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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The courses of 276 acute tubular necrosis patients referred for dialysis were reviewed in search for prognostic indicators. Sixty-three percent survived. Of 28 possible predictor variables, a posttoxic cause and nonoliguria were favorable, whereas myocardial infarction and peritonitis affected survival unfavorably. Total pareneral nutrition influenced survival favorably only in those with multiple complications or peritonitis. No single variable or combination predicted a lethal outcome. Since survivors were frequently restored to complete health, we advocate an aggressive therapeutic approach even in the face of multiple complications.
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PMID:Prevailing patterns and predictor variables in patients with acute tubular necrosis. 64 66

The objective of this study was to evaluate the renal tolerance of a new magnetic resonance contrast agent, AMI 25. This agent has an affinity for the reticuloendothelial system and is used for the detection of focal liver lesions. A combination of renal ischemia and intra-arterial iodinated contrast agent infusion (diatrizoate) leads to a reproducible and reversible model of acute renal failure in the rat. Using this model, AMI 25 was perfused directly into the aorta at the dose of 1 ml/kg--ten times the dose used in humans. AMI 25 induced no change in serum creatinine (45 +/- 7, 40 +/- 6, 40 +/- 9 mumol/L before infusion and at 24 and 48 hours, respectively), in creatinine clearance (2.1 +/- 0.6, 2.1 +/- 0.6, 2.1 +/- 0.6 mL/mn), or in urinary N-acetyl glucosaminidase (NAG) excretion (72 +/- 16, 98 +/- 12, 58 +/- 9.8 mumol hour-1/mmol creatinine). Blinded histologic analysis of 11 kidneys perfused with AMI 25 revealed no abnormalities, whereas diatrizoate induced acute tubular necrosis in four of the seven kidneys examined. In our animal model, AMI 25 has no nephrotoxicity, even at ten times the expected clinical dose for humans.
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PMID:Renal tolerance of AMI 25. 196 29

Ex vivo renal artery surgery has been reported by several investigators and has extended the role of revascularization in the treatment of lesions previously managed by nephrectomy alone. Several techniques are available for use, and selection of the most appropriate method can be tailored to the specific anatomy being managed. Our total experience included 27 kidneys that have been managed by ex vivo renal artery reconstruction. Lesions managed in this manner include two kidneys with renal artery stenosis and renal tumors, one kidney with a congenital branch arteriovenous malformation, and 24 kidneys with branch occlusive or aneurysmal disease from fibromuscular dysplasia. Postoperative angiography was performed in 22 cases and defined successful revascularization without technical error in 20 cases. One operative death occurred as a result of myocardial infarction. One patient required reoperation to control bleeding, and two patients had temporary acute tubular necrosis during the postoperative period. Techniques employed included ex vivo repair with autotransplantation to the iliac system (six kidneys), mobilization and perfusion without transection of the renal vein (10 kidneys), and ex vivo perfusion and repair with replacement into the original renal fossa (11 kidneys). The authors believe this latter technique of reconstruction to be preferable to autotransplantation for the usual patient undergoing ex vivo repair of complex renovascular lesions.
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PMID:Ex vivo renal artery reconstructions: indications and techniques. 378 29

Four patients are presented aged over 65 years in whom a state of cardiogenic shock was present due to myocardial infarction of the following localization: anterior in two and posterior in two. According to the parameters all patients satisfied the criteria of cardiogenic shock. Of the four patients three died. In all patients parameters of renal lesion were analyzed after establishment of diureses: sodium in urine, creatinine quotient in urine and plasma, osmolality of urine, osmolality quotient of urine and plasma, the renal failure index and the excretional fraction of filtered sodium. The parameters quoted were analyzed the day after diuresis was established. All parameters, apart from sodium in urine, indicated functional oliguria. In corroboration of this were the values of creatinine clearance which were determined the day after establishing diuresis, amounting in all patients to more than 20 ml/min./1.73 m2, i.e. ranging from 20.6 to 59.0 ml/min./1.73 m2. Of the cases which ended fatally all had fibroses and myocardial scars, apart from recent infarction of the myocardium, generalized atherosclerosis particularly of the coronary arteries, and in all patients hypertrophy of the left ventricle and dilatation of the whole heart. In one patient anaemic infarction of one kidney was found and in another acute tubular necrosis (with the renal failure index of 0.3 and the excretional fraction of filtered sodium of 0.2), while in third patient no renal changes were found.
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PMID:The characteristics of acute renal failure in cardiogenic shock in the elderly. 378 19

Since 1973, 11 patients have had emergency valve replacement for severe mitral insufficiency and cardiogenic shock within 1 month (mean 10.0 days) of acute myocardial infarction. Mean age was 60 years (range 44 to 71 years). Nine infarcts affected the inferior wall, one patient had a prior myocardial infarction, and only two patients had a history of cardiac symptoms. Ten patients had pulmonary edema, five were oliguric (less than 0.5 ml/kg/hr for 12 hours), four required endotracheal intubation, nine required preoperative intra-aortic balloon support, and three had had a cardiac arrest. Preoperative cardiac index averaged 1.7 L/m2/min even with pharmacologic and circulatory support. Eight patients had cardiac catheterization and nine had echocardiograms. Left ventricular ejection fraction varied from 23% to 83% (mean 51%) and was not prognostic. Five patients had papillary muscle rupture and six patients had papillary muscle dysfunction. The mitral valve was replaced with a mechanical prosthesis in all patients. Five had simultaneous coronary artery bypass grafts. Three of five patients with papillary muscle rupture and two of six with papillary muscle dysfunction survived hospitalization. Two patients could not be weaned from cardiopulmonary bypass, two patients died within 24 hours of low cardiac output, and two patients died 3 weeks postoperatively of acute tubular necrosis and sepsis following prolonged preoperative cardiogenic shock. The interval from onset of shock to operative therapy averaged 1.7 days for survivors versus 9.3 days for nonsurvivors. Although the amount of viable left ventricular mass cannot be measured preoperatively, we recommend early operation, before other organ systems fail, for patients having severe mitral insufficiency and cardiogenic shock within 30 days of acute myocardial infarction.
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PMID:Operation for acute postinfarction mitral insufficiency and cardiogenic shock. 387 81

We report on 4 cases of reversible acute renal failure (ARF), appearing within the first days after institution of a sulfinpyrazone treatment (600 mg p. day) early after a myocardial infarction. Urinary data were consistent with an acute tubular necrosis. A renal biopsy, performed in 3 patients, revealed only very discrete tubular and interstitial lesions, not helpful in the understanding of the ARF. Three pathogenetic mechanisms could be evoked. Data in favour of an acute tubular precipitation of uric acid or an immunologically induced acute interstitial nephritis are lacking. More probably this ARF is due to an inhibitory effect of sulfinpyrazone on the renal prostaglandin synthesis. Early after a myocardial infarction, renal prostaglandins could play an important protective role in maintaining the renal circulation. Renal function should be monitored closely when sulfinpyrazone is prescribed, especially early after a myocardial infarction.
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PMID:[Acute renal failure induced by sulfinpyrazone (author's transl)]. 730 Oct 34

The vascular endothelium is an important mediator of vascular tone, angiogenesis, inflammatory-immune reactions, vascular permeability, and hemostasis. Thus, it plays an important role in the pathogenesis of numerous critical care processes, including septic shock, myocardial infarction, the adult respiratory distress syndrome, and acute tubular necrosis. Endothelial functions may be altered by changes in the local cellular environment, particularly changes in PO2. The ability of endothelial cells (EC) to not only sense, but also to adapt to, acute and chronic changes in PO2 is critical to maintaining endothelial metabolic functions and, in turn, to maintaining homeostasis, particularly in the critical care setting. Recent studies have shown that the EC is one of the more hypoxia-tolerant mammalian cell types; however, the mechanisms by which ECs respond and adapt to hypoxia are unknown. Our laboratory has shown that cultured ECs exposed to hypoxia upregulate a set of stress proteins, termed hypoxia-associated proteins (HAPs), that are distinct from the classically described stress proteins induced by heat shock (heat-shock proteins) or glucose deprivation (glucose-regulated proteins). We have recently identified one of these proteins as the glycolytic enzyme glyceraldehyde-3-phosphate dehydrogenase (GAPDH). Further studies have shown that GAPDH expression is regulated by hypoxia, primarily at the transcriptional level. Subcellular fractionation of hypoxic EC has shown that GAPDH is upregulated in the cytoplasmic fraction as would be expected with a glycolytic enzyme; however, a protein corresponding to GAPDH is also upregulated in the nuclear fraction. This suggests that the upregulation of GAPDH in EC during hypoxia is related to the potential nonglycolytic functions of this enzyme. Furthermore, the upregulation of GAPDH and the other HAPs (that have yet to be identified) may be related to the relative hypoxia tolerance of EC.
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PMID:Hypoxia-associated proteins. 758 62

Programmed cell death (PCD) had been widely used synonymously to caspase-mediated apoptosis until caspase-independent cell death was described. Identification of necrosis as a regulated process in ischaemic conditions has recently changed our understanding of PCD. At least three pathways of programmed necrosis (PN) have been identified. First, receptor-interacting protein kinase 3 (RIP3)-dependent necroptosis causes organ failure following stroke, myocardial infarction and renal ischaemia/reperfusion injury. Necroptosis can be mediated either by a large intracellular caspase-8-containing signalling complex called the ripoptosome or by the RIP1-/RIP3-containing necroptosome and is controlled by a caspase-8/FLICE inhibitory protein(long) heterodimer at least in the latter case. Second, mitochondrial permeability transition mediates apoptotic or necrotic stimuli and depends on the mitochondrial protein cyclophilin D. The third PN pathway involves the poly(ADP-ribose) polymerase-calpain axis that contributes to acute kidney injury (AKI). Preclinical interference with the PN pathways therefore raises expectations for the future treatment of ischaemic conditions. In this brief review, we aim to summarize the clinically relevant PCD pathways and to transfer the basic science data to settings of AKI. We conclude that pathologists were quite right to refer to ischaemic kidney injury as 'acute tubular necrosis'.
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PMID:Programmed necrosis in acute kidney injury. 2294 73