Since pressure/volume relationships are largely determined by heart compliance, a high CVP indicates volume overload, cardiac dysfunction, or both [
28,
29]. Traditionally, AKI in congestive heart failure or cardiorenal syndrome is attributed to a reduction in CO and MAP which elicits a series of neurohumoral events resulting in increased renal vascular resistance and decreased renal function [
30]. The degree of AKI is closely associated with congestive venous “backward failure.” In 2557 patients who underwent right heart catheterization, Damman et al. found that an increased CVP was not only associated with impaired renal function but also independently related to all-cause mortality [
31]. A study in patients with advanced decompensated heart failure showed that those with worsening renal function had a higher CVP on admission and after intensive medical therapy [
32]. Worsening renal function occurred less frequently in patients in whom CVP was kept below 8 mmHg. An apparent potential of CVP for AKI risk stratification was noted across the spectrum of systemic blood pressure, pulmonary capillary wedge pressure, cardiac index, and estimated glomerular filtration rate [
32]. In adults with chronic heart disease after biventricular repair, Ohuchi et al. found that a high CVP predicted kidney enlargement and abnormal intrarenal flow dynamics that were closely associated with severity of heart failure and with cardiovascular events [
33]. Right ventricular dysfunction and increased CVP are frequently observed in cardiac surgery patients and may lead to congestive renal dysfunction [
34]. Studies in patients with acute right ventricular failure suggest that a high CVP is associated with a marked reduction in RBF by increasing renal backward pressure [
35,
36]. A strong relationship was observed between CVP and RBF in both acute and chronic heart failure. Reducing CVP markedly improved renal function [
35]. Cardiovascular surgery patients with progressive AKI had greater diastolic perfusion pressure deficits as compared to patients without AKI progression. Almost 25% of the diastolic perfusion pressure deficit was due to an increase in CVP [
36]. This underscores the strong relationship between back (renal venous) pressure and CVP in the development of AKI.
Taken together, more attention must be paid to the pressure effect of CVP in heart failure/cardiorenal syndrome, regardless of whether fluid overload is present or not.