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)

We have compared 23 cadaver kidneys preserved with cryoprecipitated plasma (CPP) with 23 consecutive cadaver kidneys preserved with plasma protein fractions (PPF). In both groups the MOX-100 Waters machine was used. The PPF solution does not contain any fibrinogen or gamma globulin. The harvesting characteristics of both groups were comparable. Pulsatile perfusion time in the PPF group was up to 46 hours and in the CPP group was up to 44 hours. In the PPF group, 20 kidneys achieved immediate function upon transplant (85 percent). Two underwent periods of acute tubular necrosis (ATN) and one kidney never worked. In the CPP group, 18 kidneys achieved immediate function (78 percent). Two underwent periods of ATN and three never achieved satisfactory function. From this clinical experience, PPF is as effective as CPP for the preservation of kidneys up to 44 hours prior to transplant. The advantages of the PPF are easy availability, long shelf life, simple preparation, low cost, freedom from risk of hepatitis, and theoretical absence of antibody against the kidney. Graft and patient survival at 6 months showed no statistical difference.
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PMID:Use of plasma protein fraction in preservation of cadaveric kidneys. 76 16

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

A woman with a history of drug allergy, renal impairment and carcinoma of the breast with pulmonary micrometastases developed haemolytic anaemia and Stevens-Johnson syndrome following the use of mefenamic acid, paracetamol (acetaminophen) and furosemide (frusemide). In addition there was severe cholestatic hepatitis in the absence of clinical evidence of sepsis, biliary obstruction or recurrent metastases. The rash resolved on steroid therapy but the patient eventually died from both renal and liver failure. Acute tubular necrosis with a background of chronic tubulointerstitial nephritis was also found at autopsy. Although in the presence of multiple drug therapy the causative agent cannot be identified with absolute certainty, the association of these severe idiosyncratic hepatic and dermatological reactions with haemolytic anaemia strongly suggests mefenamic acid as the most likely culprit.
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PMID:A case of Stevens-Johnson syndrome, cholestatic hepatitis and haemolytic anaemia associated with use of mefenamic acid. 206 63

The raw carp bile has both nephrotoxic and hepatotoxic effects which are not well known. Recently, we studied 13 patients who had toxic acute renal failure and toxic hepatitis after ingestion of raw bile of carp in 3, grass carp in 8 and silver carp in 2 cases. The purpose of this report is to alert physicians to this very rare cause of toxic acute renal failure and hepatitis. All patients presented initially with gastrointestinal upset after eating. These symptoms were followed by oliguria in 7 patients (54%), hematuria was noted in 10 (77%) and jaundice in 8 patients (62%). Elevation of blood urea nitrogen, creatinine and transaminases lasted for about 3 weeks. The severity of the symptoms depended on the amount of bile ingested. All the patients recovered with conservative therapy and hemodialysis. Biopsy of the kidney revealed findings compatible with acute tubular necrosis similar to that produced by other nephrotoxins. Biopsy of the liver revealed findings consistent with acute toxic hepatitis. Both suggest toxic effects of carp bile as a cause of toxic acute renal failure and hepatitis.
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PMID:Toxic acute renal failure and hepatitis after ingestion of raw carp bile. 224 75

We report two cases of aluminium phosphide poisoning who presented with rare manifestations, one with bleeding diathesis, hepatitis and acute tubular necrosis and the other with acute respiratory failure.
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PMID:Aluminium phosphide poisoning. Two cases with rare presentation. 229 63

Combined hepatocellular injury and renal tubular necrosis developed in five alcoholic patients who were receiving acetaminophen therapeutically. Two patients were taking doses prescribed by a physician. The hepatitis was characterized by extremely high serum transaminase values that were maximal on admission. Two patients died, and autopsy disclosed hepatic centrizonal necrosis and acute renal tubular necrosis. The three who survived had clinical features typical of acute tubular necrosis. All five had measurable concentrations of acetaminophen in plasma, although measurements were requested on admission only in two patients. When an alcoholic presents with combined hepatic and renal insufficiency, acetaminophen should be considered as a possible inciting agent. This diagnosis should be considered when serum transaminase levels are markedly elevated and when renal failure is due to acute tubular necrosis.
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PMID:Combined hepatic and renal injury in alcoholics during therapeutic use of acetaminophen. 406 53

Due to a combination of ingested ethanol and inhaled trichloroethylene (Tri) a 28 year old man developed toxic hepatitis and acute oliguric renal failure, both of which had a favorable evolution. Tri has been described as a cause of hepatic disfunction and acute renal failure due to acute tubular necrosis, although some of the cases described are controversial, because Tri was either contaminated by other dissolvents or could not be proven pure, with the exception of one case. In many there was ethanol ingestion. The Tri inhaled by our patient was found to contain less than 1% of carbon tetrachloride (C-Tchl). This would suggest the C-Tchl to be responsible for the clinical picture although the combination Tri/ethanol cannot be discarded as the causal agent, due to the small amount of contaminant present.
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PMID:[Toxic hepatitis and acute renal failure after inhalation of chloride solvents: report of one case (author's transl)]. 732 30

We report two cases of acute renal failure induced by sciadopitysin, a type of flavonoid, and review related papers of flavonoid-induced acute nephropathy in the literature. A total of eight patients were studied. The purpose of this report is to alert physicians to consider this cause of acute renal failure with hemolysis, because flavonoids are widely used in the world. All patients initially presented with fever and gastrointestinal upset after the ingestion of a single large dose or long-term small doses. Symptoms that followed were cola-colored urine and jaundice. Elevation of blood nitrogen and serum creatinine lasted for 2 to 9 weeks. Hemolysis (100%), cholestatic hepatitis (50%), and disseminated intravascular coagulopathy (50%) were also noted in flavonoid-induced oliguric acute renal failure patients. All of these patients required hemodialysis and all but one who died completely recovered within 2 to 9 weeks. Renal biopsy was performed and showed acute interstitial nephritis with acute tubular necrosis. Moreover, we first demonstrated multiple polymorphous inclusion bodies within tubular epithelial cells in electron microscopic examinations. The definite pathogenetic mechanism of flavonoid-induced acute nephropathy needs further elucidation.
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PMID:Flavonoid-induced acute nephropathy. 812 47

Here, we report a 35-year-old man with non-fulminant acute non A, non B, non C hepatitis which developed into acute renal failure. The patient was admitted to hospital with the chief complaints of general fatigue, nausea and a high-grade fever of 40 degrees C. Laboratory examination revealed severe liver dysfunction and renal insufficiency on admission: his serum glutamic oxaloacetic transaminase was 3.203 IU/ml, serum glutamic pyruvic transaminase was 3.825 IU/ml, lactic dehydrogenase was 2.840 IU/ml, blood urea nitrogen was 65 mg/dl, and creatinine was 7.6 mg/dl. Hemodialysis was conducted during the initial 19-day period after admission because anuria was manifested on admission. On the 36th day after onset, renal functions returned to normal and the patient was negative for IgM-HA antibody. HBs antigen, IgM-HBC antibody, HCV antibody, cytomegalovirus antibody, and Epstein-Barr virus antibody. However, liver biopsy for histological examination on the 44th day after onset revealed no specific findings except the healing stage of acute hepatitis. Renal biopsy on the 49th day showed the healing stage of acute tubular necrosis without any glomerular change. It has been infrequently reported that acute renal failure develops following a non-fulminant acute state without hepatitis A, B or C virus infection. It is necessary to take acute renal failure into account in the clinical course of non-fulminant non A, non B, non C hepatitis.
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PMID:[Acute renal failure in non-fulminant acute hepatitis without hepatitis A, B or C virus infection]. 951 78

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


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