Cardiorenal Syndrome in the Hospital

Abstract

The cardiorenal syndrome refers to a group of complex, bidirectional pathophysiological pathways involving dysfunction in both the heart and kidney. Upward of 60% of patients admitted for acute decompensated heart failure have CKD, as defined by an eGFR of <60 ml/min per 1.73 m 2 . CKD, in turn, is one of the strongest risk factors for mortality and cardiovascular events in acute decompensated heart failure. Although not well understood, the mechanisms in the cardiorenal syndrome include venous congestion, arterial underfilling, neurohormonal activation, inflammation, and endothelial dysfunction. Arterial underfilling may lead to activation of the renin-angiotensin-aldosterone system and sympathetic nervous system, leading to sodium reabsorption and vasoconstriction. Venous congestion likely also mediates and perpetuates these maladaptive pathways. To rule out intrinsic kidney disease that is distinct from the cardiorenal syndrome, one should obtain a careful history, review longitudinal eGFR trends, assess albuminuria and proteinuria, and review the urine sediment and kidney imaging. The hallmark of the cardiorenal syndrome is intense sodium avidity and diuretic resistance, often requiring a combination of diuretics with varying pharmacological targets, and monitoring of urinary response to guide escalations in therapy. Invasive means of decongestion may be required including ultrafiltration or KRT such as peritoneal dialysis, which is often better tolerated from a hemodynamic perspective than intermittent hemodialysis. Strategies for increasing forward perfusion in states of low cardiac output and cardiogenic shock may include afterload reduction and inotropes and, in the most severe cases, mechanical circulatory support devices, many of which have kidney-specific considerations.

Trial registration: ClinicalTrials.gov NCT05318105.

Figure 1

Proposed pathophysiological pathways leading to the cardiorenal syndrome and its complications. The inciting event is usually an acute decompensation of heart failure. This may lead to either arterial underfilling or venous congestion as mediators that promote neurohormonal activity, inflammation, and endothelial dysfunction. In combination, these pathways lead to reductions in glomerular filtration rate. Complications include sodium avidity and fluid retention, reduced kidney clearance, and endocrine function, all of which further perpetuate the pathophysiology. HFpEF, heart failure with preserved ejection fraction; HFrEF, heart failure with reduced ejection fraction.