# Acute Kidney Injury in Acute Heart Failure Revisited: Marker of Cardiorenal Disease Severity Rather Than Isolated Renal Injury

## TL;DR

The paper argues that kidney function decline in acute heart failure is a sign of overall disease severity, not just kidney damage.

## Contribution

It challenges traditional definitions of acute kidney injury by emphasizing cardiorenal interactions and context in acute heart failure.

## Key findings

- Worsening renal function often occurs during effective decongestion and isn't linked to poor outcomes without residual congestion.
- Persistent congestion and reduced renal reserve are stronger predictors of worse prognosis than creatinine-based definitions.
- Nephrology-derived AKI definitions miss the hemodynamic and therapeutic context of acute heart failure.

## Abstract

Background: Renal function deterioration during hospitalization for acute heart failure (AHF) is common and is traditionally classified as acute kidney injury (AKI) or worsening renal function (WRF) based on changes in serum creatinine (Cr). However, Cr-based definitions may inadequately reflect the complex cardiorenal interactions occurring in AHF. Purpose: This narrative review summarizes and compares definitions of AKI and WRF used in AHF, evaluates their prognostic significance, and explores whether renal function deterioration should be interpreted as a marker of cardiorenal disease severity rather than isolated kidney injury. Methods: A narrative review of randomized trials, observational studies, post hoc analyses, and meta-analyses was conducted, focusing on Cr-based and nephrology-derived AKI definitions (RIFLE, AKIN, KDIGO), timing and baseline selection, congestion status, and the role of biomarkers and imaging in clinical interpretation. Results: The most widely used definition of WRF is an absolute increase in serum Cr ≥ 0.3 mg/dL. Multiple studies demonstrate that such changes frequently occur during effective decongestion and are not independently associated with adverse outcomes in the absence of residual congestion. In contrast, persistent congestion, impaired diuretic response, reduced renal reserve, and advanced cardiorenal comorbidity consistently predict worse prognosis. Nephrology-derived AKI definitions identify higher-risk patients but incompletely account for the hemodynamic and therapeutic context of AHF. Conclusions: In AHF, AKI and WRF often act as markers of underlying cardiorenal disease severity rather than direct indicators of irreversible kidney injury. Interpretation of renal function deterioration should be contextual, integrating congestion status, perfusion, renal reserve, and dynamic response to therapy. Achieving effective and complete decongestion remains the primary therapeutic objective in AHF, even in the presence of transient Cr increases.