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)

The toxic effects of imidocarb diproprionate (3,3'-bis [2 imidazolin-2yl]-carbanilde diproprionate) were evaluated in adult goats given (intramuscular injection) a lethal dose (6.75 mg/kg). The immediate clinical signs of toxicosis were transient excessive salivation and diarrhea. Anorexia, dyspnea, recumbency, and death occurred between postinjection days (PID) 4 and 8, during which time 7 goats died and 4 moribund goats were euthanatized. There were marked increases in mean serum urea nitrogen concentration and significant increases in serum glutamic oxalacetic transminase activity and in the mean number of circulating neutrophils after PID 4. Renal hyperemia and enlargement were evident by PID1. Serosanguineous fluid in the trachea and major bronchi, pulmonary congestion and edema, hydrothorax, hydroperitoneum, and less frequently hydropericardium were observed on and after day 4. Microscopic renal tubular lesions rapidly progressed from pyknotic epithelial nuclei observed at 6 and 12 hours to acute tubular necrosis of epithelium of the proximal convoluted tubules on days 1 and 2. Pulmonary congestion and edema; hemorrhage into alveoli, bronchioles, and bronchi; and intracytoplasmic lipid vacuoles within the hepatocytes in the periacinar zones of the hepatic lobules were observed on or after day 4. Succinic dehydrogenase and adenosine triphosphatase activities decreased progressively in the epithelial cells of the proximal convoluted tubules. The decreases in cellular enzymatic activity occurred shortly after the appearance of microscopic lesions in the tubular epithelium.
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PMID:Clinical, histologic, and histochemical study of imidocarb diproprionate toxicosis in goats. 13 83

A 63-year-old male with liver cirrhosis due to type-C hepatitis virus was admitted on June 14, 1999 to our hospital with complaints of dyspnea, and blisters, swelling and purpuras on his legs. He had consumed raw fish one or two days before. He was already in a state of shock with sepsis and disseminated intravascular coagulation shortly after the admission. Although treatment with MEPM and MINO for sepsis, and daltepalin sodium, antithrombin III and gabexate mesilate for disseminated intravascular coagulation was begun within 12 hours, he died only 30 hours after admission. The causative organism was detected from the blood and the contents of blisters, and was determined as Vibrio vulnificus. On autopsy, Vibrio vulnificus was also detected from skin and muscular tissue of his legs, but necrotizing fasciitis were not apparently revealed. Coagulating necrosis and acute tubular necrosis were verified in intestine and kidneys respectively probably due to ischemic changes. Pseudolobuli were formed and a small hepatocellular carcinoma was detected in the liver. Vibrio vulnificus has two infection channels; one is oral intake and the other is an external wound. The former is said to become serious. It has a rather short period from the starting of the symptom to death, and is highly fatal. If this bacteria is suspected by the clinical coarse of the patients or the laboratory examinations, it is necessary to dose effective antibiotics in its early stage. And for prevention, susceptible patients must be informed of the existence of this disease and the necessity of adequately heating raw seafood.
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PMID:[An autopsied case of septicemia due to Vibrio vulnificus]. 1185 76

A retrospective study was conducted in nine patients with rabies admitted to a hospital of Fortaleza, Brazil. Autopsy was performed in all cases. The ages ranged from three to 81 years and six were males. They all were bitten by dogs. The time between the accident and the hospital admission ranged from 20 to 120 days (mean 45 +/- 34 days). The time until death ranged from one to nine days (mean 3.3 +/- 5.5 days). The signs and symptoms presented were fever, hydrophobia, aerophobia, agitation, disorientation, dyspnea, sialorrhea, vomiting, oliguria, sore throat, pain and hypoesthesia in the site of the bite, headache, syncope, cough, hematemesis, mydriasis, hematuria, constipation, cervical pain and priapism. In three out of six patients, there was evidence of acute renal failure, defined as serum creatinine > or = 1.4 mg/dL. The post-mortem findings in the kidneys were mild to moderate glomerular congestion and mild to intense peritubular capillary congestion. Acute tubular necrosis was seen in only two cases. This study shows some evidence of renal involvement in rabies. Histopathologic findings are nonspecific, so hemodynamic instability, caused by autonomic dysfunction, hydrophobia and dehydration must be responsible for acute renal failure in rabies.
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PMID:Renal involvement in human rabies: clinical manifestations and autopsy findings of nine cases from northeast of Brazil. 1655 20