TY - JOUR AU - Matsushita K. AU - Jee S. AU - Yatsuya H. AU - Ishani A. AU - Warnock D. AU - Woodward Mark AU - Fox C. AU - Kitamura A. AU - Black C. AU - Gansevoort R. AU - Tonelli M. AU - Coresh J. AU - Inker L. AU - de Jong P. AU - Rothenbacher D. AU - Grams M. AU - Naimark D. AU - Nally J. AU - Drion I. AU - Lea J. AU - Peralta C. AU - Ryu S. AB -

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 m2 per year, whereas 7% and 4% had a slope >5 ml/min per 1.73 m2 per year, respectively. Compared with a slope of 0 ml/min per 1.73 m2 per year, a slope of -6 ml/min per 1.73 m2 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 m2 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 versus <3 years). We conclude that prior decline or rise in eGFR associates with an increased risk of mortality, independent of current eGFR.

AD - Division of Nephrology, Sunnybrook Health Sciences Centre and Institute of Health Policy Management and Evaluation, Faculty of Medicine, University of Toronto, Toronto, Ontario, Canada;
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland; Division of Nephrology, Department of Medicine, Johns Hopkins University, Baltimore, Maryland;
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland;
Institute of Applied Health Science, University of Aberdeen, Aberdeen, United Kingdom;
Diabetes Centre, Isala Clinics, Zwolle, The Netherlands;
National Heart, Lung, and Blood Institute's Framingham Heart Study, Center for Population Studies, Framingham, Massachusetts; Division of Endocrinology, Brigham and Women's Hospital and Harvard Medical School, Boston, Massachusetts;
Division of Nephrology, Tufts Medical Center, Boston, Massachusetts;
Section of Nephrology, Minneapolis Veterans Affairs Health Care System, Minneapolis, Minnesota;
Department of Epidemiology and Health Promotion, Institute for Health Promotion, Graduate School of Public Health, Yonsei University, Seoul, Korea;
Osaka Center for Cancer and Cardiovascular Disease Prevention, Osaka, Japan;
Renal Division, Emory University School of Medicine, Atlanta, Georgia;
Department of Nephrology and Hypertension, Glickman Urological and Kidney Institute, Cleveland, Ohio;
Department of Medicine, University of California and San Francisco Veterans Affairs Medical Center, San Francisco, California;
Division of Clinical Epidemiology and Aging Research, German Cancer Research Center, Heidelberg, Germany; Institute of Epidemiology and Medical Biometry, Ulm University, Ulm, Germany;
Kangbuk Samsung Hospital, Sunkgyunkwan University School of Medicine, Seoul, Korea;
Department of Medicine, University of Calgary, Calgary, Alberta, Canada;
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland; ckdpc@jhmi.edu.
Department of Nephrology, University Medical Center Groningen, University of Groningen, Groningen, The Netherlands;
Department of Medicine, University of Alabama at Birmingham, Birmingham, Alabama;
Department of Epidemiology, Johns Hopkins Bloomberg School of Public Health, Baltimore, Maryland; The George Institute for Global Health, Nuffield Department of Population Health, University of Oxford, Oxford, United Kingdom; and The George Institute for Global Health, University of Sydney, Sydney, Australia. AN - 26657865 BT - Journal of the American Society of Nephrology DP - NLM ET - 2015/12/15 LA - Eng LB - AUS
UK
PROF
FY16 N1 - Naimark, David M J
Grams, Morgan E
Matsushita, Kunihiro
Black, Corri
Drion, Iefke
Fox, Caroline S
Inker, Lesley A
Ishani, Areef
Jee, Sun Ha
Kitamura, Akihiko
Lea, Janice P
Nally, Joseph
Peralta, Carmen Alicia
Rothenbacher, Dietrich
Ryu, Seungho
Tonelli, Marcello
Yatsuya, Hiroshi
Coresh, Josef
Gansevoort, Ron T
Warnock, David G
Woodward, Mark
de Jong, Paul E
CKD Prognosis Consortium
K08 DK092287/DK/NIDDK NIH HHS/United States
J Am Soc Nephrol. 2015 Dec 11. pii: ASN.2015060688. N2 -

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 m2 per year, whereas 7% and 4% had a slope >5 ml/min per 1.73 m2 per year, respectively. Compared with a slope of 0 ml/min per 1.73 m2 per year, a slope of -6 ml/min per 1.73 m2 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 m2 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 versus <3 years). We conclude that prior decline or rise in eGFR associates with an increased risk of mortality, independent of current eGFR.

PY - 2015 SN - 1533-3450 (Electronic)
1046-6673 (Linking) T2 - Journal of the American Society of Nephrology TI - Past Decline Versus Current eGFR and Subsequent Mortality Risk Y2 - FY16 ER -