Creatinine Bump: An Indication of AKI in Patients With Acute Heart Failure?

Tejas P. Desai, MD


April 05, 2018

The "creatinine bump" is not the latest dance craze sweeping the nation. Yet when it is mentioned, you can be nearly assured that a delicate dance between the kidneys and the heart has already begun. This dance is rooted in the contradictory manner in which nephrologists and cardiologists recommend treating the creatinine bump [also known as acute kidney injury (AKI)]. These recommendations, to increase diuresis or increase volume, leave many physicians frustrated and confused.

A number of previous studies[1,2,3,4,5,6] have tried to uncover the exact nature-and, therefore, appropriate treatment-of AKI during the treatment of decompensated heart failure (HF), but the current study[7] published in Circulation approaches the "bump" from an interesting and novel perspective.

Ahmad and colleagues[7] hypothesized that the creatinine bump is not an indication of AKI. Rather, the acute rise in creatinine during the treatment of decompensated HF is an innocuous change in concentration and not an indicator of true tubular damage. Proving this hypothesis would mean that the creatinine bump would no longer be a source of confusion and frustration for physicians.

Study Outcomes

The current study[7] was a subgroup analysis of the ROSE-HF[8] trial. In that trial, patients with decompensated HF and chronic kidney disease were randomly assigned to receive either nesiritide vs placebo or dopamine vs placebo. Investigators measured a number of markers of kidney function and found that renal function did not improve with either treatment.

In this new analysis, 283 of the 360 randomly assigned ROSE-HF patients were further split into two groups: those who developed worsening renal failure (rise in serum creatinine or cystatin C as measured by at least a 20% drop in estimated glomerular filtration rate [eGFR]) and those who did not. In each group, markers of tubular injury (KIM-1, NGAL, NAG) were evaluated to determine if true tubular damage (ie, AKI) was correlated with changes in eGFR (and, therefore, creatinine). The concentration of each tubular marker was measured at baseline (before the initiation of high-dose loop diuretic for treatment of decompensated HF) and 72 hours later.

Within the 72-hour period, the patients were exposed to high-dose furosemide (median dose, 560 mg IV) and had a median total urine output of nearly 8 L. Despite adequate diuresis, the investigators uncovered no changes in KIM-1, NGAL, and NAG from baseline and after 72 hours when cystatin C was used to calculate eGFR. Similarly, neither KIM-1 nor NGAL changed in the group in which eGFR was measured by serum creatinine (ie, those patients who experienced the creatinine bump). In fact, the investigators found a paradoxical improvement in survival when KIM-1, NGAL, and NAG increased!


At this point, it is important to remind you that this subgroup analysis was not randomized. The results obtained are likely affected by the suboptimal study design. Indeed, the paradoxical improvement in survival raises many doubts about the integrity of this analysis. For fun, you may want to read the explanations that the authors provide for this paradoxical observation; they do not appear to mention that the study design could have contributed to this finding.

This trial is an interesting effort to debunk the belief that AKI occurs when patients with acute HF are heavily diuresed. Rather than trying to determine the best treatment that would limit collateral organ (kidney) damage, the investigators simply wanted to disprove that AKI even occurs.

My fear is that this trial will lend support to those clinicians who want to ignore the creatinine bump as a true indicator of kidney damage. The creatinine bump and the concomitant debate between nephrologists and cardiologists have furthered our understanding of kidney injury in the face of heavy diuresis. These debates may become antiquated if an increasing number of clinicians believe that the creatinine bump is more an innocuous finding than an ominous sign.

Follow Tejas P. Desai, MD, on Twitter: @nephondemand

Follow Medscape Nephrology on Twitter for more nephrology news: @MedscapeKidney


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