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There is a strong association between congestive heart failure (CHF) and kidney disease, and either one can precipitate the other. The term “cardiorenal syndrome” is often used as an umbrella term to describe the interdependency of the two organs in the disease state.

This section will focus on the prerenal state that may occur in the setting of CHF. For a discussion of the cardiovascular sequelae of chronic kidney disease, refer to the overview of the latter (see Plate 4-66).


Heart failure is defined as the inability of the heart to provide sufficient output to meet perfusion and oxygenation requirements while maintaining normal filling pressures. Insufficient forward flow in the setting of heart failure is sensed by central vascular receptors, and it stimulates the release of norepinephrine, angiotensin II, endothelin, and other cytokines that cause vasoconstriction. These hormones favor perfusion of tissues with high oxygen extraction (brain, heart, skeletal muscle) over tissues with low oxygen extraction (skin, kidneys, splanchnic organs).
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.

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.


Patients with CHF typically complain of dyspnea with exertion, orthopnea, and paroxysmal nocturnal dyspnea. Physical examination may reveal stigmata of advanced CHF, including low blood pressure, crackles on lung examination, elevated jugular venous pressure, ascites, and edema.
If an elevation in serum creatinine concentration is noted, prerenal state must be distinguished from causes of intrinsic AKI, such as acute tubular necrosis. In addition to a detailed history, several laboratory findings can help facilitate the distinction. For a detailed discussion, see Plates 4-1 and 4-2.

Diuretics, as well as salt and water restriction, are the main treatment for controlling symptoms of volume overload in patients with CHF and prerenal state. In advanced stages of disease, however, they are often unsuccessful in reversing volume overload. Loop diuretics (e.g., furosemide) are highly protein-bound and thus enter the tubular lumen primarily by secretion in the proximal tubule, rather than filtration across the glomerulus. In the setting of decreased renal perfusion, patients may develop diuretic resistance because of decreased diuretic secretion. In such cases, thiazide diuretics (oral metolazone or intravenous chlorothiazide) may need to be added for synergy.
In addition, randomized trials have shown that ACE inhibitor therapy leads to symptomatic improvement, reduced hospitalization, and enhanced survival in patients with systolic heart failure. ACE inhibitors are also widely used in patients with chronic kidney disease because of their cardioprotective and renal protective benefits; however, they must be used with caution in heart failure patients with significant renal insufficiency because of the risk for hyperkalemia and the possibility of worsening GFR.
Renal replacement therapy, in the form of isolated or continuous ultrafiltration for fluid removal, with or without a component of solute clearance (i.e., hemofiltration or hemodialysis), has been increasingly used as a therapeutic tool when diuretics have failed to control symptoms of volume overload.
Heart transplantation is the only potential “cure” for a patient with advanced CHF and kidney dysfunction that is thought to be reversible. Differentiating between prerenal state versus renal parenchymal damage is important when considering heart transplantation alone versus combined heart-kidney transplantation.
Unfortunately, based on a recent series of heart transplant candidates, simple laboratory tests at the time of heart transplant evaluation, such as measurement of urine protein excretion and estimated glomerular filtration rate, do not correlate with the degree of fibrosis on renal biopsy. Therefore, in patients with advanced CHF who require transplantation, a renal biopsy may be a crucial step in the preoperative assessment.