The management of the cardiorenal syndrome (CRS) in decompensated heart failure (HF) is challenging, with high-quality evidence lacking.
The pathophysiology of CRS in decompensated HF is complex, with glomerular filtration rate (GFR) and urine output representing different aspects of kidney function. GFR depends on structural factors (number of functional nephrons and integrity of the glomerular membrane) versus hemodynamic alterations (volume status, renal perfusion, arterial blood pressure, central venous pressure or intra-abdominal pressure) and neurohumoral activation. In contrast, urine output and volume homeostasis are mainly a function of the renal tubules. Treatment of CRS in decompensated HF patients should be individualized based on the underlying pathophysiological processes.
Congestion, defined as elevated cardiac filling pressures, is not a surrogate for volume overload. Transient decreases in GFR might be accepted during decongestion, but hypotension must be avoided. Paracentesis and compression therapy are essential to remove fluid overload from third spaces. Increasing the effective circulatory volume improves renal function when cardiac output is depressed. As mechanical support is invasive and inotropes are related to increased mortality, afterload reduction through vasodilator therapy remains the preferred strategy in patients who are normo- or hypertensive. Specific therapies to augment renal perfusion (rolofylline, dopamine or nesiritide) have rendered disappointing results, but recently, serelaxin has been shown to improve renal function, even with a trend towards reduced all-cause mortality in selected patients. Diuretic resistance is associated with worse outcomes, independent of the underlying GFR. Combinational diuretic therapy, with ultrafiltration as a bail-out strategy, is indicated in case of diuretic resistance.
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