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1. Relationship Between Urinary Phosphate and All-Cause and Cardiovascular Mortality in a National Population-Based Longitudinal Cohort Study

Author

Toussaint, ND, Damasiewicz, MJ, Holt, SG, Lu, ZX, Magliano, DJ, Atkins, RC, Chadban, SJ, Shaw, JE, Polkinghorne, KR, Toussaint, ND, Damasiewicz, MJ, Holt, SG, Lu, ZX, Magliano, DJ, Atkins, RC, Chadban, SJ, Shaw, JE, and Polkinghorne, KR

Abstract

OBJECTIVES: High dietary phosphate intake may lead to adverse outcomes including cardiovascular disease (CVD). Urinary phosphate excretion, a marker of intestinal phosphate absorption, may be a more reliable marker of phosphate homeostasis in steady state than serum phosphate. Studies report good agreement between urine phosphate-to-creatinine ratio (uPiCr) and 24-hour urinary phosphate; however, whether uPiCr is associated with increased risk of CVD or mortality remains uncertain. This study aimed to assess the relationship between uPiCr and all-cause and CVD mortality. DESIGN AND METHODS: This is an observational longitudinal cohort study using data from the population-based national Australian Diabetes, Obesity and Lifestyle study (n = 10,014 participants). Non-linear association between uPiCr and all-cause and CVD mortality was assessed using fractional polynomial transformations. Cox proportional hazards regression models were used to estimate adjusted hazard ratios for all-cause and CVD mortality. RESULTS: Median age [interquartile range] was 50 [41-62] years, and 46% were male. Median uPiCr was 1.38 [1.02-1.79] mmol/mmol. Median follow-up time was 16.9 years with 1,735 deaths. uPiCr was associated with all-cause and CVD mortality in univariate models and when adjusted for age and gender. However, associations were not significant in multivariate models. Sensitivity analyses excluding participants with chronic kidney disease (CKD) revealed a significant J-shaped association between uPiCr and all-cause mortality. Urine phosphate alone showed an association with increased all-cause mortality in a similar J-shape relationship. CONCLUSION: Although no association between uPiCr and all-cause and CVD mortality was observed in multivariate analyses in the whole cohort, a significant relationship between uPiCr and mortality in those without CKD suggests that uPiCr may have predictive validity for future adverse outcomes in people with no CKD.

Published
2022

3. Relative risks of Chronic Kidney Disease for mortality and End Stage Renal Disease across races is similar

Author

Wright, Jt, Appel, L, Greene, T, Astor, Bc, Chalmers, J, Macmahon, S, Woodward, M, Arima, H, Yatsuya, H, Yamashita, K, Toyoshima, H, Tamakoshi, K, Coresh, J, Matsushita, K, Atkins, Rc, Polkinghorne, Kr, Chadban, S, Shankar, A, Klein, R, Klein, Be, Lee, Ke, Wang, H, Wang, F, Zhang, L, Zuo, L, Liu, L, Levin, A, Djurdjev, O, Tonelli, M, Sacks, F, Curhan, G, Shlipak, M, Peralta, C, Katz, R, Fried, L, Iso, H, Kitamura, A, Ohira, T, Yamagishi, K, Jafar, Th, Islam, M, Hatcher, J, Poulter, N, Chaturvedi, N, Landray, Mj, Emberson, J, Townend, J, Wheeler, Dc, Rothenbacher, D, Brenner, H, Müller, H, Schöttker, B, Fox, Cs, Hwang, Sj, Meigs, Jb, Perkins, Rm, Fluck, N, Clark, L, Prescott, Gj, Marks, A, Black, C, Cirillo, Massimo, Hallan, S, Aasard, K, Øien, Cm, Radtke, M, Irie, F, Sairenchi, T, Smith, Dh, Weiss, J, 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, L, Menon, V, Fried, Lf, Kramer, H, Boer, De, I, Kronenberg, F, Kollerits, B, Ritz, E, Roderick, P, Nitsch, D, Fletcher, A, Bulpitt, C, Ishani, A, Neaton, J, 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, Bakker, Sj, Bernardo, R, Kaur, Jassal, S, Barrett Connor, E, Bergstrom, J, Heerspink, Hj, Brenner, B, Zeeuw, De, D, Warnock, Dg, Muntner, P, Judd, S, Mcclellan, W, Jee, Sh, Kimm, H, Jo, J, Mok, Y, Choi, E, Rossing, P, Parving, Hh, Tangri, N, Naimark, D, Wen, Cp, Wen, Sf, Tsao, Ck, Tsai, Mk, Wu, Be, Ärnlöv, J, Lannfelt, L, Larsson, A, Bilo, Hj, Joosten, H, Kleefstra, N, Groenier, Kh, Drion, I, Hemmelgarn, Br, Ballew, Sh, Grams, M, Sang, Y, Camarata, L, Hui, X, Seltzer, J, Winegrad, H., Cardiovascular Centre (CVC), Groningen Kidney Center (GKC), Wright, Jt, Jr, Appel, L, Greene, T, Astor, Bc, Chalmers, J, Macmahon, S, Woodward, M, Arima, H, Yatsuya, H, Yamashita, K, Toyoshima, H, Tamakoshi, K, Coresh, J, Matsushita, K, Atkins, Rc, Polkinghorne, Kr, Chadban, S, Shankar, A, Klein, R, Klein, Be, Lee, Ke, Wang, H, Wang, F, Zhang, L, Zuo, L, Liu, L, Levin, A, Djurdjev, O, Tonelli, M, Sacks, F, Curhan, G, Shlipak, M, Peralta, C, Katz, R, Fried, L, Iso, H, Kitamura, A, Ohira, T, Yamagishi, K, Jafar, Th, Islam, M, Hatcher, J, Poulter, N, Chaturvedi, N, Landray, Mj, Emberson, J, Townend, J, Wheeler, Dc, Rothenbacher, D, Brenner, H, Müller, H, Schöttker, B, Fox, C, Hwang, Sj, Meigs, Jb, Perkins, Rm, Fluck, N, Clark, L, Prescott, Gj, Marks, A, Black, C, Cirillo, Massimo, Hallan, S, Aasard, K, Øien, Cm, Radtke, M, Irie, F, Sairenchi, T, Smith, Dh, Weiss, J, 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, L, Menon, V, Fried, Lf, Kramer, H, De, Boer, I, Kronenberg, F, Kollerits, B, Ritz, E, Roderick, P, Nitsch, D, Fletcher, A, Bulpitt, C, Ishani, A, Neaton, J, 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, Bakker, Sj, Bernardo, R, Kaur, Jassal, S, Barrett Connor, E, Bergstrom, J, Heerspink, Hj, Brenner, B, De, Zeeuw, D, Warnock, Dg, Muntner, P, Judd, S, Mcclellan, W, Jee, Sh, Kimm, H, Jo, J, Mok, Y, Choi, E, Rossing, P, Parving, Hh, Tangri, N, Naimark, D, Wen, Cp, Wen, Sf, Tsao, Ck, Tsai, Mk, Be, Wu, Ärnlöv, J, Lannfelt, L, Larsson, A, Bilo, Hj, Joosten, H, Kleefstra, N, Groenier, Kh, Drion, I, Hemmelgarn, Br, Ballew, Sh, Grams, M, Sang, Y, Camarata, L, Hui, X, Seltzer, J, and Winegrad, H.

Subjects
Male, GLOMERULAR-FILTRATION-RATE, Cohort Studies, Risk Factors, eGFR, Odds Ratio, ASSOCIATIONS, African Continental Ancestry Group, Aged, 80 and over, education.field_of_study, end-stage renal disease, Hazard ratio, PROTEINURIA, Urology & Nephrology, Middle Aged, CKD-EPI EQUATION, 3. Good health, PREVALENCE, Nephrology, Cardiovascular Diseases, Creatinine, ethnicity, Female, medicine.symptom, epidemiology and outcomes, Glomerular Filtration Rate, Asian Continental Ancestry Group, Adult, medicine.medical_specialty, Population, European Continental Ancestry Group, Renal function, Black People, ALL-CAUSE, Article, White People, End stage renal disease, Asian People, Internal medicine, medicine, Chronic Kidney Disease Prognosis Consortium, Albuminuria, Humans, Renal Insufficiency, Chronic, education, Aged, business.industry, 1103 Clinical Sciences, Odds ratio, POPULATION COHORTS, medicine.disease, INDIVIDUALS, Endocrinology, Relative risk, COLLABORATIVE METAANALYSIS, mortality risk, Kidney Failure, Chronic, Renal disorders Radboud Institute for Health Sciences [Radboudumc 11], business, HIGHER ALBUMINURIA, chronic kidney disease, Kidney disease
Abstract

Item does not contain fulltext Some suggest race-specific cutpoints for kidney measures to define and stage chronic kidney disease (CKD), but evidence for race-specific clinical impact is limited. To address this issue, we compared hazard ratios of estimated glomerular filtration rates (eGFR) and albuminuria across races using meta-regression in 1.1 million adults (75% Asians, 21% Whites, and 4% Blacks) from 45 cohorts. Results came mainly from 25 general population cohorts comprising 0.9 million individuals. The associations of lower eGFR and higher albuminuria with mortality and end-stage renal disease (ESRD) were largely similar across races. For example, in Asians, Whites, and Blacks, the adjusted hazard ratios (95% confidence interval) for eGFR 45-59 versus 90-104 ml/min per 1.73 m(2) were 1.3 (1.2-1.3), 1.1 (1.0-1.2), and 1.3 (1.1-1.7) for all-cause mortality, 1.6 (1.5-1.7), 1.4 (1.2-1.7), and 1.4 (0.7-2.9) for cardiovascular mortality, and 27.6 (11.1-68.7), 11.2 (6.0-20.9), and 4.1 (2.2-7.5) for ESRD, respectively. The corresponding hazard ratios for urine albumin-to-creatinine ratio 30-299 mg/g or dipstick 1+ versus an albumin-to-creatinine ratio under 10 or dipstick negative were 1.6 (1.4-1.8), 1.7 (1.5-1.9), and 1.8 (1.7-2.1) for all-cause mortality, 1.7 (1.4-2.0), 1.8 (1.5-2.1), and 2.8 (2.2-3.6) for cardiovascular mortality, and 7.4 (2.0-27.6), 4.0 (2.8-5.9), and 5.6 (3.4-9.2) for ESRD, respectively. Thus, the relative mortality or ESRD risks of lower eGFR and higher albuminuria were largely similar among three major races, supporting similar clinical approach to CKD definition and staging, across races.

Published
2014

4. 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

5. 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

6. 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

7. 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

8. 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

9. Incidence of chronic kidney disease among people with diabetes: a systematic review of observational studies

Author

Koye, DN, Shaw, JE, Reid, CM, Atkins, RC, Reutens, AT, Magliano, DJ, Koye, DN, Shaw, JE, Reid, CM, Atkins, RC, Reutens, AT, and Magliano, DJ

Abstract

AIMS: The aim was to systematically review published articles that reported the incidence of chronic kidney disease among people with diabetes. METHODS: A systematic literature search was performed using MEDLINE, Embase and CINAHL databases. The titles and abstracts of all publications identified by the search were reviewed and 10 047 studies were retrieved. RESULTS: A total of 71 studies from 30 different countries with sample sizes ranging from 505 to 211 132 met the inclusion criteria. The annual incidence of microalbuminuria and albuminuria ranged from 1.3% to 3.8% for Type 1 diabetes. For Type 2 diabetes and studies combining both diabetes types, the range was from 3.8% to 12.7%, with four of six studies reporting annual rates between 7.4% and 8.6%. In studies reporting the incidence of eGFR < 60 ml/min/1.73 m2 using the Modification of Diet on Renal Disease (MDRD) equation, apart from one study which reported an annual incidence of 8.9%, the annual incidence ranged from 1.9% to 4.3%. The annual incidence of end-stage renal disease ranged from 0.04% to 1.8%. CONCLUSIONS: The annual incidence of microalbuminuria and albuminuria is ~ 2-3% in Type 1 diabetes, and ~ 8% in Type 2 diabetes or mixed diabetes type. The incidence of developing eGFR < 60 ml/min/1.73 m2 is ~ 2-4% per year. Despite the wide variation in methods and study design, within a particular category of kidney disease, there was only modest variation in incidence rates. These findings may be useful in clinical settings to help understand the risk of developing kidney disease among those with diabetes.

Published
2017

10. Association of estimated glomerular filtration rate and albuminuria with all-cause and cardiovascular mortality in general population cohorts: a collaborative meta-analysis

Author

Chronic Kidney Disease Prognosis Consortium, Matsushita, K, van der Velde, M, Astor, Bc, Woodward, M, Levey, As, de Jong PE, Coresh, J, Investigators/Collaborators: Levey AS, Gansevoort R. T., El Nahas, M, Eckardt, Ku, Kasiske, Bl, Tonelli, M, Hemmelgarn, B, Wang, Y, Atkins, Rc, Polkinghorne, Kr, Chadban, Sj, Shankar, A, Klein, R, Klein, Be, Wang, H, Wang, F, Zhang, L, Liu, L, Shlipak, M, Sarnak, Mj, Katz, R, Fried, Lp, Jafar, T, Islam, M, Hatcher, J, Poulter, N, Chaturvedi, N, Rothenbacher, D, Brenner, H, Raum, E, Koenig, W, Fox, Cs, Hwang, Sj, Meigs, Jb, Cirillo, Massimo, Hallan, S, Lydersen, S, Holmen, J, Roderick, P, Nitsch, D, Fletcher, A, Bulpitt, C, Ohkubo, T, Metoki, H, Nakayama, M, Kikuya, M, Imai, Y, Gansevoort, Rt, Jassal, Sk, Barrett Connor, E, Bergstrom, J, Warnock, Dg, Muntner, P, Judd, S, Mcclellan, Wm, Cushman, M, Howard, G, Mcclure, La, Jee, Sh, Kimm, H, Yun, Je, Wen, Cp, Wen, Sf, Tsao, Ck, Tsai, Mk, Arnlöv, J, Auguste, P, Veldhuis, K, Camarata, L, Thomas, B, Manley, T., Chronic Kidney Disease Prognosis, Consortium, Matsushita, K, van der Velde, M, Astor, Bc, Woodward, M, Levey, A, de Jong, Pe, Coresh, J, Investigators/Collaborators: Levey AS, Gansevoort R. T., El Nahas, M, Eckardt, Ku, Kasiske, Bl, Tonelli, M, Hemmelgarn, B, Wang, Y, Atkins, Rc, Polkinghorne, Kr, Chadban, Sj, Shankar, A, Klein, R, Klein, Be, Wang, H, Wang, F, Zhang, L, Liu, L, Shlipak, M, Sarnak, Mj, Katz, R, Fried, Lp, Jafar, T, Islam, M, Hatcher, J, Poulter, N, Chaturvedi, N, Rothenbacher, D, Brenner, H, Raum, E, Koenig, W, Fox, C, Hwang, Sj, Meigs, Jb, Cirillo, Massimo, Hallan, S, Lydersen, S, Holmen, J, Roderick, P, Nitsch, D, Fletcher, A, Bulpitt, C, Ohkubo, T, Metoki, H, Nakayama, M, Kikuya, M, Imai, Y, Gansevoort, Rt, Jassal, Sk, Barrett Connor, E, Bergstrom, J, Warnock, Dg, Muntner, P, Judd, S, Mcclellan, Wm, Cushman, M, Howard, G, Mcclure, La, Jee, Sh, Kimm, H, Yun, Je, Wen, Cp, Wen, Sf, Tsao, Ck, Tsai, Mk, Arnlöv, J, Auguste, P, Veldhuis, K, Camarata, L, Thomas, B, Manley, T., Cardiovascular Centre (CVC), and Groningen Kidney Center (GKC)

Subjects
Male, CHRONIC KIDNEY-DISEASE, medicine.medical_specialty, Pathology, Population, Urology, Renal function, POOLED ANALYSIS, chemistry.chemical_compound, RISK-FACTOR, CYSTATIN-C, medicine, Risk of mortality, EQUATION, Albuminuria, Humans, Risk factor, Mortality, education, OLDER-ADULTS, Aged, Proportional Hazards Models, Creatinine, education.field_of_study, OUTCOMES, SERUM CREATININE, business.industry, Hazard ratio, General Medicine, Middle Aged, medicine.disease, PREVALENCE, RENAL-DISEASE, chemistry, Cardiovascular Diseases, Chronic Disease, Female, Kidney Diseases, medicine.symptom, business, Kidney disease, Glomerular Filtration Rate
Abstract

BACKGROUND: Substantial controversy surrounds the use of estimated glomerular filtration rate (eGFR) and albuminuria to define chronic kidney disease and assign its stages. We undertook a meta-analysis to assess the independent and combined associations of eGFR and albuminuria with mortality. METHODS: In this collaborative meta-analysis of general population cohorts, we pooled standardised data for all-cause and cardiovascular mortality from studies containing at least 1000 participants and baseline information about eGFR and urine albumin concentrations. Cox proportional hazards models were used to estimate hazard ratios (HRs) for all-cause and cardiovascular mortality associated with eGFR and albuminuria, adjusted for potential confounders. FINDINGS: The analysis included 105,872 participants (730,577 person-years) from 14 studies with urine albumin-to-creatinine ratio (ACR) measurements and 1,128,310 participants (4,732,110 person-years) from seven studies with urine protein dipstick measurements. In studies with ACR measurements, risk of mortality was unrelated to eGFR between 75 mL/min/1.73 m(2) and 105 mL/min/1.73 m(2) and increased at lower eGFRs. Compared with eGFR 95 mL/min/1.73 m(2), adjusted HRs for all-cause mortality were 1.18 (95% CI 1.05-1.32) for eGFR 60 mL/min/1.73 m(2), 1.57 (1.39-1.78) for 45 mL/min/1.73 m(2), and 3.14 (2.39-4.13) for 15 mL/min/1.73 m(2). ACR was associated with risk of mortality linearly on the log-log scale without threshold effects. Compared with ACR 0.6 mg/mmol, adjusted HRs for all-cause mortality were 1.20 (1.15-1.26) for ACR 1.1 mg/mmol, 1.63 (1.50-1.77) for 3.4 mg/mmol, and 2.22 (1.97-2.51) for 33.9 mg/mmol. eGFR and ACR were multiplicatively associated with risk of mortality without evidence of interaction. Similar findings were recorded for cardiovascular mortality and in studies with dipstick measurements. INTERPRETATION: eGFR less than 60 mL/min/1.73 m(2) and ACR 1.1 mg/mmol (10 mg/g) or more are independent predictors of mortality risk in the general population. This study provides quantitative data for use of both kidney measures for risk assessment and definition and staging of chronic kidney disease. FUNDING: Kidney Disease: Improving Global Outcomes (KDIGO), US National Kidney Foundation, and Dutch Kidney Foundation.

Published
2010

12. Proteinuria reduction and progression to renal failure in patients with type 2 diabetes mellitus and overt nephropathy

Author

Atkins, Rc, Briganti, Em, Lewis, Jb, Hunsicker, Lg, Braden, G, Champion, De, Crespigny, Pj, Deferrari, Giacomo, Drury, P, Locatelli, F, Wiegmann, Tb, and Lewis, E. J.

Subjects
Adult, Male, Nephrology, medicine.medical_specialty, Urology, Tetrazoles, Blood Pressure, Type 2 diabetes, urologic and male genital diseases, Diabetic nephropathy, Irbesartan, Double-Blind Method, Internal medicine, Diabetes mellitus, medicine, Humans, Diabetic Nephropathies, Renal Insufficiency, Aged, Proteinuria, urogenital system, business.industry, Biphenyl Compounds, Middle Aged, medicine.disease, Angiotensin II, female genital diseases and pregnancy complications, Endocrinology, Diabetes Mellitus, Type 2, Hypertension, Female, Amlodipine, medicine.symptom, business, Follow-Up Studies, Kidney disease, medicine.drug
Abstract

Little is known of the effects of blood pressure reduction by specific classes of antihypertensive drugs on the association between proteinuria reduction and progression of kidney insufficiency and development of end-stage kidney disease in patients with overt diabetic nephropathy in type 2 diabetes mellitus.Associations between baseline proteinuria and proteinuria reduction by either irbesartan, amlodipine, or control for similar decrements in blood pressure and the cumulative incidence of renal end points were examined using the Kaplan-Meier method in patients enrolled in the Irbesartan Diabetic Nephropathy Trial.Risk for kidney failure doubled for each doubling of baseline proteinuria level (hazard ratio, 2.04; 95% confidence interval, 1.87 to 2.22; P0.001). For each halving of proteinuria level between baseline and 12 months with treatment, risk for kidney failure was reduced by more than half (hazard ratio, 0.44; 95% confidence interval, 0.40 to 0.49; P0.001). For the same proportional change in proteinuria, the reduction in risk for kidney failure was significantly greater for irbesartan compared with amlodipine ( P = 0.048), but not control ( P = 0.245). Proteinuria reduction in the first 12 months of therapy with irbesartan is associated with 36% of the total renoprotective effect observed.Baseline proteinuria is an important risk factor for kidney failure and provides a means to identify patients at greatest risk. Halving proteinuria halves the kidney risk. Proteinuria reduction using an angiotensin receptor-blocking agent, such as irbesartan, should be regarded as an important therapeutic goal in renoprotective strategies.

Published
2005

13. 25-hydroxyvitamin D Levels and chronic kidney disease in the AusDiab (Australian Diabetes, Obesity and Lifestyle) study

Author

Damasiewicz, MJ, Magliano, DJ, Daly, RM, Gagnon, C, Lu, ZX, Ebeling, PR, Chadban, SJ, Atkins, RC, Kerr, PG, Shaw, JE, Polkinghorne, KR, Damasiewicz, MJ, Magliano, DJ, Daly, RM, Gagnon, C, Lu, ZX, Ebeling, PR, Chadban, SJ, Atkins, RC, Kerr, PG, Shaw, JE, and Polkinghorne, KR

Abstract

BACKGROUND: Low 25-hydroxy vitamin D (25(OH)D) levels have been associated with an increased risk of albuminuria, however an association with glomerular filtration rate (GFR) is not clear. We explored the relationship between 25(OH)D levels and prevalent chronic kidney disease (CKD), albuminuria and impaired GFR, in a national, population-based cohort of Australian adults (AusDiab Study). METHODS: 10,732 adults ≥ 25 years of age participating in the baseline survey of the AusDiab study (1999-2000) were included. The GFR was estimated using an enzymatic creatinine assay and the CKD-EPI equation, with CKD defined as eGFR <60 ml/min/1.73 m(2). Albuminuria was defined as a spot urine albumin to creatinine ratio (ACR) of ≥ 2.5 mg/mmol for men and ≥ 3.5 for women. Serum 25(OH)D levels of <50 nmol/L were considered vitamin D deficient. The associations between 25(OH)D level, albuminuria and impaired eGFR were estimated using multivariate regression models. RESULTS: 30.7% of the study population had a 25(OH)D level <50 nmol/L (95% CI 25.6-35.8). 25(OH)D deficiency was significantly associated with an impaired eGFR in the univariate model (OR 1.52, 95% CI 1.07-2.17), but not in the multivariate model (OR 0.95, 95% CI 0.67-1.35). 25(OH)D deficiency was significantly associated with albuminuria in the univariate (OR 2.05, 95% CI 1.58-2.67) and multivariate models (OR 1.54, 95% CI 1.14-2.07). CONCLUSIONS: Vitamin D deficiency is common in this population, and 25(OH)D levels of <50 nmol/L were independently associated with albuminuria, but not with impaired eGFR. These associations warrant further exploration in prospective and interventional studies.

Published
2012

14. Nonalbuminuric Renal Impairment in Type 2 Diabetic Patients and in the General Population (National Evaluation of the Frequency of Renal Impairment cO-existing with NIDDM [NEFRON] 11)

Author

Thomas, MC, MacIsaac, RJ, Jerums, G, Weekes, A, Moran, J, Shaw, JE, Atkins, RC, Thomas, MC, MacIsaac, RJ, Jerums, G, Weekes, A, Moran, J, Shaw, JE, and Atkins, RC

Abstract

OBJECTIVE Most diabetic patients with impaired renal function have a urinary albumin excretion rate in the normal range. In these patients, the etiology of renal impairment is unclear, and it is also unclear whether this nonalbumunuric renal impairment is unique to diabetes. RESEARCH DESIGN AND METHODS In this study, we examined the frequency and predictors of nonalbumunuric renal impairment (estimated glomerular filtration rate [eGFR] <60 ml/min per 1.73 m(2)) in a nationally representative cohort of 3,893 patients with type 2 diabetes and compared our findings with rates observed in the general population from the Australian Diabetes, Obesity and Lifestyle Study (AusDiab) survey (n = 11,247). RESULTS Of the 23.1% of individuals with type 2 diabetes who had eGFR <60 ml/min per 1.73 m(2) (95% CI 21.8-24.5%), more than half (55%) had a urinary albumin excretion rate that was persistently in the normal range. This rate of renal impairment was predictably higher than that observed in the general population (adjusted odds ratio 1.3, 95% CI 1.1-1.5, P < 0.01) but was solely due to chronic kidney disease associated with albuminuria. In contrast, renal impairment in the absence of albuminuria was less common in those with diabetes than in the general population, independent of sex, ethnicity, and duration of diabetes (0.6, 0.5-0.7, P < 0.001). CONCLUSIONS Nonalbuminuric renal impairment is not more common in those with diabetes. However, its impact may be more significant. New studies are required to address the pathogenesis, prevention, and treatment of nonalbuminuric renal disease.

Published
2009

15. Interleukin-10 differentially modulates MHC class II expression by mesangial cells and macrophages in vitro and in vivo

Author

Chadban, Sj, Tesch, Gh, Foti, R., Hui-yao Lan, Atkins, Rc, and Nikolic-Paterson, Dj

Subjects
Male, Macrophages, Histocompatibility Antigens Class II, Gene Expression, Blotting, Northern, Recombinant Proteins, Glomerular Mesangium, Interleukin-10, Rats, Immunoenzyme Techniques, Rats, Sprague-Dawley, Interferon-gamma, Glomerulonephritis, Culture Techniques, Animals, Research Article
Abstract

Inhibition of major histocompatibility complex (MHC) class II expression by macrophages is the primary mechanism by which interleukin-10 (IL-10) exerts immune suppression. Little, however, is known of the effects of IL-10 on other types of cells which can be induced to express MHC class II during an inflammatory response. We therefore studied the effects of IL-10 treatment on the expression of MHC class II molecules in a rat model of immunologically induced glomerulonephritis. MHC class II mRNA levels in whole kidney were increased in saline-treated (control) animals with glomerulonephritis (2.6-fold increase versus normal, P = 0.028) and this was partially inhibited by treatment with IL-10 (P = NS). Double immunostaining of tissue sections was used to compare MHC class II expression by infiltrating macrophages and resident glomerular cells. IL-10 treatment reduced the proportion of glomerular macrophages which expressed detectable MHC class II (70% reduction, P = 0.03). In contrast, IL-10 treatment was associated with an increase in the number of resident glomerular cells expressing MHC class II, particularly within mesangial areas. Therefore, the effects of IL-10 on macrophages and mesangial cells were compared in vitro. IL-10 reduced constitutive MHC class II mRNA and cell surface expression by peritoneal macrophages. In contrast, IFN-gamma-stimulated mesangial cells (1097 cell line) cultured with IL-10 for 24 hr showed increased MHC class II mRNA (26% increase) and surface expression (72% increase in percentage MHC II+ by flow cytometry, P = 0.04) as compared with cells stimulated with IFN-gamma alone. IL-10 also directly up-regulated expression of ICAM-1 by 1997 cells. In conclusion, IL-10 was found to have contrasting effects on the production and cell surface expression of MHC class II molecules by mesengial cells and by macrophages, both in vitro and in vivo. The implications of these findings for IL-10-mediated immunosuppression are discussed.

Published
1998

24. HEROIN OVERDOSE AND MYOGLOBINURIC ACUTE RENAL FAILURE

Author

Rice Ek, McMahon Lp., Isbel Nm, Becker Gj, and Atkins Rc

Subjects
medicine.medical_specialty, Nephrology, business.industry, Emergency medicine, Heroin overdose, Medicine, General Medicine, business, Myoglobinuric acute renal failure
Published
2000

28. The role of transcription factor Egr‐1 in IL‐1 up‐regulation of tubular CD44 expression

Author

David J. Nikolic-Paterson, Rita Foti, Kazunori Takazoe, Hurst La, and Atkins Rc

Subjects
Sp1 transcription factor, General transcription factor, biology, business.industry, Response element, E-box, General Medicine, TCF4, Activating transcription factor 2, Cell biology, Sp3 transcription factor, Nephrology, Serum response factor, biology.protein, Medicine, business
Published
2000

29. Induction of neutrophil apoptosis through cross‐linking of the adhesion molecule CD44

Author

Nikolic-Paterson D.-J., Lan Hy, Hill Pa, Hurst La, Tesch Gh, Atkins Rc, and Takazoe K.

Subjects
biology, Cell adhesion molecule, business.industry, CD44, Soluble cell adhesion molecules, Neutrophil apoptosis, General Medicine, Adhesion, Intercellular adhesion molecule, Nephrology, biology.protein, Biophysics, Medicine, Molecule, business, Cell adhesion
Published
2000

32. Comparison of the prevalence and mortality risk of CKD in Australia using the CKD Epidemiology Collaboration (CKD-EPI) and Modification of Diet in Renal Disease (MDRD) Study GFR estimating equations: the AusDiab (Australian Diabetes, Obesity and...

Author

White SL, Polkinghorne KR, Atkins RC, and Chadban SJ

Abstract

BACKGROUND: The Chronic Kidney Disease Epidemiology Collaboration (CKD-EPI) is more accurate than the Modification of Diet in Renal Disease (MDRD) Study equation. We applied both equations in a cohort representative of the Australian adult population. STUDY DESIGN: Population-based cohort study. SETTING & PARTICIPANTS: 11,247 randomly selected noninstitutionalized Australians aged >or= 25 years who attended a physical examination during the baseline AusDiab (Australian Diabetes, Obesity and Lifestyle) Study survey. PREDICTORS & OUTCOMES: Glomerular filtration rate (GFR) was estimated using the MDRD Study and CKD-EPI equations. Kidney damage was defined as urine albumin-creatinine ratio >or= 2.5 mg/mmol in men and >or= 3.5 mg/mmol in women or urine protein-creatinine ratio >or= 0.20 mg/mg. Chronic kidney disease (CKD) was defined as estimated GFR (eGFR) >or= 60 mL/min/1.73 m(2) or kidney damage. Participants were classified into 3 mutually exclusive subgroups: CKD according to both equations; CKD according to the MDRD Study equation, but no CKD according to the CKD-EPI equation; and no CKD according to both equations. All-cause mortality was examined in subgroups with and without CKD. MEASUREMENTS: Serum creatinine and urinary albumin, protein, and creatinine measured on a random spot morning urine sample. RESULTS: 266 participants identified as having CKD according to the MDRD Study equation were reclassified to no CKD according to the CKD-EPI equation (estimated prevalence, 1.9%; 95% CI, 1.4-2.6). All had an eGFR >or= 45 mL/min/1.73 m(2) using the MDRD Study equation. Reclassified individuals were predominantly women with a favorable cardiovascular risk profile. The proportion of reclassified individuals with a Framingham-predicted 10-year cardiovascular risk >or= 30% was 7.2% compared with 7.9% of the group with no CKD according to both equations and 45.3% of individuals retained in stage 3a using both equations. There was no evidence of increased all-cause mortality in the reclassified group (age- and sex-adjusted hazard ratio vs no CKD, 1.01; 95% CI, 0.62-1.97). Using the MDRD Study equation, the prevalence of CKD in the Australian population aged >or= 25 years was 13.4% (95% CI, 11.1-16.1). Using the CKD-EPI equation, the prevalence was 11.5% (95% CI, 9.42-14.1). LIMITATIONS: Single measurements of serum creatinine and urinary markers. CONCLUSIONS: The lower estimated prevalence of CKD using the CKD-EPI equation is caused by reclassification of low-risk individuals. [ABSTRACT FROM AUTHOR]

Published
2010
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33. Nonalbuminuric renal impairment in type 2 diabetic patients and in the general population (national evaluation of the frequency of renal impairment cO-existing with NIDDM [NEFRON] 11).

Author

Thomas MC, Macisaac RJ, Jerums G, Weekes A, Moran J, Shaw JE, Atkins RC, Thomas, Merlin C, Macisaac, Richard J, Jerums, George, Weekes, Andrew, Moran, John, Shaw, Jonathan E, and Atkins, Robert C

Abstract

OBJECTIVE Most diabetic patients with impaired renal function have a urinary albumin excretion rate in the normal range. In these patients, the etiology of renal impairment is unclear, and it is also unclear whether this nonalbumunuric renal impairment is unique to diabetes. RESEARCH DESIGN AND METHODS In this study, we examined the frequency and predictors of nonalbumunuric renal impairment (estimated glomerular filtration rate [eGFR] <60 ml/min per 1.73 m(2)) in a nationally representative cohort of 3,893 patients with type 2 diabetes and compared our findings with rates observed in the general population from the Australian Diabetes, Obesity and Lifestyle Study (AusDiab) survey (n = 11,247). RESULTS Of the 23.1% of individuals with type 2 diabetes who had eGFR <60 ml/min per 1.73 m(2) (95% CI 21.8-24.5%), more than half (55%) had a urinary albumin excretion rate that was persistently in the normal range. This rate of renal impairment was predictably higher than that observed in the general population (adjusted odds ratio 1.3, 95% CI 1.1-1.5, P < 0.01) but was solely due to chronic kidney disease associated with albuminuria. In contrast, renal impairment in the absence of albuminuria was less common in those with diabetes than in the general population, independent of sex, ethnicity, and duration of diabetes (0.6, 0.5-0.7, P < 0.001). CONCLUSIONS Nonalbuminuric renal impairment is not more common in those with diabetes. However, its impact may be more significant. New studies are required to address the pathogenesis, prevention, and treatment of nonalbuminuric renal disease. [ABSTRACT FROM AUTHOR]

Published
2009
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34. Predictive value of nephelometric and high-performance liquid chromatography assays of urine albumin for mortality in a high-risk Aboriginal population.

Author

Wang Z, Hoy WE, Nicol JL, Su Q, Atkins RC, and Polkinghorne KR

Abstract

BACKGROUND: Urine albumin assays by high-performance liquid chromatography (HPLC) yield greater values than immunoassays at lower albumin levels. We compared predictive values of albumin-creatinine ratios (ACRs) by these 2 techniques for mortality in Aboriginal people. STUDY DESIGN & SETTING: This was a longitudinal study of 741 adults in a remote Aboriginal community who participated in a baseline health survey between 1992 and 1998 at ages ranging from 18 to 84 years (mean, 34 years). All natural deaths were documented on follow-up until 2006. Urine albumin concentrations were measured simultaneously by using both nephelometric and HPLC techniques on baseline urine samples retrieved from -70 degrees C storage, as well as creatinine concentrations, and ACRs were derived. Age- and sex-specific tertiles of ACR were compiled. Cox regression analyses were used to evaluate the predictive value of ACR for natural deaths by ACR tertiles and again by z score changes in ACRs as continuous variables. RESULTS: Participants were followed up for a median of 11 years, during which a total of 119 natural deaths were documented. ACRs on baseline urine samples were greater by HPLC than immunoassay at lower ACR ranges, but were fairly concordant at levels greater than 100 mg/mmol. Levels of ACR by both techniques were strong predictors of death, but correlations of death with ACR tertiles and with ACR levels on a continuum were similar for the 2 techniques. LIMITATIONS: The age- and sex-specific tertiles used might introduce some risk of bias in the assessment of predictive value. In addition, assays were performed on urine after more than 10 years of cold storage. CONCLUSION: Despite different absolute values, this study did not show that ACR level by either technique was superior in predicting deaths. Copyright © 2008 National Kidney Foundation, Inc. [ABSTRACT FROM AUTHOR]

Published
2008
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35. Combined interleukin 1 and tumour necrosis factor α blockade in rat crescentic anti-glomerular basement membrane glomerulonephritis.

Author

Atkins, Rc, Lan, Hui Y, Song, Qing, Nikolic-Paterson, David J, Tesch, Greg H, Mu, Wei, and Atkins, Robert C

Subjects
*GLOMERULONEPHRITIS, *INTERLEUKIN-1, *TUMOR necrosis factors, *RATS, *GENETICS
Abstract

SUMMARY: Studies in experimental models have established that blockade of either interleukin 1 (IL-1) or tumour necrosis factor α (TNF-α) is effective in suppressing crescentic glomerulonephritis. However, it is not known whether simultaneous blockade of both cytokines will provide additional disease suppression compared with that produced by single cytokine blockade. We have addressed this question in a study of accelerated crescentic anti-glomerular basement membrane (GBM) glomerulonephritis in the rat. Groups of six animals were treated with an IL-1 receptor antagonist (IL-1ra), TNF-α-binding protein (TNFbp), IL-1ra + TNFbp (combined) or saline (control) from the time of anti-GBM serum injection until being killed, 10 days later. Saline-treated animals developed crescentic glomerulonephritis with tubulointerstitial damage, heavy proteinuria and renal impairment. Compared with saline, treatment with either IL-1ra or TNFbp alone resulted in significant suppression of crescent formation (3.0% and 3.3%, respectively, vs. 21.0%; both P < 0.001 vs. control), tubulointerstitial leucocytic infiltration (262 ± 31 and 282 ± 32 cells/mm2 vs. 481 ± 71 cells/mm2; both P < 0.001 vs. control) and proteinuria (167 ± 44 and 164 ± 23 mg/24 h vs. 279 ± 36 mg/24 h; both P < 0.001 vs. control) and prevented the loss of renal function. Combined IL-1ra and TNFbp treatment resulted in a virtually identical degree of disease suppression as individual cytokine blockade in terms of crescent formation (2.7%), interstitial leucocytic infiltration (274 ± 45 cells/mm2), proteinuria (190 ± 18 mg/24 h) and renal function preservation. In conclusion, this study has demonstrated that blockade of either IL-1 or TNF-α alone substantial suppresses experimental crescentic glomerulonephritis to a similar extent to that achieved by simultaneous blockade of both cytokines. These findings provide a rationale... [ABSTRACT FROM AUTHOR]

Published
2001
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36. Local macrophage and myofibroblast proliferation in progressive renal injury in the rat remnant kidney.

Author

Yang, N, Wu, LL, Nikolic-Paterson, DJ, Ng, YY, Yang, WC, Mu, W, Gilbert, RE, Cooper, ME, Atkins, RC, and Lan, HU

Abstract

Background. We have recently shown that blockade of angiotensin II activity inhibits local macrophage and myofibroblast proliferation in progressive non-immune renal injury in the rat remnant kidney. However, it is not known whether this local proliferation contributes to macrophages and myofibroblast accumulation and the development of renal injury. Therefore, we examined this issue in a detailed time-course study of the rat remnant kidney. [ABSTRACT FROM PUBLISHER]

Published
1998
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37. Total body nitrogen predicts long-term mortality in haemodialysis patients - a single-centre experience.

Author

Arora, P, Strauss, BJG, Borovnicar, D, Stroud, D, Atkins, RC, and Kerr, PG

Abstract

Background: It has been estimated that 30-50% of adult haemodialysis patients have moderate to severe malnutrition. We have previously shown that estimation of total body nitrogen, expressed as a nitrogen index (NI) by in vivo neutron activation analysis (IVNAA) is an accurate tool for estimating total body protein in dialysis patients. It is not clear whether the nitrogen index is predictive of mortality and morbidity in dialysis patients. [ABSTRACT FROM PUBLISHER]

Published
1998
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39. THE EFFECTS OF DEOXYSPERGUALIN ON LYMPHOCYTES AND MONOCYTES IN VIVO AND IN VITRO

Author

Peter G. Kerr and Atkins Rc

Subjects
Transplantation, Kidney, Monocyte, Lymphocyte, Cyclosporins, Stimulation, Lymphocyte proliferation, Biology, Lymphocyte Activation, Guanidines, Kidney Transplantation, Monocytes, medicine.anatomical_structure, Immune system, Mechanism of action, In vivo, Immunology, medicine, Humans, Interleukin-2, Lymphocytes, Lymphocyte Culture Test, Mixed, medicine.symptom, Immunosuppressive Agents
Abstract

It has been suggested that deoxyspergualin, a new immunosuppressant, may be immunosuppressive via a purely antimonocyte action. As this appears to be unlikely, this study examines the effect of deoxyspergualin on lymphocyte and monocyte function in vivo and in vitro. It is demonstrated that deoxyspergualin inhibits human lymphocyte proliferation in response to mitogens and allogeneic stimulation. Furthermore, it is demonstrated that this inhibition occurs no matter whether the monocytes or lymphocytes are treated with the drug. The drug appears to have a more significant effect on the lymphocyte component; rhIL-2 appears partly to overcome the deoxyspergualin-induced inhibition of lymphocyte proliferation in response to allogeneic stimulation. In a rat renal transplant model, deoxyspergualin-treated animals demonstrated a moderate interstitial infiltrate in their transplant kidneys that comprised approximately 50% each of macrophages and lymphocytes. There was significantly less activation (e.g. IL-2R expression) in the treated kidney infiltrates compared to rejected controls. Thus deoxyspergualin is an agent with immunosuppressive effects on both lymphocytes and monocytes and would appear to have more marked effects on lymphocytes.

Published
1989

40. Antigenic heterogeneity of human mononuclear phagocytes: immunohistologic analysis using monoclonal antibodies

Author

Hancock, WW, Zola, H, and Atkins, RC

Abstract

Eight monoclonal antibodies to cell surface antigens of human monocytes were evaluated as immunologic markers for recognition of macrophages in sections of normal and diseased tissues, using immunoperoxidase and enzyme histochemical techniques. Monoclonal antibodies assessed were PHM2, PHM3, FMC17, FMC32, FMC33, FMC34, OKM1, and 63D3. Sites studied were human bone marrow, blood, lymph node, spleen, thymus, liver, kidney, lung, and peritoneal lavages, rejecting renal allografts containing inflammatory macrophages, and granulomata showing epithelioid and multinucleate giant cell formation. All antibodies bound to at least some tissue macrophages and, except for FMC32 and FMC33 antibodies, which were identically distributed, each antibody had a distinctive tissue distribution. Some antigens were shared by other bone-marrow-derived cells (megakaryocytes and cortical thymocytes), endothelium, epithelium, and dendritic cells. Antigenic differences were also detected between mononuclear phagocytes present at different sites, different stages of differentiation, and likely different states of activation. These studies provide evidence of major antigenic differences between various populations of human mononuclear phagocytes. They therefore indicate the need for careful evaluation of experiments involving the recognition of macrophages in tissue sections and smears based solely on the use of antimonocyte monoclonal antibodies.

Published
1983
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41. PROLONGED ANTIBIOTIC PERITONEAL LAVAGE IN THE MANAGEMENT OF GROSS GENERALIZED PERITONITIS

Author

Atkins Rc, Davidson Aj, Scott Df, and Holdsworth

Subjects
medicine.medical_specialty, medicine.drug_class, business.industry, Treatment regimen, Convalescence, media_common.quotation_subject, Antibiotics, Peritonitis, Kanamycin, General Medicine, medicine.disease, Surgery, Lesion, Diffuse peritonitis, medicine, medicine.symptom, Intensive care medicine, business, medicine.drug, media_common
Abstract

Since there is a high mortality and morbidity with conventional therapy in generalized peritonitis, a treatment regime of prolonged continuous peritoneal lavage (two to 10 days) with the lavage solution containing kanamycin (40 mug/ml) and cephalothin (100 mug/ml) was undertaken in 14 cases of gross, well established, diffuse peritonitis. Antibiotics were also given systemically. In 11 cases, in which the causative lesion was definitively repaired, no intraperitoneal complications developed and convalescence was rapid. Three patients, in whom causative lesion was not definitively repaired at operation, subsequently died. Prolonged antibiotic peritoneal lavage appears to be beneficial for patients with gross and diffuse peritoneal soiling, after the causative lesion has been repaired.

Published
1962

42. SURGICAL CORRECTION OF COMBINED MYOCARDIAL ANEURYSM AND INTERVENTRICULAR SEPTAL DEFECT FOLLOWING MYOCARDIAL INFARCTION

Author

Morris Kn, Atkins Rc, Stafford Eg, Anderson St, and Mirams Ja

Subjects
Heart Septal Defects, Ventricular, Male, Cardiac Catheterization, medicine.medical_specialty, business.industry, Myocardial Infarction, Electrocardiography in myocardial infarction, General Medicine, Middle Aged, Surgical correction, medicine.disease, Aneurysm, Internal medicine, Interventricular septal defect, Cardiology, Humans, Medicine, Myocardial infarction, Heart Aneurysm, business
Published
1968

44. REVERSIBLE ACUTE RENAL FAILURE IN THE NEPHROTIC SYNDROME WITH MINIMAL GLOMERULAR PATHOLOGY

Author

Holdsworth Dr, Stephenson P, Atkins Rc, and Dowling Jp

Subjects
medicine.medical_specialty, Nephrotic Syndrome, medicine.medical_treatment, Remission, Spontaneous, Urology, Renal function, Spontaneous remission, urologic and male genital diseases, Glomerulonephritis, medicine, Humans, Dialysis, Proteinuria, business.industry, Nephrosis, Lipoid, Acute kidney injury, General Medicine, Acute Kidney Injury, Middle Aged, medicine.disease, Acute Disease, Female, medicine.symptom, business, Complication, Nephrotic syndrome
Abstract

A case of minimal change glomerulonephritis, associated with the nephrotic syndrome and prolonged acute renal failure requiring two months of dialysis, is reported. Complete recovery of renal function occurred, but proteinuria recurred, responding to a course of steroids. Normal renal function without proteinuria has been observed for two years subsequently. The full return of renal function without specific therapy demonstrates that spontaneous recovery is possible in this rare complication of minimal change glomerulonephritis.

Published
1977

48. Renoprotective effect of the angiotensin-receptor antagonist irbesartan in patients with nephropathy due to type 2 diabetes.

Author

Lewis EJ, Hunsicker LG, Clarke WR, Berl T, Pohl MA, Lewis JB, Ritz E, Atkins RC, Rohde R, Raz I, Collaborative Study Group, Lewis, E J, Hunsicker, L G, Clarke, W R, Berl, T, Pohl, M A, Lewis, J B, Ritz, E, Atkins, R C, and Rohde, R

Abstract

Background: It is unknown whether either the angiotensin-II-receptor blocker irbesartan or the calcium-channel blocker amlodipine slows the progression of nephropathy in patients with type 2 diabetes independently of its capacity to lower the systemic blood pressure.Methods: We randomly assigned 1715 hypertensive patients with nephropathy due to type 2 diabetes to treatment with irbesartan (300 mg daily), amlodipine (10 mg daily), or placebo. The target blood pressure was 135/85 mm Hg or less in all groups. We compared the groups with regard to the time to the primary composite end point of a doubling of the base-line serum creatinine concentration, the development of end-stage renal disease, or death from any cause. We also compared them with regard to the time to a secondary, cardiovascular composite end point.Results: The mean duration of follow-up was 2.6 years. Treatment with irbesartan was associated with a risk of the primary composite end point that was 20 percent lower than that in the placebo group (P=0.02) and 23 percent lower than that in the amlodipine group (P=0.006). The risk of a doubling of the serum creatinine concentration was 33 percent lower in the irbesartan group than in the placebo group (P=0.003) and 37 percent lower in the irbesartan group than in the amlodipine group (P<0.001). Treatment with irbesartan was associated with a relative risk of end-stage renal disease that was 23 percent lower than that in both other groups (P=0.07 for both comparisons). These differences were not explained by differences in the blood pressures that were achieved. The serum creatinine concentration increased 24 percent more slowly in the irbesartan group than in the placebo group (P=0.008) and 21 percent more slowly than in the amlodipine group (P=0.02). There were no significant differences in the rates of death from any cause or in the cardiovascular composite end point.Conclusions: The angiotensin-II-receptor blocker irbesartan is effective in protecting against the progression of nephropathy due to type 2 diabetes. This protection is independent of the reduction in blood pressure it causes. [ABSTRACT FROM AUTHOR]

Published
2001

49. Relationship Between Urinary Phosphate and All-Cause and Cardiovascular Mortality in a National Population-Based Longitudinal Cohort Study.

Author

Toussaint ND, Damasiewicz MJ, Holt SG, Lu ZX, Magliano DJ, Atkins RC, Chadban SJ, Shaw JE, and Polkinghorne KR

Subjects
Australia epidemiology, Cohort Studies, Female, Humans, Longitudinal Studies, Male, Middle Aged, Phosphates, Proportional Hazards Models, Risk Factors, Cardiovascular Diseases, Renal Insufficiency, Chronic complications
Abstract

Objectives: High dietary phosphate intake may lead to adverse outcomes including cardiovascular disease (CVD). Urinary phosphate excretion, a marker of intestinal phosphate absorption, may be a more reliable marker of phosphate homeostasis in steady state than serum phosphate. Studies report good agreement between urine phosphate-to-creatinine ratio (uPiCr) and 24-hour urinary phosphate; however, whether uPiCr is associated with increased risk of CVD or mortality remains uncertain. This study aimed to assess the relationship between uPiCr and all-cause and CVD mortality., Design and Methods: This is an observational longitudinal cohort study using data from the population-based national Australian Diabetes, Obesity and Lifestyle study (n = 10,014 participants). Non-linear association between uPiCr and all-cause and CVD mortality was assessed using fractional polynomial transformations. Cox proportional hazards regression models were used to estimate adjusted hazard ratios for all-cause and CVD mortality., Results: Median age [interquartile range] was 50 [41-62] years, and 46% were male. Median uPiCr was 1.38 [1.02-1.79] mmol/mmol. Median follow-up time was 16.9 years with 1,735 deaths. uPiCr was associated with all-cause and CVD mortality in univariate models and when adjusted for age and gender. However, associations were not significant in multivariate models. Sensitivity analyses excluding participants with chronic kidney disease (CKD) revealed a significant J-shaped association between uPiCr and all-cause mortality. Urine phosphate alone showed an association with increased all-cause mortality in a similar J-shape relationship., Conclusion: Although no association between uPiCr and all-cause and CVD mortality was observed in multivariate analyses in the whole cohort, a significant relationship between uPiCr and mortality in those without CKD suggests that uPiCr may have predictive validity for future adverse outcomes in people with no CKD., (Copyright © 2021 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.)

Published
2022
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50. Incidence of chronic kidney disease among people with diabetes: a systematic review of observational studies.

Author

Koye DN, Shaw JE, Reid CM, Atkins RC, Reutens AT, and Magliano DJ

Subjects
Diabetic Nephropathies epidemiology, Disease Progression, Glomerular Filtration Rate, Humans, Incidence, Kidney Failure, Chronic complications, Kidney Failure, Chronic epidemiology, Kidney Failure, Chronic physiopathology, Observational Studies as Topic, Renal Insufficiency, Chronic epidemiology, Renal Insufficiency, Chronic physiopathology, Severity of Illness Index, Diabetes Mellitus, Type 1 complications, Diabetes Mellitus, Type 2 complications, Diabetic Nephropathies physiopathology, Global Health, Kidney physiopathology, Renal Insufficiency, Chronic complications
Abstract

Aims: The aim was to systematically review published articles that reported the incidence of chronic kidney disease among people with diabetes., Methods: A systematic literature search was performed using MEDLINE, Embase and CINAHL databases. The titles and abstracts of all publications identified by the search were reviewed and 10 047 studies were retrieved., Results: A total of 71 studies from 30 different countries with sample sizes ranging from 505 to 211 132 met the inclusion criteria. The annual incidence of microalbuminuria and albuminuria ranged from 1.3% to 3.8% for Type 1 diabetes. For Type 2 diabetes and studies combining both diabetes types, the range was from 3.8% to 12.7%, with four of six studies reporting annual rates between 7.4% and 8.6%. In studies reporting the incidence of eGFR < 60 ml/min/1.73 m 2 using the Modification of Diet on Renal Disease (MDRD) equation, apart from one study which reported an annual incidence of 8.9%, the annual incidence ranged from 1.9% to 4.3%. The annual incidence of end-stage renal disease ranged from 0.04% to 1.8%., Conclusions: The annual incidence of microalbuminuria and albuminuria is ~ 2-3% in Type 1 diabetes, and ~ 8% in Type 2 diabetes or mixed diabetes type. The incidence of developing eGFR < 60 ml/min/1.73 m 2 is ~ 2-4% per year. Despite the wide variation in methods and study design, within a particular category of kidney disease, there was only modest variation in incidence rates. These findings may be useful in clinical settings to help understand the risk of developing kidney disease among those with diabetes., (© 2017 Diabetes UK.)

Published
2017
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