Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0033687 (proteinuria)
 24,015 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Acute fatty liver of pregnancy is a rare clinical entity unique to pregnancy that can lead to hepatic failure and encephalopathy and, if the diagnosis is delayed, to death for the baby and the mother. The characteristic histological picture demonstrates microvesicular fatty infiltration of hepatocytes. Acute fatty liver of pregnancy is a disease of the third trimester of pregnancy. The most significant clinical findings are nausea or vomiting, abdominal pain, jaundice, hepatic encephalopathy, increased transaminase levels, decreased platelet count, increased prothrombin time, and renal failure. Hypertension and proteinuria are common. Liver biopsy is not always necessary for diagnosis but may be useful in atypical cases. The primary therapy is early delivery and supportive care. Both the obstetric team and the medical consultants must have a high index of suspicion for this disease because early delivery is lifesaving and has transformed the prognosis for the mother and the baby. Collaboration between obstetricians and gastroenterologists is necessary to make the diagnosis and also to improve our understanding of this disease of unknown etiology.
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PMID:Acute fatty liver of pregnancy: the hepatologist's view. 805 22

Four cases of typhoid fever complicated by both acute oliguric renal failure and hepatitis are presented. Two patients had type II hepatitis according to criteria proposed by Khosla et al. (30) with hepatomegaly, hyperbilirubinaemia and markedly elevated asparate transaminase (AST); the others had type III hepatitis, characterized clinically and biochemically by profound jaundice, hepatomegaly, hepatic encephalopathy (one case only), hyperbilirubinemia and markedly elevated serum AST. Renal biopsy was not performed in any of our patients. However, a combination of proteinuria and abnormal urinary sediments containing red cell casts and granular casts, as noted in these patients, is considered highly suggestive of glomerulonephritis. Although isolated renal failure and hepatitis with hepatomegaly and deranged liver enzyme values have been reported previously in typhoid fever, their occurrence simultaneously in the same patient in distinctly rare, having been reported only twice in the English language literature.
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PMID:Typhoid fever complicated by acute renal failure and hepatitis: case reports and review. 964 38

A 22-year-old woman developed sudden hepatic encephalopathy and severe intestinal bleeding. She was diagnosed with acute fatty liver and hypersensitivity vasculitis and was successfully treated with whole plasma exchange, methylprednisolone pulse therapy, and transcatheter arterial embolization. Twenty-seven months later, she began complaining of lower abdominal fullness, tenderness, and nausea and vomiting. Histologic examination showed that she had developed gastrointestinal and renal amyloidosis with intestinal pseudoobstruction and proteinuria. The immunohistochemical study of the stomach, rectum, and kidney with anti-amyloid A fluorescent antibody showed that the systemic amyloid deposit was secondary to her underlying disease. This is the first report of amyloidosis occurring secondary to hypersensitivity vasculitis.
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PMID:Gastrointestinal amyloidosis secondary to hypersensitivity vasculitis presenting with intestinal pseudoobstruction. 972 75

It has been reported that glomerulosclerosis with IgA deposition is likely to be complicated with alcoholic liver cirrhosis. On the other hand, it is said that complications of nephrotic syndrome or rapidly progressive glomerulonephritis (RPGN) are relatively rare. We experienced two patients with alcoholic liver cirrhosis complicated with RPGN syndrome who had obtained favorable outcomes through the use of steroids and immune system suppressors. Case 1 was a 55-year-old male. He was being treated for alcoholic liver cirrhosis, but as bloody urine was noticed macroscopically, his renal function rapidly decreased. Specimens from a renal biopsy showed endocapillary proliferative lesions accompanying necrotic lesions. Granular deposition of IgA (IgA1) and C3 was seen along the capillary walls and in the mesangial areas. After the combined treatments of bilateral palatotonsillectomy, three courses of steroid semi-pulse therapy and post-therapy with steroids and mizoribin (MZR)were started, his hematuria and proteinuria disappeared and renal function improved markedly. Case 2 was a 37-year-old male with alcoholic liver cirrhosis complicated with hepatic encephalopathy. Although he was being treated at another hospital, nephritic syndrome occurred with rapidly worsening renal function and massive ascites. After continuous drainage of the ascites, we performed a renal biopsy. Mild proliferative lesions and notable wrinkling, thickening and doubling of the basal membrane were seen. Crescent formations were found in about half of the glomeruli. The fluorescent antibody technique showed positive pictures of IgA (IgA1) and C3. When three courses of steroid semi-pulse therapy and post therapy with steroids and MZR were combined, his proteinuria and serum Cre level decreased and stagnated ascites markedly decreased. The two cases were diagnosed as having secondary IgA nephropathy induced by the deposition of the IgA1 derived mainly from the intestinal tract, which had increased in the blood due to alcoholic liver cirrhosis. Active use of immune system suppressor therapy was effective.
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PMID:[Two cases of rapidly progressive nephritic syndrome complicated with alcoholic liver cirrhosis]. 2137 May 79

We present a case of a 75-year-old man with nephrotic syndrome and renal insufficiency caused by immune complex-mediated secondary membranoproliferative glomerulonephritis. He developed hepatic encephalopathy. A congenital portosystemic shunt was identified, indicating a diagnosis of membranoproliferative glomerulonephritis with noncirrhotic portosystemic shunt. Proteinuria resolved after shunt ratio reduction by percutaneous transhepatic portal vein embolization. Renal function and histopathological findings improved without immunosuppressive therapy. This case emphasizes the role of a high shunt ratio and reduced hepatic clearance of circulating immune complexes in such nephropathy. Membranoproliferative glomerulonephritis with a shunt may cause refractory nephrotic syndrome, but embolization is effective.
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PMID:Remission of membranoproliferative glomerulonephritis associated with a noncirrhotic portosystemic shunt after percutaneous transhepatic portal vein embolization. 2598 97