Kidney Failure in Cardiogenic Shock

Acute kidney injury (AKI) is a frequent and prognostically decisive complication of cardiogenic shock (CS), conferring substantially increased short- and long-term mortality. As understanding of CS has evolved beyond an isolated low-output model, AKI is increasingly recognized as a consequence of multifactorial pathophysiology encompassing venous congestion, neurohormonal dysregulation, microcirculatory dysfunction, inflammation, and iatrogenic injury from shock therapies. Despite this expanded mechanistic framework, approaches to the diagnosis and management of AKI in CS remain highly variable, and no single strategy has consistently improved renal or survival outcomes. Emerging data suggest multiple biologically distinct phenotypes of AKI in CS that may enable future targeted therapeutics. This review synthesizes contemporary evidence on the classification, epidemiology, and mechanisms of AKI in CS across distinct phenotypes, including early- versus late-onset, acute versus acute-on-chronic, and cardiorenal versus cardiometabolic presentations. We further discuss the renal effects of contemporary shock therapies, including vasoactive agents, temporary mechanical circulatory support, and renal replacement strategies. Finally, we highlight emerging diagnostic tools, including noninvasive vascular imaging and renal biomarkers, alongside novel device-based approaches to improve renal perfusion and congestion. Advancing care in CS will depend on redefining AKI not only as a binary marker of renal dysfunction but also as a mechanistically heterogeneous component of shock biology amenable to targeted intervention.