title: Portosystemic encephalopathy in a patient treated with peritoneal dialysis.
abstract: We present a case of a 75-year-old man with end-stage renal disease caused by immunoglobulin A nephropathy who developed hepatic encephalopathy 15 months after starting continuous ambulatory peritoneal dialysis therapy. Liver test results were normal except for hyperammonemia (ammonia, 317 microg/dL [186 micromol/L]) and mildly increased alkaline phosphatase and gamma-glutamyl transpeptidase levels. Abdominal ultrasonography showed normal liver architecture, and color Doppler ultrasonography showed a normal splenic-portal axis with hepatopetal blood flow. Histological examination of a laparoscopic liver biopsy specimen showed moderate fibrosis limited to portal tracts without necrosis or inflammation. Magnetic resonance angiography and percutaneous transhepatic portal angiography showed a large shunt between the left gastric and azygous veins, with blood flowing from the portal vein to the superior vena cava. The patient was transferred to hemodialysis treatment, and although his condition improved slightly, episodes of encephalopathy did not disappear. Surgical ligation of the left gastric vein was performed. In the 8 months after surgery, he has experienced no further episodes of hepatic encephalopathy or hyperammonemia. We speculate that increased intra-abdominal pressure and vasodilation caused by peritoneal dialysis solutions in a patient with a spontaneous portosystemic shunt resulted in ammonia-rich blood flow from the portal vein to the superior vena cava and encephalopathy. In addition, it is possible that chronic hepatic hypoxia caused by hypoperfusion from portosystemic shunting contributed to the development of liver fibrosis. To our knowledge, this is the first report of spontaneous portosystemic shunt encephalopathy in a patient with a noncirrhotic liver undergoing peritoneal dialysis.
authors.affiliation: Service of Nephrology, Hospital Ntra Sra de Sonsoles, Avila, Spain. vparaiso@hnss.sacyl.es
authors.forename: Vicente
authors.initials: V
authors.lastname: Paraíso
authors.forename: Marcelo
authors.initials: M
authors.lastname: Francos
authors.forename: Fernando
authors.initials: F
authors.lastname: Rodríguez-Berzosa
authors.forename: Carmen
authors.initials: C
authors.lastname: Felipe
authors.forename: Eva
authors.initials: E
authors.lastname: López-Valdés
authors.forename: Rocío
authors.initials: R
authors.lastname: Martín
authors.forename: Javier
authors.initials: J
authors.lastname: Blázquez
authors.forename: Carlos
authors.initials: C
authors.lastname: Chacón
authors.forename: Amelia
authors.initials: A
authors.lastname: Fidalgo
authors.forename: Jesús
authors.initials: J
authors.lastname: Martín
mesh_terms: D000368:Aged; D006501:Hepatic Encephalopathy / Q000209:etiology* / Q000503:physiopathology; D006801:Humans; D007676:Kidney Failure, Chronic / Q000628:therapy; D008026:Ligation; D008102:Liver Circulation / Q000502:physiology; D008103:Liver Cirrhosis / Q000209:etiology / Q000503:physiopathology; D018810:Magnetic Resonance Angiography; D008297:Male; D010531:Peritoneal Dialysis, Continuous Ambulatory / Q000009:adverse effects*; D011169:Portal Vein / Q000503:physiopathology; D011170:Portasystemic Shunt, Surgical; D013152:Splanchnic Circulation / Q000502:physiology; D013270:Stomach / Q000098:blood supply; D018615:Ultrasonography, Doppler, Color; D014655:Vascular Resistance