Traditionally, renal dysfunction in congestive heart failure (cardiorenal syndrome type 1) has been attributed to reduced cardiac output and low mean arterial perfusion pressure, which elicit a series of neurohumoral activations resulting in increased renal vascular resistance and decreased renal function.During the last decade, several studies have shown that the extent of renal dysfunction is not so closely associated with indices of forward failure-such as the cardiac index or mean arterial pressure-but rather with indicators of congestion, such as left ventricular enddiasystolic pressure or central venous pressure (CVP), which are indicators of backward failure. The impact of backward failure on renal function is not confined to an elevation of CVP, the renal drainage pressure, but includes a broad spectrum of mechanisms. Involved are the organ systems right heart, lung, the liver, the proinflammatory signals originating from the intestines, but also renal interstitial edema (renal compartment syndrome) and the intraabdominal pressure.The therapeutic measures must focus on the modulation of the preload adapted to the specific situation of an individual patient. This includes diuretics aiming at different segments of the tubulus system including antagonists of aldosteron and ADH, extracorporeal fluid elimination by ultrafiltration or peritoneal dialysis.