Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019209 (hepatomegaly)
 5,798 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The occurrence of ascites after Renal Transplant (RT) is infrequent, and may be a consequence of surgical or medical complications. Case report: 61 year-old, male, history of arterial hypertension, tongue carcinoma and alcoholic habits 12-20g/day. He had chronic kidney disease secondary to autosomal dominant polycystic kidney disease, without hepatic polycystic disease. He underwent cadaver donor RT in September 2017. He had delayed graft function by surgically corrected renal artery stenosis. He was admitted in January 2018 for ascites de novo, with no response to diuretics. HE had visible abdominal collateral circulation. Graft dysfunction, adequate tacrolinemia, Innocent urinary sediment, mild anemia, without thrombocytopenia. Serum albumin 4.0g / dL. Normal hepatic biochemistry. Peritoneal fluid with transudate characteristics and serum albumin gradient > 1.1. Ultrasound showed hepatomegaly, permeable vascular axes, without splenomegaly. Mycophenolate mofetil was suspended, with reduced remaining immunosuppression. He maintained refractory ascites: excluded infectious, metabolic, autoimmune and neoplastic etiologies. No nephrotic proteinuria and no heart failure. MRI: micronodules compatible with bile cysts. Upper Digestive Tract Endoscopy did not show gastroesophageal varicose veins. Normal abdominal lymphoscintigraphy. He underwent exploratory laparoscopy with liver biopsy: incomplete septal cirrhosis of probable vascular etiology some dilated bile ducts. He maintained progressive RT dysfunction and restarted hemodialysis. The proposed direct measurement of portal pressure was delayed by ascites resolution. There was further recovery of the graft function. Discussion: Incomplete septal cirrhosis is an uncommon cause of non-cirrhotic portal hypertension. Its definition is not well known, morphological and pathophysiological. We have not found published cases of post-RT ascites secondary to this pathology, described as possibly associated with drugs, immune alterations, infections, hypercoagulability and genetic predisposition.
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PMID:Refractory ascites and graft dysfunction in early renal transplantation. 3089 91

We presently report the case of hantavirus infection in a 45-year-old male who was hospitalized to our clinic of infectious diseases, with fever, myalgia, vomiting, nausea, headache, and abdominal pain. The physical findings included hepatomegaly, splenomegaly, rash, and conjunctival injection. Eight days before the start of complaints, the patient has cut trees in the mountain. An acute renal failure was observed with an oliguria and an increase of serum creatinine and blood urea nitrogen. Urinalysis shows albuminuria and hematuria. Elevations of amylase, lipase, and liver enzymes levels, low serum albumin level, and thrombocytopenia were observed. A positive ELISA test for hantavirus IgM/IgG antibodies confirmed hemorrhagic fever with renal syndrome. On the third day of hospitalization, the patient had seizures. The unenhanced head computed tomography (CT) performed after seizures showed subcortical bilateral hypodensities within frontal, parietal, and occipital regions corresponding to areas of increased signal intensity in magnetic resonance imaging (MRI) associated with cerebral edema in posterior reversible encephalopathy syndrome (PRES). The treatment consisted of supportive therapy. The patient underwent another head MRI with contrast enhancement after 2 months, which resulted normal.
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PMID:Posterior Reversible Encephalopathy Syndrome in a Patient with Hemorrhagic Fever with Renal Syndrome. 3218 Oct 28


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