Normotensive Ischemic Acute Renal Failure

Acute renal failure is defined as a rapid decrease in the glomerular filtration rate, occurring over a period of minutes to days. Because the rate of production of metabolic waste exceeds the rate of renal excretion in this circumstance, serum concentrations of markers of renal function, such as urea and creatinine, rise. The causes of acute renal failure are classically divided into three categories: prerenal, postrenal (or obstructive), and intrinsic. Prerenal azotemia is considered a functional response to renal hypoperfusion, in which renal structure and microstructure are preserved. Postrenal azotemia — obstruction of the urinary tract — is initially accompanied by few microscopical changes (early hydronephrosis, with enlargement of the pelvic cavity and minimal distention or blunting of the renal papilla) or none. In contrast, intrinsic renal azotemia is due to parenchymal injury of the blood vessels, glomeruli, tubules, or interstitium. In prerenal and postrenal azotemia, complete recovery may be seen 1 to 2 days after relief of the offending lesion, provided that normal perfusion or urinary outflow is reestablished before structural changes occur. A research focus group organized by the American Society of Nephrology recent­ ly recommended that the term “acute kidney injury” replace the term “acute renal failure.” 1 However, the group left the actual definition of acute kidney injury to be determined in the future. Thus, whether acute kidney injury refers only to acute tubular necrosis or includes prerenal and postrenal azotemia and parenchymal dis­ eases such as acute glomerulonephritis remains unclear. Most clinicians still use the term acute renal failure as defined above. The two forms of ischemic acute renal failure, prerenal azotemia and acute tubular necrosis, account for more than half the cases of renal failure seen in hospitalized patients and are familiar to most clinicians. 2-4 Yet in many patients with acute renal failure, the contribution of ischemia is initially unrecognized. Patients with ischemic acute renal failure typically have low systemic perfusion, sometimes caused by volume depletion, although their blood pressure may not fall dramatically but instead may remain within the normal range (in an adult, systolic blood pressure >90 to 100 mm Hg). In such cases, in the absence of frank hypo­ tension, the clinician may speculate that an unobserved drop in blood pressure must have caused the renal failure. Although this scenario cannot be ruled out, other causative mechanisms can usually be identified. This type of ischemic acute renal failure (termed normotensive, because the patient’s blood pressure is — at least temporarily — within the normal range) can occur as a result of several processes, most of which involve increased renal susceptibility to modest reductions in perfu­ sion pressure. Fortunately, the factors that lead to ischemic renal failure in patients with apparently normal blood pressure are discernible in most instances. Recogni­ tion of these factors allows the physician to make an early diagnosis and facilitates the interventions that can help to reestablish normal renal hemodynamics. The importance of addressing even mild renal failure is illustrated by a recent study showing that hospitalized patients with a modest increase in the serum