*; Viola Vaccarino, MD, PhD; Mikhail Kosiborod, MD; Judith H. Lichtman, PhD§; Susan Cheng, BA; Suzanne G. Watnick, MD*; Harlan M. Krumholz, MD‡∥¶">
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Volume 9, Issue 1, Pages 13-25 (February 2003)


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Worsening renal function: What is a clinically meaningful change in creatinine during hospitalization with heart failure?☆☆

Grace L. Smith, MPH*, Viola Vaccarino, MD, PhD, Mikhail Kosiborod, MD, Judith H. Lichtman, PhD§, Susan Cheng, BA, Suzanne G. Watnick, MD*, Harlan M. Krumholz, MD‡∥¶

Received 26 July 2002; received in revised form 26 November 2002 and 27 November 2002

Abstract 

Introduction: Worsening renal function during hospitalization for heart failure, defined as elevation in creatinine during admission, predicts adverse outcomes. Prior studies define worsening renal function using various creatinine elevations, but the relative value of definitions is unknown. Methods and Results: In a prospective cohort of 412 patients hospitalized for heart failure, we compared a spectrum of worsening renal function definitions (absolute creatinine elevations ≥0.1 to ≥0.5 mg/dL and 25% relative elevation from baseline) and associations with 6-month mortality, readmission, and functional decline. Creatinine elevation ≥0.1 mg/dL occurred in 75% of patients, and elevation ≥0.5 mg/dL occurred in 24% of patients. Risk of death rose with higher creatinine elevations (adjusted hazard ratio [HR] = 0.89, 1.19, 1.67, 1.91, and 2.90 for elevations ≥0.1 to ≥0.5 mg/dL). Maximum sensitivity of any definition for predicting mortality was 75% and maximum specificity was 79%. High creatinine elevation was a more important predictor of death than was a single measure of baseline creatinine. Conclusions: Larger creatinine elevations predict highest risk of death, yet even minor changes in renal function are associated with adverse outcomes. The choice of a “best definition” for worsening renal function has implications for the number of patients identified with this risk factor and the magnitude of risk for mortality.

KeywordsSensitivity, mortality

New Haven, Connecticut

Atlanta, Georgia

From the *Department of Medicine, Yale University School of Medicine, New Haven, Connecticut; Division of Cardiology, Emory University School of Medicine, Atlanta, Georgia; Section of Cardiovascular Medicine, Department of Medicine, Yale University School of Medicine, New Haven, Connecticut, §Section of Chronic Disease Epidemiology, Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut; Center for Outcomes Research and Evaluation, Yale-New Haven Hospital, New Haven, Connecticut (current affiliation: McMaster University, Hamilton, Ontario, Canada); and Section of Health Policy and Administration, Department of Epidemiology and Public Health, Yale University School of Medicine, New Haven, Connecticut

 Reprint requests to: Dr. Krumholz, Yale University School of Medicine, 333 Cedar Street, PO Box 208025, New Haven, CT 06520-8025.

☆☆ Dr. Watnick was a Robert Wood Johnson Clinical Scholar at Yale University during the time the work was conducted. She is currently affiliated with the Section of Nephrology, Oregon Health Sciences University and Portland VA Hospital.

PII: S1071-9164(02)25403-2

doi:10.1054/jcaf.2003.3


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