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 52-year-old male suffered from acute viral myocarditis with severe cardiogenic shock. On his admission, he underwent the inotropic and IABP supports, and subsequently was treated effectively by V-A bypass, which was continued for 35 hours. But he died in the period of 69 hours after V-A bypass from extended bowel necrosis and septic shock. The small and large intestinal mucosal necrosis, hemorrhagic hepatic necrosis and acute tubular necrosis were confirmed at necropsy. It is well known that the nonocclusive mesenteric vascular spasm is concerned strongly in their pathogenesis, after prolonged severe cardiogenic shock.
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PMID:[Nonocclusive intestinal necrosis after the successful veno-arterial bypass]. 195 43

Histopathological study was made of 12 Merino sheep - five splenectomized and seven intact - experimentally infected with Babesia ovis. Non-purulent encephalitis; initially exudative and subsequently interstitial pneumonia; pericarditis, myocarditis and haemorrhagic endocarditis; centrilobular necrotic hepatitis; hyperplasia of the lymphoreticular system; necrosis and vascular changes in adrenal glands were observed. The kidney was the most severely affected organ, exhibiting acute tubular necrosis typical of kidney shock syndrome. The lesions observed were suggestive of hypovolemic shock culminating in haemorrhagic diathesis owing to consumptive coagulopathy. Additionally, the massive release of catabolites from lysis and necrosis apparently produced endotoxic shock.
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PMID:Histopathological changes in sheep experimentally infected with Babesia ovis. 202 25

Dengue is a public health problem, with several gaps in understanding its pathogenesis. Studies based on human fatal cases are extremely important and may clarify some of these gaps. In this work, we analyzed lesions in different organs of four dengue fatal cases, occurred in Brazil. Tissues were prepared for visualization in optical and electron microscopy, with damages quantification. As expected, we observed in all studied organ lesions characteristic of severe dengue, such as hemorrhage and edema, although other injuries were also detected. Cases presented necrotic areas in the liver and diffuse macro and microsteatosis, which were more accentuated in case 1, who also had obesity. The lung was the most affected organ, with hyaline membrane formation associated with mononuclear infiltrates in patients with pre-existing diseases such as diabetes and obesity (cases 1 and 2, respectively). These cases had also extensive acute tubular necrosis in the kidney. Infection induced destruction of cardiac fibers in most cases, with absence of nucleus and loss of striations, suggesting myocarditis. Spleens revealed significant destruction of the germinal centers and atrophy of lymphoid follicles, which may be associated to decrease of T cell number. Circulatory disturbs were reinforced by the presence of megakaryocytes in alveolar spaces, thrombus formation in glomerular capillaries and loss of endothelium in several tissues. Besides histopathological and ultrastructural observations, virus replication were investigated by detection of dengue antigens, especially the non-structural 3 protein (NS3), and confirmed by the presence of virus RNA negative strand (in situ hybridization), with second staining for identification of some cells. Results showed that dengue had broader tropism comparing to what was described before in literature, replicating in hepatocytes, type II pneumocytes and cardiac fibers, as well as in resident and circulating monocytes/macrophages and endothelial cells.
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PMID:The pathology of severe dengue in multiple organs of human fatal cases: histopathology, ultrastructure and virus replication. 2473 95

In February 2012, 100% mortality was reported in a herd with 79 local sheep that were kept around of Abhar, Northwest of Iran. The ration for adult sheep was daily mixed (40 kg straw, 25 kg wheat and 2 kg Vit-C premix) and accidentally 1 500 g of salinomycin (Salinomycin 12% Premix; Aras Bazar Laboratories, Iran) had been added to the ration (22388 mg/kg = 22388 ppm) and overnight was fed to herd. At the morning, 78 sheep were founded dead and one of them showed convulsive seizures. Postmortem examination revealed pulmonary congestion and edema, hemorrhages in abomasum, large pale kidney and white streak lines in myocardium. Main histopathologic lesions were extensive subepicardial and intercardiomyofibers hemorrhages, extensive cardiomyolysis and myocarditis in heart, severe hyperemia and extensive acute tubular necrosis (ATN) in kidneys and focal necrosis and retention of bile cholangitis in the liver. In this study, on the basis of the history, observation of the ionophore remnant in the ration, clinical signs, gross and histopathological findings, acute salinomycin intoxication is definitely diagnosed.
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PMID:High mortality due to accidental salinomycin intoxication in sheep. 2610 96

Acute kidney injury has been reported in as many as 29% of COVID-19 patients. Reported risk factors include elevated baseline serum creatinine, elevated blood urea nitrogen, acute kidney injury, proteinuria, and hematuria. Suspected causes include sepsis and acute tubular necrosis resulting from renal hypoperfusion, cytokine release syndrome, direct viral invasion, renal medullary hypoxia secondary to alveolar damage, rhabdomyolysis, and cardiorenal syndrome due to viral myocarditis.
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PMID:Management of acute kidney injury in COVID-19. 3243 6