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  • Prerenal azotemia and acute tubular necrosis account for the overwhelming majority of hospital-acquired acute renal failure cases, whereas acute glomerulonephritis and vasculitides are more common causes of acute renal failure developing outside the hospital.
  • Acute renal failure occurs in at least 10% to 30% of patients admitted to an ICU and is associated with a mortality rate of about 50% despite advances in supportive care and technology.
  • The most important diagnostic classification to be made in the evaluation of patients with acute renal failure is based on the site of the renal lesion (pre-, intra-, or postrenal).
  • Since there are few specific therapies available in patients with established acute tubular necrosis, the major clinical focus is on prevention of ARF by identification of subjects at highest risk.
  • All aspects of treatment of acute tubular necrosis, including renal replacement therapy, are basically supportive. The nondialytic measures of greatest importance are maintenance of nutritional, volume, and electrolyte homeostasis.
  • Emergent renal replacement therapy is indicated in the management of acute renal failure when pulmonary edema, hyperkalemia, refractory acidosis, or symptomatic uremia develops.
  • Prophylactic renal replacement therapy should be considered in patients with sustained anuria, persistent oliguria with progressive azotemia and glomerular filtration rate <10 mL/ min, and to prevent uncontrolled positive fluid balance.

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Acute renal failure (ARF) is defined as rapid decline (over hours to days) in glomerular filtration rate (GFR). This manifests as a rapid increase in blood urea nitrogen (BUN; azotemia) and serum creatinine, and may or may not be accompanied by a decline in urine output; specific definitions (e.g., absolute or fractional increase of serum creatinine) vary widely between studies.1 ARF occurs in 2% to 5% of general medical-surgical admissions, but up to 10% to 30% of ICU admissions. Acute renal failure can be classified into three broad etiologic/anatomic categories: prerenal ARF, intrarenal ARF, and postrenal ARF. Prerenal ARF is caused by renal hypoperfusion with intact renal parenchyma (55% to 60% of instances of ARF). Intrarenal ARF is caused by parenchymal renal diseases (35% to 40% of instances of ARF). Postrenal ARF is caused by urinary tract obstruction (∼5% of instances of ARF).2

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Most ARF in the ICU is caused by prerenal azotemia, and the rest predominantly by renal parenchymal injury with acute tubular necrosis (ATN); the former may convert to the latter. Despite advances in critical care and dialysis technologies, the mortality of ARF requiring dialysis in critically ill patients remains 50% to 80%.3–5 Although there is evidence that isolated ARF itself increases mortality, it is clear that mortality of ICU ARF increases with every additional nonrenal organ failure present at the time of initiation of renal replacement therapy (RRT).3,5 Emerging data suggest that renal ischemia-reperfusion injury and the uremic milieu actually contribute to the development of distant organ injury (increased pulmonary vascular permeability and cardiac and splanchnic organ apoptosis).6–8 Outcome is particularly poor in septic ARF; in one study, mortality of septic ARF was 74%, compared to 45% in nonseptic cases.9...

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