Are We Barking Up the Wrong Tree? Rise in Serum Creatinine and Heart Failure

A significant subset of patients with heart failure (HF) experience small to moderate rise in serum creatinine (RSC) in the setting of otherwise beneficial therapies such as aggressive diuresis or renin-angiotensin-aldosterone system (RAAS) inhibition. Accumulating data suggest that RSC in this setting is dissimilar from conventional causes of renal insult in that it has a negligible impact on the outcomes. There is also emerging evidence on the lack of association between biomarkers of renal injury and RSC in the setting of aggressive diuresis. A similar pattern has been observed in recent hypertension trials where the RSC in patients with intensive blood pressure control has not been associated with biomarker evidence of renal injury or adverse outcomes. Based on these findings, RSC, rather than acute kidney injury, appears to be the preferred terminology in HF (and possibly in hypertension) because of its purely descriptive nature that lacks any potentially inaccurate implication of mechanistic or prognostic reference. From a pragmatic viewpoint, we believe that small to moderate RSC is to be anticipated and tolerated with RAAS inhibition and/or aggressive diuresis in acute or chronic HF and should not prompt discontinuation of the therapy unless complications such as hypotension and severe hyperkalemia develop.