CONGESTIVE HEART
FAILURE
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).
PATHOPHYSIOLOGY
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.
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.
PRESENTATION AND DIAGNOSIS
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.
TREATMENT
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.
