Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0268494 (ATN)
 694 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Fifty-three children, ages one day to 15 years, were treated with hemodialysis for acute renal failure between 1968 and 1977. Twenty-three had acute tubular necrosis. Nine had ATN associated with catastrophic medical illnesses; all died. Fourteen had ATN following major surgical procedures; ten died. Thirty had ARF due to primary nephrologic disorders; 27 survived. Thus it was not the ARF per se but the underlying and concomitant disorders which had the major influences on survival. As prognostic indications of survival in patients with postoperative ATN cannot be clearly defined, these patients almost always deserve aggressive management, including dialysis therapy. Patients with ATN associated with severe medical illness often have fatal underlying conditions which cannot be influenced by presently available technologies.
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PMID:Acute renal failure in infants and children: outcome of 53 patients requiring hemodialysis treatment. 71 76

This study was intended to elucidate the mechanism(s) of protection afforded by splenectomy against EPI-induced ATN and myocardial necrosis. Renal function parameters, hematocrit, circulating catecholamines (EPI and NE), serum enzymes (CPK and SGOT), and urinary PGE2 were measured before and during intravenous infusion of EPI (4 micrograms/kg/min for 6 hr) in intact and chronically splenectomized animals. All but serum enzymes were measured in another group of splenectomized animals that were implanted with small fragments of the autologous spleen (autoimplanted animals) 2 weeks prior to EPI infusion. Renal function tests and urinary PGE2 levels were monitored for several hours during the recovery period. The development of ARF in intact animals was accompanied by marked increases in circulating catecholamine levels, hematocrit, and serum enzymes and by a marked decrease in urinary PGE2 levels. These animals had diffuse ATN and hemorrhagic lesions of the heart (myocardial necrosis), and none survived. Chronically splenectomized animals were protected against the adverse effects of EPI infusion. The protected animals showed minimal elevation of circulating catecholamine levels and no changes in urinary PGE2 levels or hematocrit. Serum enzymes and renal and cardiac histopathology remained essentially normal in these animals. Implantation of autologous splenic tissue in splenectomized animals caused reversal of the protective effect of splenectomy. The response of autoimplanted animals to EPI infusion was in all respects similar to that in intact animals with the exception of hematocrit, which did not rise. All autoimplanted animals survived. They showed prompt recovery of renal function associated with significant increase of urinary PGE2 levels during the recovery period. Focal ATN was observed but no hemorrhagic lesion of the heart was found. From these observations we conclude the following: (1) high circulating NE and/or low renal (urinary) PGE2 activity are important in the pathogenesis of EPI-induced ARF, (2) the spleen may release some factor(s) that modulate plasma NE level and/or renal PGE2 activity during EPI infusion, (3) EPI-induced ARF may occur independently of myocardial necrosis, and (4) hematocrit has no major role in EPI-induced ARF.
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PMID:Mechanisms of splenectomy protection in epinephrine-induced renal and cardiac necrosis. 657 17

Previous experimental and human data suggests a detrimental effect on the course of acute renal failure related to exposure of blood to artificial dialysis membranes of poor biocompatibility. We performed a 2.5-year prospective randomized trial to compare the clinical course of acute renal failure (post-operative ischemic acute tubular necrosis, ATN) in patients receiving a cadaveric renal transplant requiring supportive hemodialysis in the immediate post-transplant setting. Patients were randomized to either a cuprophane or polymethylmethacrylate (PMMA) conventional hollow fiber dialyzer. All patients received a standard immunosuppressive regimen which included induction therapy with either horse anti-thymocyte gamma globulin (ATGAM) or the murine anti-CD3 monoclonal antibody (OKT3). Of 53 patients randomized, 17 were excluded (2 for intervening biopsy-proven rejection prior to recovery from ATN, 10 for primary graft nonfunction and 5 for other reasons), leaving 36 evaluable cases of uncomplicated ATN, 18 in each group. There was no difference by age, race, gender, cause of ESRD, immunosuppressive regimen, cold or warm ischemia time, use of pre-transplant dialysis, percent oliguria or the incidence of intra-dialytic hypotension between the 2 groups. There was no difference in the mean time to recovery from ATN posttransplant (8.9 days in the cuprophane group vs 9.5 days in the PMMA group, p = NS) or in the average number of hemodialysis treatments required (3.6 in both groups, p = NS). There was also no difference in long term allograft outcome in terms of the nadir serum creatinine, the number of episodes of subsequent acute rejection or in the development of chronic rejection. An intent-to-treat analysis of all 53 originally randomized patients similarly yielded no significant differences. A subsequent, non-randomized study using a membrane of intermediate biocompatibility (Hemophan) also showed no difference in recovery time from ATN. Bioincompatible membranes do not seem to have a significant clinical impact on the course of recovery of this form of acute renal failure. The striking benefits of biocompatibility in the course of ARF seen in other human trials may relate more to the non-renal systemic toxic effects of bioincompatibility.
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PMID:Biocompatible dialysis membranes and acute renal failure: a study in post-operative acute tubular necrosis in cadaveric renal transplant recipients. 898 57

In this study we have analyzed incidence, causes and clinical course of ARF due to primary intrarenal disease other than acute tubular necrosis. Thousand hundred and twenty two cases of ARF of diverse etiology were studied over a period of 16 years; July 1984 to Dec, 1999. Surgical ARF 231 (20.6%) were not included in the present study. Intrinsic renal diseases were responsible for ARF in 891 (79.4%) of cases. The most common intrinsic renal diseases 705 (79.4%) causing ARF were ischemic/toxic acute tubular necrosis, but not included in this study. Acute renal failure was related to acute glomerulonephritis (9.3%), acute interstitial nephritis (7%), and renal cortical necrosis in (4.6%) of cases. Therefore intrinsic renal diseases other than ATN were the causative factor for acute renal failure in 186 (20.8%) patients in our study. Crescentic (51.8%) and endocapillary proliferative glomerulonephritis (34.9%), were the main glomerular diseases responsible for ARF and 75.9% of GN was related to infectious etiology. Fifty three percent of acute interstitial nephritis was drug induced and in 25 (40%) patients it was related to an infectious etiology. Renal cortical necrosis due to HUS was observed in 16 (39%) children and majority (76.47%) of the cases had a diarrhoeal prodrome. Obstetrical complications were the main causes (61%) of cortical necrosis in adults with acute renal failure. Thus, intrinsic renal diseases other than ATN were responsible for ARF in 186 (20.8%) cases. Post-infectious glomerulonephritis, acute interstitial nephritis and renal cortical necrosis (complicating HUS in children and obstetrical complications in adult) are the main causes of acute renal failure in our study. Both acute GN and interstitial nephritis had excellent prognosis, however renal cortical necrosis was associated with a very high mortality.
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PMID:Acute renal failure due to intrinsic renal diseases: review of 1122 cases. 1273 29