Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022672 (acute tubular necrosis)
 2,175 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A renal transplant patient in whom acute pancreatitis developed 2 1/2 years after surgery is presented. Pancreatisis was accompanied by hyperlipaemia, diabetes mellitus and acute renal failure possibly due to acute tubular necrosis. Pancreatic abscesses necessitated subtotal pancreatectomy 2 months later. Because of generalized tuberculosis finally the patient succumbed 6 weeks thereafter. As aetiological factors cytomegalovirus disease, disorders in lipid metabolism and immunosuppressive therapy must be discussed. It is concluded that prophylactic measures as well as early diagnosis, intensive care and therapy are necessary for reducing the high risks of pancreatis in renal transplant recipients.
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PMID:[Pancreatitis after renal transplantation (author's transl)]. 20 57

Eight autopsy cases of paraquat poisoning from 1980 to 1990 were studied by light microscopy. An attempt was made to correlate the severity of poisoning, as assessed by the blood paraquat concentrations and the time between ingestion and treatment, with the survival periods and pathological changes. Six of the patients were male. The mean age was 21 years (range 12-33 years). The blood paraquat concentrations on admission ranged from 0.04 to 4.27 micrograms/ml. The survival periods were between 26 hours and 59 days. The main causes of death included circulatory collapse in one patient with 26 hours survival, and acute alveolar injury of the lungs and acute tubular necrosis or diffuse cortical necrosis of the kidneys in 4 patients who survived less than 7 days. Pulmonary proliferative changes leading to respiratory failure were detected in the remaining patients, who survived 11, 17, and 59 days. The liver revealed bile duct injury in the portal areas, centrolobular cholestasis, fatty metamorphosis, and inconspicuous centrolobular hepatic necrosis. The adrenal glands showed diffuse cortical necrosis in 3 severe cases. Mild acute pancreatitis was evident in one case. The brain was edematous with or without focal minimal hemorrhages. Toxic myocarditis, myositis, and aplasia of erythropoiesis, as previously described, were not present in this study. The severity of poisoning seems to correlate reversely with the survival periods and directly with degrees of pulmonary damage and adrenal cortical necrosis.
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PMID:Fatal paraquat poisoning: a light microscopic study in eight autopsy cases. 140 91

We have described a spectrum of pancreatic surgery after cardiopulmonary bypass. At one end is a subclinical lesion which was manifested only by elevations in serum isoamylase levels (27 percent of patients) and increased ribonuclease levels (13 percent of patients) in asymptomatic patients followed after cardiac surgery. At the other end is a severe and often lethal necrotizing pancreatitis. Acute necrotizing pancreatitis was found at autopsy in 25 percent of 138 patients who died after cardiac surgery, and it correlated strongly with low output, acute tubular necrosis, and infarction of the liver, spleen, or bowel. It was the principal cause of death in 4 percent of these patients. In addition, 24 percent of 38 nonsurgical patients who died from cardiac failure and hypoperfusion had acute pancreatitis at autopsy, whereas acute pancreatitis was not observed in 55 nonsurgical patients who died without a significant period of low output. Acute pancreatitis was recognized postoperatively in 12 patients (0.2 percent). Three had mild pancreatitis, and all responded well to conservative therapy. In nine patients, fulminant necrotizing pancreatitis developed. Their courses were characterized by significant early postoperative hemodynamic compromise, abdominal distention, ileus, fever, and episodes of late vascular instability associated with hypocalcemia. The diagnosis of pancreatitis was usually missed because of the absence of pain, tenderness and hyperamylasemia. The diagnosis was confirmed at laparotomy in eight patients and at autopsy in one. The only two survivors among the nine with severe cases had aggressive mobilization, debridement, and wide drainage of the necrotic pancreas. We suggest that a mild subclinical injury to the pancreas may occur as a consequence of cardiopulmonary bypass and may progress to severe ischemic necrosis if hypoperfusion follows in the postoperative period, the presentation of necrotizing pancreatitis may be atypical in the cardiac surgical patient and should be considered if nonspecific abdominal symptoms are present, and aggressive debridement and drainage may be the optimal treatment for aggressive forms of this disease.
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PMID:Acute pancreatitis after cardiopulmonary bypass. 258 Apr 53

A case is reported of a patient with renal failure and developing systemic and renal oxalosis due to pyridoxine-resistant type I primary hyperoxaluria. In spite of vigorous haemodialysis and hydration before and after operation, an allografted cadaveric kidney failed because of oxalate deposits in the transplant. The patient was treated by combined hepatic and renal transplantation. The liver allograft functioned well but the kidney had poor function due to primary acute tubular necrosis aggravated by steroid-associated acute pancreatitis, systemic cytomegalovirus infection and high cyclosporin A levels. The patient died from generalised cytomegalovirus infection. The early course after operation was associated with a reduced rate of oxalate production, which would slow the rate of oxalate deposition in the tissues. The size of the oxalate metabolic pool was also diminished. These observations are compatible with the grafted liver having corrected the metabolic lesion.
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PMID:Primary hyperoxaluria (type I): attempted treatment by combined hepatic and renal transplantation. 390 98

To verify whether renal tubular dysfunction may account for the CAm/CCr enhancement in acute pancreatitis (AP), we have measured the renal excretion of amylase, lysozyme, and gamma-glutamyl-transpeptidase (GGTP) in 22 patients with AP and in 8 with acute tubular necrosis. While the CAm/CCr ratio was elevated in most patients with AP, the CLys/CCr ratio fell within the normal range in 60% of these patients. The subdivision of patients with AP in subgroups with elevated and normal CLys/CCr ratios revealed a mean CAm/CCr not statistically different. Moreover, no correlation was present in AP between amylase vs. both lysozyme and GGTP clearances. These data suggest that tubular dysfunction does occur in some but not in all the patients with AP and seems not to play a major role in the pathogenesis of the increased CAm/CCr ratio in this condition.
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PMID:Does renal tubular dysfunction account for the enhanced CAm/CCr ratio in acute pancreatitis? 615 8