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Acute renal failure (ARF) or acute kidney injury (AKI), defined as a measurable increase in the serum creatinine (Cr) concentration (usually relative increase of 50% or absolute increase by 44–88 μmol/L [0.5–1.0 mg/dL]), occurs in ~5–7% of hospitalized pts. It is associated with a substantial increase in in-hospital mortality and morbidity. AKI can be anticipated in some clinical circumstances (e.g., after radiocontrast exposure or major surgery), and there are no specific pharmacologic therapies proven helpful at preventing or reversing the condition. Maintaining optimal renal perfusion and intravascular volume appears to be important in most clinical circumstances; important cofactors in AKI include hypovolemia and drugs that interfere with renal perfusion and/or glomerular filtration (nonsteroidal anti-inflammatory drugs [NSAIDs], angiotensin-converting enzyme [ACE] inhibitors, and angiotensin receptor blockers).


The separation into three broad categories (prerenal, intrinsic renal, and postrenal failure) is of considerable clinical utility (Table 138-1). Prerenal failure is most common among hospitalized pts. It may result from true volume depletion (e.g., diarrhea, vomiting, GI or other hemorrhage) or “arterial underfilling,” i.e., reduced renal perfusion in the setting of adequate or excess blood volume. Reduced renal perfusion may be seen in congestive heart failure (CHF) (due to reduced cardiac output and/or potent vasodilator therapy), hepatic cirrhosis (due mostly to peripheral vasodilation and arteriovenous shunting), nephrotic syndrome and other states of severe hypoproteinemia (total serum protein <54 g/L [<5.4 g/dL]), and renovascular disease (because of fixed stenosis at the level of the main renal artery or large branch vessels). Several drugs can reduce renal perfusion, most notably NSAIDs. ACE inhibitors and angiotensin II receptor antagonists may reduce glomerular filtration rate but do not tend to reduce renal perfusion.


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