ARF is common in ambulatory HIV patients. Immunosuppression, infection, and HCV are important conditions associated with ARF in the post-HAART era.

Contrast-induced nephropathy (CIN), an impairment of renal function following intravascular injection of contrast media, is commonly defined as an increase in the baseline serum creatinine concentration of >25% or 0.5 mg/dl (44 micromol/l). The incidence of CIN does not appear to have changed appreciably in the last three decades, and it continues to be the third leading cause of hospital-acquired acute renal failure (ARF). In the general population, the incidence of CIN is estimated to be 1-2%. However, the risk for developing CIN may be as high as 50% in some high-risk patient subgroups, such as those with diabetes mellitus and pre-existing renal impairment. Patients who develop CIN after percutaneous coronary intervention sustain an increase in both short- and long-term mortality whether or not chronic kidney disease was present prior to contrast exposure. The diminished long-term survival in patients with CIN has been observed for both, those whose ARF is not severe enough to require dialysis as well as those requiring dialysis. Treatment is limited to supportive measures while awaiting the resolution of the renal impairment. At times, this does not occur. Because of the lack of treatment options and because CIN is associated with serious short- and long-term sequelae, emphasis needs to be directed at preventative measures, identification of high-risk patients and education of all physicians involved in the care of these patients in order to reduce the incidence of CIN.

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In this study, we characterized the sequence of several intrarenal events and evaluated their relative importance in the pathogenesis of unilateral oliguric acute renal failure induced experimentally in rats by complete occlusion of a renal artery for 1 hour. Kidneys were studied prior to occlusion and 1-3 hours and 22-26 hours after release of the temporary occlusion. Renal blood flow measured by an electromagnetic flow transducer was reduced to 40-50% of control during both postocclusion periods. Flow of tubular fluid was markedly reduced, and the damaged kidneys were oliguric. Proximal and distal convolutions were filled with fluid and dilated 1-3 hours after occlusion; their pressures were greatly heterogeneous and were elevated, on the average, to 31 and 16 mm Hg, respectively. Glomerular capillary pressure at this time was normal or slightly increased. Histological sections showed extensive tubular obstruction. We conclude that initially the oliguria is primarily due to intraluminal obstruction in the absence of predominant increases in preglomerular vascular resistance. Observations at 22-26 hours after occlusion indicated acute tubular necrosis. Moreover, the combined involvement of preglomerular vasoconstriction, persisting tubular obstruction, and passive backflow of tubular fluid appeared to be important in the maintenance of the oliguria. Glomerular capillary, proximal intratubular, and peritubular capillary hydrostatic pressures were reduced below control values. After acute volume expansion, the reduced pressures and renal blood flow were reversed, yet the experimental kidneys remained oliguric. Thus, it is clear that tubular obstruction is a significant factor responsible for both the genesis and the maintenance of oliguria in this experimental model of ischemia-induced acute renal failure.• A controversy concerning the nature and sequence of events involved in the development and maintenance of oliguria in acute renal failure persists despite the application of a number of investigative techniques in a variety of experimental models. Studies of acute renal failure have been performed in an attempt to determine the relative importance of the following etiologic factors: (1) primary failure to filter fluid across glomerular membranes which might result from arteriolar vasomotor changes lowering glomerular capillary pressure or plasma flow or from reductions in the glomerular ultrafiltration coefficient, (2) This investigation was supported in part by a grant-in-aid from the American Heart Association, by U. S. Public Health Service Grant HE-02334 from the National Heart and Lung Institute, by NIH Training Grant 5 T01 AM05054, and by Grant 1973-74-A-36 from the North Carolina Heart Association.Dr. Gottschalk is a Career Investigator of the American Heart Association.A preliminary report of this work was presented to the 6th Annual Meeting of the American Society of Nephrology, Washington, D. C, November, 1973. Received April 21, 1975. Accepted for publication July 17. 1975. 558epithelium. ...

Abstract. N-acetylcysteine has been recommended for patients with renal insufficiency who are to receive radiocontrast media. However, trials of oral N-acetylcysteine for the prevention of radiocontrast-induced nephropathy have yielded inconsistent results. A systematic review of patient and study characteristics was undertaken to discover possible explanations of the inconsistencies. The databases MEDLINE, EMBASE, and CENTRAL (1966 to March 2003) were searched in all languages, and conference proceedings from several professional societies from the years 1999 to 2003 were also searched. Only prospective controlled trials of oral N-acetylcysteine were included. Risk difference estimates and 95% confidence intervals were calculated. The estimates were examined for evidence of publication bias and heterogeneity. Stratified and meta-regression analyses were used to compare estimates by study and patient characteristics. Identified were 16 studies, 15 published and 1 unpublished. There was no evidence of publication bias, but there was substantial evidence of heterogeneity, thus precluding reliance on a meaningful summary effect estimate. Meta-regression identified several patient and study characteristics, with some evidence of association with study-specific estimates. None of these characteristics, however, formed subsets of studies with results that were homogeneous enough to aggregate. Research on N-acetylcysteine and the incidence of radiocontrast nephropathy is too inconsistent at present to warrant a conclusion on efficacy or a recommendation for its routine use. Identified patient and study characteristics may be responsible for some, but not all, of this inconsistency. A large, randomized, placebo-controlled trial, a pooled analysis of patient-level data, or both may resolve this issue.Over the last 3 yr, enthusiasm for the use of oral N-acetylcysteine to prevent radiocontrast-induced nephropathy has been growing (1). A breakthrough study (2) first reported a large and significant reduction in the risk of radiocontrast-induced nephropathy compared with placebo among patients with moderate renal dysfunction. Subsequent studies produced mixed results (3-6). Recently, a large study (7), arguably with a relatively high degree of power and sound methods, seemed to confirm the beneficial effect of this agent. N-acetylcysteine is now being routinely recommended as preventative therapy, as an additive to low-osmolar contrast media and intravenous hydration, for patients with reduced renal function who are to undergo a planned exposure to radiocontrast media (8,9). Yet the reasons for discrepant findings among the trials need investigation before the widespread use of N-acetylcysteine can be recommended.We therefore performed a systematic review and metaanalysis of available prospective controlled trials to quantify and compare reported associations of oral N-acetylcysteine with the incidence of nephropathy after exposure to radiocontrast media. For this review, we examined several key questions. Is there evidenc...

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Phosphate binders include calcium acetate or carbonate, sevelamer hydrochloride or carbonate, magnesium and lanthanum carbonate, and aluminum carbonate or hydroxide. Their relative phosphate-binding capacity has been assessed in human, in vivo studies that have measured phosphate recovery from stool and/or changes in urinary phosphate excretion or that have compared pairs of different binders where dose of binder in each group was titrated to a target level of serum phosphate. The relative phosphate-binding coefficient (RPBC) based on weight of each binder can be estimated relative to calcium carbonate, the latter being set to 1.0. A systematic review of these studies gave the following estimated RPBC: for elemental lanthanum, 2.0, for sevelamer hydrochloride or carbonate 0.75, for calcium acetate 1.0, for anhydrous magnesium carbonate 1.7, and for "heavy" or hydrated, magnesium carbonate 1.3. Estimated RPBC for aluminum-containing binders were 1.5 for aluminum hydroxide and 1.9 for aluminum carbonate. The phosphate-binding equivalent dose was then defined as the dose of each binder in g × its RPBC, which would be the binding ability of an equivalent weight of calcium carbonate. The phosphate-binding equivalent dose may be useful in comparing changes in phosphate binder prescription over time when multiple binders are being prescribed, when estimating an initial binder prescription, and also in phosphate kinetic modeling.

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