BACKGROUND Atherosclerotic renal-artery stenosis is a common problem in the elderly. Despite two randomized trials that did not show a benefit of renal-artery stenting with respect to kidney function, the usefulness of stenting for the prevention of major adverse renal and cardiovascular events is uncertain. METHODS We randomly assigned 947 participants who had atherosclerotic renal-artery stenosis and either systolic hypertension while taking two or more antihypertensive drugs or chronic kidney disease to medical therapy plus renal-artery stenting or medical therapy alone. Participants were followed for the occurrence of adverse cardiovascular and renal events (a composite end point of death from cardiovascular or renal causes, myocar-dial infarction, stroke, hospitalization for congestive heart failure, progressive renal insufficiency, or the need for renal-replacement therapy). RESULTS Over a median follow-up period of 43 months (interquartile range, 31 to 55), the rate of the primary composite end point did not differ significantly between participants who underwent stenting in addition to receiving medical therapy and those who received medical therapy alone (35.1% and 35.8%, respectively; hazard ratio with stenting, 0.94; 95% confidence interval [CI], 0.76 to 1.17; P = 0.58). There were also no significant differences between the treatment groups in the rates of the individual components of the primary end point or in all-cause mortality. During follow-up, there was a consistent modest difference in systolic blood pressure favoring the stent group (−2.3 mm Hg; 95% CI, −4.4 to −0.2; P = 0.03). CONCLUSIONS Renal-artery stenting did not confer a significant benefit with respect to the prevention of clinical events when added to comprehensive, multifactorial medical therapy in people with atherosclerotic renal-artery stenosis and hypertension or chronic kidney disease. (Funded by the National Heart, Lung and Blood Institute and others; ClinicalTrials.gov number, NCT00081731.)

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A prospective analysis of the value of urinary diagnostic indices in ascertaining the cause of acute renal failure was undertaken. Our results show that in the setting of acute oliguria a diagnosis of potentially reversible prerenal azotemia is likely with urine osmolality greater than 500 mosm/kg H2O, urine sodium concentration less than 20 meq/litre, urine/plasma urea nitrogen ratio greater than 8, and urine/plasma creatinine ratio greater than 40. Conversely, a urine osmolality less than 350 mosm/kg, urine sodium concentration greater than 40 meq/liter, urine/plasma urea nitrogen ratio less than 3, and urine/plasma creatinine ratio less than 20 suggest acute tubular necrosis. A significant number of oliguric patients will not have urinary indices that fall within these guidelines. In this setting, urine sodium concentration divided by the urine-to-plasma creatinine ratio (the renal failure index) and the fractional excretion of filtered sodium provide a reliable means of differentiating reversible prerenal azotemia from acute tubular necrosis.

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A symptomatic reduction in BP during or immediately after dialysis occurs in approximately 20 to 30% of dialysis sessions. The treatment includes stopping or slowing the rate of ultrafiltration, placing the patient in the Trendelenburg position, decreasing the blood flow rate, and restoring intravascular volume. Such episodes predispose the patient to leave the dialysis unit volume overloaded and if repetitive can lead to inadequate clearance. Intradialytic hypotension and orthostatic hypotension after the procedure are significant and independent risk factors affecting mortality in dialysis patients. 1 This clinical commentary focuses on recent advances in the prevention and management of intradialytic hypotension.Dialysis hypotension is the result of an inadequate cardiovascular response to the reduction in blood volume that occurs when a large volume of water is removed during a short period of time. In a typical dialysis procedure, an ultrafiltrate volume that is equal to or greater that the entire plasma volume is often removed.Despite the large ultrafiltrate volume, plasma volume typically decreases by only approximately 10 to 20%. This ability to maintain plasma volume during ultrafiltration requires mobilization of fluid from the interstitial into the intravascular space. Vascular refilling is influenced by both patient-specific and treatment-related factors that dictate the distribution of water between the body fluid compartments.The amount of interstitial fluid available for vascular refilling is influenced by the dry weight set for the patient. When the volume of interstitial fluid is small, any ultrafiltrate volume will more likely be associated with hemodynamic instability. This explains the development of hypotension when patients undergo dialysis below their true dry weight. By contrast, increased amounts of interstitial fluid will expand the volume of fluid accessible for refilling of the intravascular space and, therefore, decrease the likelihood of hypotension. In most patients, a dry weight that minimizes the amount of interstitial fluid present is selected because chronic volume overload has long-term deleterious effects on the cardiovascular system.The determination of dry weight is largely assessed empirically by trial and error. The dry weight is set at the weight below which unacceptable symptoms, such as cramping, nausea, and vomiting, or hypotension occur. The dry weight is highly variable in many patients and can fluctuate with intercurrent illnesses (e.g., diarrhea, infection) and with changes in hematocrit (as with erythropoietin). A number of methods have been proposed to define more objectively the dry weight of the patient (Table 1). Comparative studies have generally favored methods based on bioimpedance measurements, which provide an assessment of extracellular and intracellular volume and total body water. 2-4 A variant of this technique in which continuous intradialytic measurements are confined to the calf shows particular promise because the relative volume of excess extrac...

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To delineate the clinical spectrum of nonliguric renal failure, we studied prospectively 90 patients with acute renal failure 54 of whom were nonoliguric throughout their periods of azotemia. Although the causes of nonoliguric renal failure varied, nephrotoxic failure occurred more frequently in nonoliguric than in oliguric subjects (P is less than 0.01). As com pared to oliguric patients, those without oliguria had significantly lower urinary sodium concentrations (P is less than 0.05) and fractional excretions of sodium (P is less than 0.02), had shorter hospital stay (P is less than 0.01), had fewer septic episodes, neurologic abnormalities, gastrointestinal bleeding and acidemia, required dialysis less frequently (P is less than 0.001) and had lower mortality rate (26 per cent in nonoliguric vs. 50 per cent in oliguric patients -- P is less than 0.05). Nonoliguric renal failure occurs more often than is generally recognized and causes less morbidity and mortality than oliguric acute renal failure.

Angiotensinogen, angiotensin-converting enzyme, and renin constitute the components of the renin-angiotensin system. The mammalian renal proximal tubule contains angiotensinogen, angiotensin-converting enzyme, and angiotensin receptors. Previous immunohistochemical studies describing the presence of renin in the proximal tubule could not distinguish synthesized renin from renin trapped from the glomerular filtrate. In the present study, we examined the presence of renin activity and mRNA in rabbit proximal tubule cells in primary culture and renin mRNA in microdissected proximal tubules. Renin activity was present in lysates of proximal tubule cells in primary culture. Cellular renin content in cultured proximal tubule cells was increased by incubation with 0-5 M isoproterenol and 10'-M forskolin by 150 and 110%, respectively. In addition, renin transcripts were detected in poly(A)+ RNA from cultured proximal tubule cells by RNA blots under high stringency conditions. In microdissected tubules from normal rats, renin mRNA was not detectable with reverse transcription and polymerase chain reaction. However, in tubules from rats administered the angiotensinogen-converting-enzyme inhibitor, enalapril, renin was easily detected in the S2 segment of the proximal tubule. We postulate the existence of a local reninangiotensin system that enables the proximal tubule to generate angiotensin II, thereby providing an autocrine system that could locally modulate NaHCO3. and NaCl absorption. (J.