Review demonstrates hemodynamic mechanisms driving acute kidney injury in cardiogenic shock, highlighting venous congestion and right ventricular failure as key therapeutic targets.
Cardiorenal syndrome (CRS) represents a complex bidirectional interaction between the heart and kidneys whereby acute or chronic failure of one organ precipitates dysfunction in the other. CRS occurring in the setting of cardiogenic shock (CS), or CRS-CS, remains one of the most severe manifestations, contributing substantially to morbidity and mortality. Historically, CRS-CS was attributed to renal hypoperfusion from reduced cardiac output. Contemporary evidence suggests that venous congestion and right ventricular dysfunction play equally important roles in the development of acute kidney injury and resultant CRS-CS. Advanced hemodynamic monitoring has further refined our understanding of this dynamic interplay. This review discusses the epidemiology, pathophysiology, hemodynamic determinants, diagnosis, and contemporary management of CRS-CS, emphasizing the importance of forward flow, venous congestion, and right ventricular performance when evaluating renal dysfunction.
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Mehta et al. (2026) studied this question.
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