A cute 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 ...

Severe hyperkalemia is a medical emergency that can cause lethal arrhythmias. Successful management requires monitoring of the electrocardiogram and serum potassium concentrations, the prompt institution of therapies that work both synergistically and sequentially, and timely repeat dosing as necessary. It is of concern then that, based on questions about effectiveness and safety, many physicians no longer use 3 key modalities in the treatment of severe hyperkalemia: sodium bicarbonate, sodium polystyrene sulfonate (Kayexalate [Concordia Pharmaceuticals Inc., Oakville, ON, Canada], SPS [CMP Pharma, Farmville, NC]), and hemodialysis with low potassium dialysate. After reviewing older reports and newer information, I believe that these exclusions are ill advised. In this article, I briefly discuss the treatment of severe hyperkalemia and detail why these modalities are safe and effective and merit inclusion in the treatment of severe hyperkalemia.

The incidence of renal failure due to vascular diseases is increasing. Two reasons for this are the epidemic of atherosclerotic vascular disease in the aging population and the widespread use of vasoactive drugs that can adversely affect renal function. These vascular causes of renal failure include vasomotor disorders such as that associated with nonsteroidal antiinflammatory drugs, small-vessel diseases such as cholesterol crystal embolization, and large-vessel diseases such as renal artery stenosis. These causes of azotemia are less familiar to physicians than more classic causes, such as acute tubular necrosis, and are less likely to be recognized in their early stages. This article describes the various vascular diseases that impair renal function and outlines the steps necessary to identify them. Although some of these conditions, such as renal artery stenosis, can gradually impair function, the vascular causes of acute renal failure are emphasized in this article. Because the vasculitides primarily cause renal failure through secondary glomerulonephritis, they are mentioned only briefly. Extensive testing is rarely necessary because the cause is usually suspected through syndrome recognition. The diagnosis can then be confirmed by the results of one or two additional tests or by improved renal function after treatment.