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Oliguria literally means “reduced” urine volume—less than that necessary to remove endogenous solute loads that are the end products of metabolism. If the patient concentrates urine in a normal fashion while consuming a regular Western diet, oliguria (for that person) is present at urine volumes <400 mL/day, or approximately 6 mL/kg body weight. If the kidney concentration is impaired and the patient can achieve a specific gravity of only 1.010, oliguria is present at urine volumes <1000–1500 mL/day.
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In an attempt to standardize the diagnosis of acute renal failure, the new terminology acute kidney injury (AKI) was coined. New staging systems have been devised to compare severity of the damage sustained across different study groups and for prognostication.
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AKI is a condition in which the glomerular filtration rate is abruptly reduced, causing a sudden retention of endogenous and exogenous metabolites (urea, potassium, phosphate, sulfate, creatinine, administered drugs) that are normally cleared by the kidneys. The urine volume is usually low (<400 mL/day). If renal concentrating mechanisms are impaired, the daily urine volume may be normal or even high (high-output or nonoliguric renal failure). In extreme cases, anuria occurs (urine output completely shuts down) in acute kidney injury.
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The causes of AKI are listed in Table 34–1. Prerenal causes are usually reversible if treated promptly, but a delay in therapy may allow it to progress to a fixed intrinsic renal failure (eg, acute tubular necrosis). The other causes of AKI are classified on the basis of their involvement with vascular lesions, intrarenal disorders, or postrenal disorders.
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The term prerenal denotes inadequate renal perfusion or lowered effective arterial circulation. The most common cause of this form of AKI is dehydration due to renal or extrarenal fluid losses from diarrhea, vomiting, excessive use of diuretics, and so on. Less common causes are septic shock, “third spacing” with extravascular fluid pooling (eg, pancreatitis), and excessive use of antihypertensive drugs. Heart failure with reduced cardiac output also can reduce effective renal blood flow. Careful clinical assessment may identify the primary condition responsible for the prerenal state, but many times several conditions can coexist. In the hospital setting, these circulatory abnormalities often are prolonged, leading to a more sustained injury (acute tubular necrosis).
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Acute reductions in glomerular filtration rate may also be noted in patients with cirrhosis (hepatorenal syndrome) or in patients taking cyclosporine, tacrolimus, nonsteroidal anti-inflammatory drugs, or angiotensin-converting enzyme inhibitors. It is felt that these conditions represent significant intrarenal hemodynamic ...