Fluid overload as a biomarker of heart failure and acute kidney injury

Abstract

Background/aims: Acute heart failure (HF) and acute kidney injury (AKI) are common. These syndromes are each associated with considerable morbidity, mortality, and health resource utilization and are increasingly encountered. Fluid accumulation and overload are common themes in the pathophysiology and clinical course of both HF and AKI.

Methods: This narrative literature review provides an overview of the pathophysiology of fluid accumulation with a focus on HF and AKI, along with a discussion of the importance of assessment of fluid balance in these syndromes and how it correlates with clinical outcome.

Results: In HF, fluid accumulation, defined as either a positive cumulative fluid balance or as an acute redistribution of fluid, represents a core precipitating mechanism of acute decompensation and is associated with worsening symptoms, hospitalization and death. Determining fluid balance in HF may be complex and depend largely on underlying pathophysiology; however, in addition to simple fluid balance (intake minus output) measurement, newer biomarkers (i.e. B-type natriuretic peptides) and novel technology (i.e. impedance cardiography) are proving to be useful for detection and risk identification for acute decompensated HF that may allow earlier intervention and translate into improved clinical outcomes. Recent data have also emerged showing the importance of fluid balance in both adult and pediatric patients with AKI. In general, a positive cumulative fluid balance portends higher morbidity and an increased risk for worse clinical outcome. Fluid balance should be recognized as a potentially modifiable biomarker and determinant of clinical outcome in these patients.

Conclusion: To date, the impact of fluid balance in both of these syndromes, more so with AKI, has likely been underappreciated. There is little to no data specifically on fluid balance in the cardiorenal syndrome, where acute/chronic heart disease can directly contribute to acute/chronic worsening of kidney function that likely exacerbates fluid homeostasis. Additional investigations are needed.