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 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

Necrotizing fasciitis can present with concomitant acute kidney injury. The etiology of acute kidney injury is often multifactorial; potential sources include volume depletion, abdominal compartment syndrome, rhabdomyolysis, and acute tubular necrosis (which may be related to hemodynamic instability, medications, or sepsis/infection). Kidney injury, defined via changes in serum creatinine, portends increased morbidity and mortality. Thus, it is crucial to accurately diagnose and assess the severity of kidney injury. We present the case of a patient with necrotizing fasciitis who endured 31 consecutive days of complete anuria. His serum creatinine decreased over this interval without the use of extracorporeal hemofiltration or dialysis. The explanation for this novel phenomenon lies in massive daily sero-sanguineous discharge and insensible losses with subsequent volume resuscitation. The patient's own convective clearance was substantial enough to maintain a modest creatinine clearance of 15 ml/min during sustained anuria. Our case emphasizes the importance of employing the creatinine, estimated glomerular filtration rate, and urine output portions of the Acute Kidney Injury Network (AKIN) or Risk Injury Failure Loss End stage (RIFLE) criteria in assessing the severity of kidney injury. It further reinforces the imperfection in using serum creatinine as a primary measure of glomerular filtration rate.
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PMID:Autologous creatinine clearance in a case of necrotizing fasciitis and anuria. 2234 4