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

Five episodes of acute renal failure due to rifampicin (R-ARF) were observed in four patients and the clinical and histological data were compared with the records of 52 episodes reported in the literature. The bulk of data supports the assumption that the by far most frequent renal injury responsible for R-ARF is acute tubular necrosis produced by a vasomotor mechanism. Nevertheless a few data, above all immunohistological findings, suggest the local presence of allergic process. It may be, that the development of an immunological renal lesion is prevented or blunted by the consequences of vasomotor effects.
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PMID:Acute renal failure due to rifampicin (R-ARF). 93 13

The FENa test, a determination of the excreted fraction of the filtered sodium, was performed in patients in the oliguric phase of acute renal failure. Patients with prerenal azotemia had an FENa of less than 1, and patients with acute tubular necrosis had an FENa of more than 3 (P less than .001). This simple test clearly differentiates between these two conditions and, thus, is of considerable clinical value.
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PMID:The FENa test. Use in the differential diagnosis of acute renal failure. 94 39

Acute renal failure of obstetric origin is common among North Indian patients and comprised 72 (22.1%) of 325 patients undergoing dialysis over an 11-year period. Of these, 46 gravidas had developed renal failure following abortion, and 29 cases were due to complications of late pregnancy. The most striking feature of this study was a high incidence of irreversible renal lesions of bilateral diffuse cortical necrosis in early (18.6%) as well as late pregnancy (37.8%). Overall incidence of diffuse cortical necrosis was 25%. In the remainder, acute tubular necrosis was seen in 52 (72.2%), patchy cortical necrosis in 1 (1.4%), and tubular necrosis along with glomerular involvement in 1 patient (1.4%). Pathogenetic factors which contributed to the development of renal failure, either singly or in combination, were loss of blood failure, either singly or in combination, were loss of blood (79.1%), septicemia (31.9%), hypotension due th hemorrhagic and septicemic shock (51.4%), eclamptic toxemia (11.1%), and disseminated intravascular coagulation in 12.5% patients. Infrequent occurrence of disseminated intravascular coagulation in the septic anc eclamptic patients who developed diffuse cortical necrosis was an interesting finding, as was the fact that coagulopathy was more frequently observed in acute tubular necrosis. Late referral, frequent sepsis, and high incidence of bilateral diffuse cortical necrosis contributed significantly to a high mortality (55.3%).
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PMID:Acute renal failure of obstetric origin. 108 92

Variable degrees of acute renal failure developed in three patients receiving therapy with cephalothin sodium. The course and findings were consistent with acute tubular necrosis of the oliguric and nonoliguric types. One patient had protracted oliguria, a second experienced transient oliguria, and one had normal urine output. All had urinary sediment changes consistent with tubular necrosis, and the two oliguric patients had elevated urine sodium concentrations. No other causes for renal failure could be detected, and all recovered after discontinuation of cephalothin therapy, although peritoneal dialysis was required in one patient. These observations indicate that cephalothin is capable of inducing renal damage in man.
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PMID:Nephrotoxicity associated with cephalothin administration. 113 Sep 24

Eight patients with acute renal failure following snakebite were studied. Intravascular hemolysis and disseminated intravascular coagulation contributed to the development of acute renal failure in 6 patients. Direct nephrotoxicity causing acute renal failure is postulated in 2 patients, 1 of whom also revealed evidence of mild, disseminated intravascular coagulation. Three patients had histopathological lesions of acute symmetrical cortical necrosis and 3 had acute tubular necrosis. In 1 patient with acute tubular necrosis, in whom direct nephrotoxicity seemed to be responsible for renal failure, the striking histological feature was a uniform debasement and disappearance of tubular epithelium. In 2 patients with a clinical course of acute tubular necrosis, histological lesions could not be documented. All the 5 patients with acute tubular necrosis regained full recovery of renal function, 3 of them with the help of dialysis and 2 with conservative management. None of the 3 patients with acute cortical necrosis survived in spite of intermittent dialysis therapy.
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PMID:Acute renal failure following snakebite. 115 3

Acute renal failure is often fatal, but usually this complication following trauma is avoidable. Of fifteen patients with acute tubular necrosis associated with severe trauma, thirteen survived. This is a marked improvement in survival rate compared with the rates previously published. We credit the improvement to aggressive medical and surgical treatment by a team of orthopaedic surgeons, nephrologists, and surgeons.
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PMID:Acute renal failure following trauma. 115 22

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, presisting 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.
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PMID:Pathogenesis of acute renal failure following temporary renal ischemia in the rat. 119 55

Marked morphologic changes were seen in all structural elements of the renal papilla during mercuric chloride-induced acute tubular necrosis. Expect for the descriptions of increased numbers of leukocytes within the medullary vasa recta, papillary changes have not been described previously. The techniques used in this study included light microscopy, scanning electron microscopy, and transmission electron microscopy. The renal interstitial cells developed an extremely irregular contour and were penetrated by large irregular cavelike structures. A marked decrease occurred in the size and number of the cytoplasmic lipid droplets in these cells. The volume of the Golgi area, and of the rough and smooth endoplasmic reticulum increased. The morphologic changes in the renal interstitial cells were indicative of increased activity rather than of cellular injury. This is of insterest because several investigators have postulated that the interstitial cells are the site of renal prostaglandin synthesis Incrreased prostaglandin synthesis and release have been proposed to play a role in the redistribution of renal blood flow seen during acute renal failure.
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PMID:Alterations of the renal papilla during mercuric chloride-induced acute tubular necrosis. 120 87

Reports of acute tubular necrosis following envenomation by hornets are rare. A 38-year-old farmer presented with evidence of haemolysis and acute renal failure following multiple hornet stings (Vespa orientalis). Biopsy of skin from the site of the stings showed evidence of vasculitis. Renal biopsy showed characteristic changes of acute tubular necrosis. Intravascular haemolysis due to haemolytic properties of the hornet venom was considered to be chiefly responsible for the renal lesions in this patient.
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PMID:Acute renal failure following hornet stings. 127 11

Out of 152 cases of Acute renal failure (ARF) 32 patients (21%) were subjected to kidney biopsy. All patients had intrinsic ARF. Prerenal azotemia and obstructive uropathy were excluded. Histologic observations were: Crescentric glomerulonephritis in 7 (21.9%), acute endocapillary proliferative glomerulonephritis 5 (15.6%), acute interstitial nephritis 7 (21.9%), necrotizing vasculitis 4 (12.5%), acute tubular necrosis in 5 (15.6%) and membrano-proliferative GN with superimposed crescent in 2 (6.2%) while renal cortical necrosis was seen in 6.2% of cases. Prebiopsy diagnosis was correct in only 10 (31.25%) cases. The result of biopsy had altered clinical diagnosis in 22 (68.75%) patients and precise renal biopsy diagnosis resulted in therapeutic changes in 54.8% of patients with ARF.
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PMID:Clinical significance of kidney biopsy in acute renal failure (ARF). 129 67


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