In the kidneys, these hormones promote avid reabsorption of salt and water throughout the tubule. In addition, they cause an overall shift in perfusion from short-looped (cortical) to long-looped (juxtamedullary) nephrons, which have a greater sodium reabsorptive capacity. The resulting increase in total volume is intended as an adaptive process, given the perceived arterial underfilling. Ultimately, however, it causes further impairment of cardiac function and worsening of pulmonary and peripheral edema.

In this setting, heart failure may cause a prerenal state because of two distinct but related phenomena. First, the decreased cardiac output (“forward failure”) and renal vasoconstriction lead to reduced renal perfusion pressure. If severe enough, the hypoperfusion may overcome normal compensation mechanisms and cause a reduction in glomerular filtration rate. In addition, the chronic increase in venous pressure (“backward failure”) behind the failing heart is transmitted to the renal veins, which further impairs renal function. It is not clear how increased renal venous pressure impairs filtration; however, the mechanism likely includes increased levels of sympathetic tone, angiotensin II, and endothelin, all of which cause intrarenal vasoconstriction.

EPIDEMIOLOGY

The incidence of chronic kidney disease in the heart failure population has been difficult to estimate, but it likely ranges somewhere between 20% and 67%, with higher incidence associated with older age, diabetes, and hypertension.

In the setting of acute decompensated CHF, both baseline renal dysfunction and worsening renal dysfunction during hospitalization have been identified as significant predictors of hospitalization length, in-hospital mortality, and mortality after discharge.

Large databases, such as the Acute Decompensated Heart Failure National Registry, have suggested that approximately 30% of patients hospitalized with acute decompensated heart failure have concomitant renal insufficiency (based on a report of the first 100,000 patients). A rise in serum creatinine of more than 0.3 mg/dL is associated with a 2.3 day increase in hospitalization length and 67% increased risk of death within 6 months of discharge. The drastic increase in mortality associated with concomitant renal dysfunction is not fully understood but is likely in part due to inflammatory risk factors that are associated with kidney disease and which accelerate cardiovascular risk.