Craven, Timothy, Pfeffer, Marc A, Shepherd, James, Keech, Anthony, Furberg, Curt D, and Braunwald, Eugene
Published: 2002

44. Effects of diet and sodium intake on blood pressure: subgroup analysis of the DASH-sodium trial.

Author: Vollmer WM, Sacks FM, Ard J, Appel LJ, Bray GA, Simons-Morton DG, Conlin PR, Svetkey LP, Erlinger TP, Moore TJ, Karanja N, DASH-Sodium Trial Collaborative Research Group, Vollmer, W M, Sacks, F M, Ard, J, Appel, L J, Bray, G A, Simons-Morton, D G, Conlin, P R, and Svetkey, L P
Abstract: Background: Initial findings from the Dietary Approaches to Stop Hypertension (DASH)-Sodium Trial demonstrated that reduction of sodium intake in two different diets decreased blood pressure in participants with and without hypertension.Objective: To determine effects on blood pressure of reduced sodium intake and the DASH diet in additional subgroups.Design: Randomized feeding study.Setting: Four clinical centers and a coordinating center.Participants: 412 adults with untreated systolic blood pressure of 120 to 160 mm Hg and diastolic blood pressure of 80 to 95 mm Hg.Intervention: Participants followed the DASH diet or a control (typical U.S.) diet for three consecutive 30-day feeding periods, during which sodium intake (50, 100, and 150 mmol/d at 2100 kcal) varied according to a randomly assigned sequence. Body weight was maintained.Measurements: Systolic and diastolic blood pressure.Results: In all subgroups, the DASH diet and reduced sodium intake were each associated with significant decreases in blood pressure; these two factors combined produced the greatest reductions. Among nonhypertensive participants who received the control diet, lower (vs. higher) sodium intake decreased blood pressure by 7.0/3.8 mm Hg in those older than 45 years of age (P < 0.001) and by 3.7/1.5 mm Hg in those 45 years of age or younger (P < 0.05).Conclusion: The DASH diet plus reduced sodium intake is recommended to control blood pressure in diverse subgroups. [ABSTRACT FROM AUTHOR]
Published: 2001
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45. Effects on blood lipids of a blood pressure-lowering diet: the Dietary Approaches to Stop Hypertension (DASH) Trial.

Author: Obarzanek E, Sacks FM, Vollmer WM, Bray GA, Miller ER III, Lin P, Karanja NM, Most-Windhauser MM, Moore TJ, Swain JF, Bales CW, Proschan MA, and Dietary Approaches to Stop Hypertension Research Group
Abstract: BACKGROUND: Effects of diet on blood lipids are best known in white men, and effects of type of carbohydrate on triacylglycerol concentrations are not well defined. OBJECTIVE: Our goal was to determine the effects of diet on plasma lipids, focusing on subgroups by sex, race, and baseline lipid concentrations. DESIGN: This was a randomized controlled outpatient feeding trial conducted in 4 field centers. The subjects were 436 participants of the Dietary Approaches to Stop Hypertension (DASH) Trial [mean age: 44.6 y; 60% African American; baseline total cholesterol: X or = 6.7 mmol/L (< or = 260 mg/dL)]. The intervention consisted of 8 wk of a control diet, a diet increased in fruit and vegetables, or a diet increased in fruit, vegetables, and low-fat dairy products and reduced in saturated fat, total fat, and cholesterol (DASH diet), during which time subjects remained weight stable. The main outcome measures were fasting total cholesterol, LDL cholesterol, HDL cholesterol, and triacylglycerol. RESULTS: Relative to the control diet, the DASH diet resulted in lower total (-0.35 mmol/L, or -13.7 mg/dL), LDL- (-0.28 mmol/L, or -10.7 mg/dL), and HDL- (-0.09 mmol/L, or -3.7 mg/dL) cholesterol concentrations (all P < 0.0001), without significant effects on triacylglycerol. The net reductions in total and LDL cholesterol in men were greater than those in women by 0.27 mmol/L, or 10.3 mg/dL (P = 0.052), and by 0.29 mmol/L, or 11.2 mg/dL (P < 0.02), respectively. Changes in lipids did not differ significantly by race or baseline lipid concentrations, except for HDL, which decreased more in participants with higher baseline HDL-cholesterol concentrations than in those with lower baseline HDL-cholesterol concentrations. The fruit and vegetable diet produced few significant lipid changes. CONCLUSIONS: The DASH diet is likely to reduce coronary heart disease risk. The possible opposing effect on coronary heart disease risk of HDL reduction needs further study. Copyright © 2001 American Society for Clinical Nutrition [ABSTRACT FROM AUTHOR]
Published: 2001

46. Effects on blood pressure of reduced dietary sodium and the dietary approaches to stop hypertension (DASH) diet.

Author: Sacks FM, Svetkey LP, Vollmer WM, Appel LJ, Bray GA, Harsha D, Obarzanek E, Conlin PR, Miller ER III, Simons-Morton DG, Karanja N, Lin P, and DASH -- Sodium Collaborative Research Group
Published: 2001

47. A prospective study of egg consumption and risk of cardiovascular disease in men and women.

Author: Hu FB, Stampfer MJ, Rimm EB, Manson JE, Ascherio A, Colditz GA, Rosner BA, Spiegelman D, Speizer FE, Sacks FM, Hennekens CH, Willett WC, Hu, F B, Stampfer, M J, Rimm, E B, Manson, J E, Ascherio, A, Colditz, G A, Rosner, B A, and Spiegelman, D
Abstract: Context: Reduction in egg consumption has been widely recommended to lower blood cholesterol levels and prevent coronary heart disease (CHD). Epidemiologic studies on egg consumption and risk of CHD are sparse.Objective: To examine the association between egg consumption and risk of CHD and stroke in men and women.Design and Setting: Two prospective cohort studies, the Health Professionals Follow-up Study (1986-1994) and the Nurses' Health Study (1980-1994).Participants: A total of 37851 men aged 40 to 75 years at study outset and 80082 women aged 34 to 59 years at study outset, free of cardiovascular disease, diabetes, hypercholesterolemia, or cancer.Main Outcome Measures: Incident nonfatal myocardial infarction, fatal CHD, and stroke corresponding to daily egg consumption as determined by a food-frequency questionnaire.Results: We documented 866 incident cases of CHD and 258 incident cases of stroke in men during 8 years of follow-up and 939 incident cases of CHD and 563 incident cases of stroke in women during 14 years of follow-up. After adjustment for age, smoking, and other potential CHD risk factors, we found no evidence of an overall significant association between egg consumption and risk of CHD or stroke in either men or women. The relative risks (RRs) of CHD across categories of intake were less than 1 per week (1.0), 1 per week (1.06), 2 to 4 per week (1.12), 5 to 6 per week (0.90), and > or =1 per day (1.08) (P for trend = .75) for men; and less than 1 per week (1.0), 1 per week (0.82), 2 to 4 per week (0.99), 5 to 6 per week (0.95), and > or =1 per day (0.82) (P for trend = .95) for women. In subgroup analyses, higher egg consumption appeared to be associated with increased risk of CHD only among diabetic subjects (RR of CHD comparing more than 1 egg per day with less than 1 egg per week among diabetic men, 2.02 [95% confidence interval, 1.05-3.87; P for trend = .04], and among diabetic women, 1.49 [0.88-2.52; P for trend = .008]).Conclusions: These findings suggest that consumption of up to 1 egg per day is unlikely to have substantial overall impact on the risk of CHD or stroke among healthy men and women. The apparent increased risk of CHD associated with higher egg consumption among diabetic participants warrants further research. [ABSTRACT FROM AUTHOR]
Published: 1999

48. Effect of pravastatin on cardiovascular events in older patients with myocardial infarction and cholesterol levels in the average range. Results of the Cholesterol and Recurrent Events (CARE) trial.

Author: Lewis SJ, Moye LA, Sacks FM, Johnstone DE, Timmis G, Mitchell J, Limacher M, Kell S, Glasser SP, Grant J, Davis BR, Pfeffer MA, Braunwald E, Lewis, S J, Moye, L A, Sacks, F M, Johnstone, D E, Timmis, G, Mitchell, J, and Limacher, M
Abstract: Background: A majority of all myocardial infarctions occur in patients who are 65 years of age or older and have average cholesterol levels, but little information is available on whether cholesterol lowering in such patients reduces the rate of recurrent cardiovascular disease.Objective: To determine whether pravastatin reduces the rate of recurrent cardiovascular events in older patients.Design: Subset analysis of a randomized, controlled trial.Setting: 80 hospitals and affiliates in the United States and Canada.Patients: 1283 patients aged 65 to 75 years who had had myocardial infarction and had a plasma total cholesterol level less than 6.2 mmol/L (240 mg/dL) and a low-density lipoprotein cholesterol level of 3.0 to 4.5 mmol/L (115 to 174 mg/dL).Intervention: Pravastatin, 40 mg/d, or placebo.Measurements: Five-year event rates of major coronary events (coronary death, nonfatal myocardial infarction, angioplasty, or bypass surgery) and stroke.Results: Major coronary events occurred in 28.1% of placebo recipients and 19.7% of pravastatin recipients (difference, 9.0 percentage points [95% CI, 4 to 13 percentage points]; relative risk reduction, 32%; P < 0.001). Coronary death occurred in 10.3% of the placebo group and in 5.8% of the pravastatin group (difference, 4.6 percentage points [CI, 1.9 to 6.5 percentage points]; relative risk reduction, 45%; P = 0.004). Stroke incidence was 7.3% in the placebo group and 4.5% in the pravastatin group (absolute reduction, 2.9 percentage points [CI, 0.3 to 4.5 percentage points]; relative reduction, 40%; P = 0.03). The numbers of older patients needed to treat for 5 years were 11 (CI, 8 to 24) to prevent a major coronary event and 22 (CI, 15 to 53) to prevent a coronary death. For every 1000 older patients treated, 225 cardiovascular hospitalizations would be prevented compared with 121 hospitalizations in 1000 younger patients.Conclusions: In older patients with myocardial infarction and cholesterol levels in the average range, pravastatin is associated with a clinically important reduction in risk for major coronary events and stroke. Given the high cardiovascular event rate in older patients, the potential for absolute benefit in this age group is substantial. [ABSTRACT FROM AUTHOR]
Published: 1998
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49. The effect of pravastatin on coronary events after myocardial infarction in patients with average cholesterol levels.

Author: Sacks FM, Pfeffer MA, Moye LA, Rouleau JL, Rutherford JD, Cole TG, Brown L, Warnica JW, Arnold JMO, Wun C, Davis BR, Braunwald E, and Cholesterol and Recurrent Events Trial Investigators
Published: 1996

50. Effect of postmenopausal estrogen replacement on plasma Lp(a) lipoprotein concentrations.

Author: Sacks FM, McPherson R, and Walsh BW
Published: 1994
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