Skip to Main Content


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. It is important to recognize that AKI is a clinical diagnosis and not a structural one. A pt may have AKI with or without injury to the kidney parenchyma. AKI can range in severity from asymptomatic and transient changes in laboratory parameters of glomerular filtration rate (GFR), to overwhelming and rapidly fatal derangements in effective circulating volume regulation and electrolyte and acid-base composition of the plasma. Maintaining optimal renal perfusion and intravascular volume is critical 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 141-1). 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 GFR but do not tend to reduce renal perfusion.

TABLE 141-1Common Causes of Acute Kidney Injury

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.