Acute Renal Failure: Introduction
Acute renal failure (ARF) is characterized by a rapid decline in glomerular filtration rate (GFR) over hours to days. Depending on the exact definition used, ARF complicates approximately 5–7% of hospital admissions and up to 30% of admissions to intensive care units. Retention of nitrogenous waste products, oliguria (urine output <400 mL/d contributing to extracellular fluid overload), and electrolyte and acid-base abnormalities are frequent clinical features. ARF is usually asymptomatic and diagnosed when biochemical monitoring of hospitalized patients reveals a new increase in blood urea and serum creatinine concentrations. For purposes of diagnosis and management, causes of ARF are generally divided into three major categories: (1) diseases that cause renal hypoperfusion, resulting in decreased function without frank parenchymal damage (prerenal ARF, or azotemia) (~55%); (2) diseases that directly involve the renal parenchyma (intrinsic ARF) (~40%); and (3) diseases associated with urinary tract obstruction (postrenal ARF) (~5%). ARF is often considered to be reversible, although a return to baseline serum creatinine concentrations postinjury might not be sufficiently sensitive to detect clinically significant irreversible damage that may ultimately contribute to chronic kidney disease. ARF is associated with significant in-hospital morbidity and mortality, the latter in the range of 30–60%, depending on the clinical setting and presence or absence of nonrenal organ system failure.
Etiology and Pathophysiology
Prerenal ARF (Prerenal Azotemia)
The most common form of ARF is prerenal ARF, which occurs in the setting of renal hypoperfusion. Prerenal ARF is generally reversible when renal perfusion pressure is restored. By definition, renal parenchymal tissue is not damaged. More severe or prolonged hypoperfusion may lead to ischemic injury, often termed acute tubular necrosis, or ATN. Thus, prerenal ARF and ischemic ATN fall along a spectrum of manifestations of renal hypoperfusion. As shown in Table 273-1, prerenal ARF can complicate any disease that induces hypovolemia, low cardiac output, systemic vasodilatation, or selective intrarenal vasoconstriction.
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