Abstract

In this issue of the Journal, Smith and colleagues report their findings that demonstrate increases in serum creatinine levels during heart failure hospitalization are associated with worsened outcomes after hospital discharge. The authors conducted a cohort study of 412 patients hospitalized at their institution over a 30-month period who survived to discharge. The change in serum creatinine level (Cr) was defined simply as the difference between the baseline and discharge levels, with “worsened renal function” defined as a Cr 0.1mg/dL. The outcomes examined in this study were survival, readmission, and change in functional status during the 6 months after hospitalization. A Cr 0.3mg/dL was associated with a 60% increased adjusted mortality risk, and surprisingly the Cr was a stronger mortality predictor than the baseline creatinine level. Furthermore, the higher mortality risk associated with Cr 0.3mg/dL was similar at all levels of baseline creatinine level. These findings build upon prior studies that have determined the importance of renal function in the prognosis and management of heart failure. Most previous analyses evaluating the effect of renal function on heart failure outcomes have used a baseline measure from the outpatient setting. 1 A prior study from this group of authors similarly found elevations of creatinine 0.3 mg/dL during heart failure hospitalization to be associated with greater inhospital length of stay and mortality risk. The current study extends these findings by demonstrating an association of increased Cr with worse outcomes for survivors of hospitalization up to 6 months after discharge, and showing a dose-dependent relationship of Cr and increased mortality risk. However, as with most interesting studies, this analysis provokes as many questions as it answers for clinicians managing heart failure patients. The primary questions that arise from this study are: (1) Can the Cr be interpreted as a “diagnostic test” for high mortality risk? (2) Is worsened renal function a causal mechanism leading to increased mortality risk or a marker of poor cardiac function and subsequent under-treatment? and (3) What are the clinical implications of these findings for inpatient and postdischarge heart failure management?

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