Christopher Maulion1, Sheldon Chen2, Veena S Rao1, Juan B Ivey-Miranda1,3, Zachary L Cox4, Devin Mahoney1, Steven G Coca5, Dan Negoianu6, Jennifer L Asher7, Jeffrey M Turner8, Lesley A Inker9, F Perry Wilson10, Jeffrey M Testani1. 1. Section of Cardiovascular Medicine, Department of Internal Medicine, Yale University School of Medicine, New Haven, Connecticut. 2. Division of Nephrology, Department of Emergency Medicine, The University of Texas MD Anderson Cancer Center, Houston, Texas. 3. Department of Heart Failure, Cardiology Hospital, XXI Century National Medical Center, Mexican Social Security Institute, Mexico City, Mexico. 4. Department of Pharmacy Practice, Lipscomb University College of Pharmacy, Nashville, Tennessee. 5. Department of Internal Medicine, Icahn School of Medicine at Mount Sinai, New York, New York. 6. Division of Renal Electrolyte and Hypertension, Department of Internal Medicine, University of Pennsylvania, Philadelphia, Pennsylvania. 7. Department of Comparative Medicine, Yale University School of Medicine, New Haven, Connecticut. 8. Division of Nephrology, Department of Medicine, Yale University School of Medicine, New Haven, Connecticut. 9. Division of Nephrology, Department of Medicine, Tufts Medical Center, Boston, Massachusetts. 10. Clinical and Translational Research Accelerator, Yale University School of Medicine, New Haven, Connecticut.
Abstract
Background: Worsening serum creatinine is common during treatment of acute decompensated heart failure (ADHF). A possible contributor to creatinine increase is diuresis-induced changes in volume of distribution (VD) of creatinine as total body water (TBW) contracts around a fixed mass of creatinine. Our objective was to better understand the filtration and nonfiltration factors driving change in creatinine during ADHF. Methods: Participants in the ROSE-AHF trial with baseline to 72-hour serum creatinine; net fluid output; and urinary KIM-1, NGAL, and NAG were included (n=270). Changes in VD were calculated by accounting for measured input and outputs from weight-based calculated TBW. Changes in observed creatinine (Crobserved) were compared with predicted changes in creatinine after accounting for alterations in VD and non-steady state conditions using a kinetic GFR equation (Cr72HR Kinetic). Results: When considering only change in VD, the median diuresis to elicit a ≥0.3 mg/dl rise in creatinine was -7526 ml (IQR, -5932 to -9149). After accounting for stable creatinine filtration during diuresis, a change in VD alone was insufficient to elicit a ≥0.3 mg/dl rise in creatinine. Larger estimated decreases in VD were paradoxically associated with improvement in Crobserved (r=-0.18, P=0.003). Overall, -3% of the change in eCr72HR Kinetic was attributable to the change in VD. A ≥0.3 mg/dl rise in eCr72HR Kinetic was not associated with worsening of KIM-1, NGAL, NAG, or postdischarge survival (P>0.05 for all). Conclusions: During ADHF therapy, increases in serum creatinine are driven predominantly by changes in filtration, with minimal contribution from change in VD.
Background: Worsening serum creatinine is common during treatment of acute decompensated heart failure (ADHF). A possible contributor to creatinine increase is diuresis-induced changes in volume of distribution (VD) of creatinine as total body water (TBW) contracts around a fixed mass of creatinine. Our objective was to better understand the filtration and nonfiltration factors driving change in creatinine during ADHF. Methods: Participants in the ROSE-AHF trial with baseline to 72-hour serum creatinine; net fluid output; and urinary KIM-1, NGAL, and NAG were included (n=270). Changes in VD were calculated by accounting for measured input and outputs from weight-based calculated TBW. Changes in observed creatinine (Crobserved) were compared with predicted changes in creatinine after accounting for alterations in VD and non-steady state conditions using a kinetic GFR equation (Cr72HR Kinetic). Results: When considering only change in VD, the median diuresis to elicit a ≥0.3 mg/dl rise in creatinine was -7526 ml (IQR, -5932 to -9149). After accounting for stable creatinine filtration during diuresis, a change in VD alone was insufficient to elicit a ≥0.3 mg/dl rise in creatinine. Larger estimated decreases in VD were paradoxically associated with improvement in Crobserved (r=-0.18, P=0.003). Overall, -3% of the change in eCr72HR Kinetic was attributable to the change in VD. A ≥0.3 mg/dl rise in eCr72HR Kinetic was not associated with worsening of KIM-1, NGAL, NAG, or postdischarge survival (P>0.05 for all). Conclusions: During ADHF therapy, increases in serum creatinine are driven predominantly by changes in filtration, with minimal contribution from change in VD.
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