Acute renal failure in
patients with congestive
heart failure occurs because
of decreased renal blood
flow. This decrease is due
to hypovolemia from
overdiuresis or hypervolemia
that causes elevated filling
pressures of the left
ventricle and leads to
decreased cardiac output.
Patients in the former group
may respond to the
discontinuation of diuretics
and gentle hydration.
Patients in the latter group
are treated with diuretics
and may need inotropes and
vasodilators. Invasive
hemodynamic monitoring may
be required for fluid
management.
The primary agents that cause prerenal acute renal failure are angiotensin-converting enzyme (ACE) inhibitors and nonsteroidal anti-inflammatory drugs (NSAIDs). The inhibition of ACE prevents the conversion of angiotensin I to angiotensin II, leading to decreased levels of angiotensin II. Angiotensin II increases the glomerular filtration rate by causing constriction of the efferent arteriole; its absence decreases the glomerular filtration rate because of dilatation of the efferent arteriole. In certain patients (e.g., those with hypovolemia or bilateral renal artery stenosis), the glomerular filtration rate is particularly dependent on the effects of angiotensin II. If these patients take an ACE inhibitor, their glomerular filtration rate decreases, and prerenal acute renal failure can develop. Potassium, BUN and creatinine levels should be obtained soon after patients start taking an ACE inhibitor. NSAIDs cause prerenal acute renal failure by blocking prostaglandin production, which also alters local glomerular arteriolar perfusion. Diminished renal blood flow causes ischemia in the renal parenchyma. If the ischemia is prolonged, acute tubular necrosis may develop. Early restoration of renal blood flow should shorten the ischemic time and prevent parenchymal injury. A response to the restoration of renal blood flow should occur in 24 to 48 hours. The keys to therapy are treating the underlying disorder, maintaining euvolemia and eliminating offending agents.
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