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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 agent causeing ARF is ACE & NSAID drugs
 
CIDPUSA.org

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.

TABLE 3
Probable Causes of Acute Renal Failure Based on the Physical Findings

Physical examination
Probable causes of acute renal failure
Vital signs  
   Temperature Possible infection
   Blood pressure Hypertension: nephrotic syndrome or malignant hypertension
Hypotension: volume depletion or sepsis
   Weight loss or gain Hypovolemia or hypervolemia
Mouth Dehydration
Jugular veins and axillae (perspiration) Hypovolemia or hypervolemia
Pulmonary system Signs of congestive heart failure
Heart New murmur of endocarditis or signs of congestive heart failure
Abdomen Bladder distention suggesting urethral obstruction
Pelvis Pelvic mass
Rectum Prostate enlargement
Skin Rash of interstitial nephritis, purpura of microvascular disease, livedo reticularis suggestive of atheroembolic disease, or splinter hemorrhages or Osler's nodes of endocarditis

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