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Hyperammonemic Encephalopathy During Hemodialysis

VINCENT J. CANZANELLO, M.D.; RAYMOND T. RASMUSSEN, B.S.; and M. DONALD McGOLDRICK, M.B.
[+] Article and Author Information

▸Requests for reprints should be addressed to M. Donald McGoldrick, M.B.; Division of Nephrology, Albany Medical College; Albany, NY 12208.


Albany Medical CollegeAlbany, New York


Ann Intern Med. 1983;99(2):190-191. doi:10.7326/0003-4819-99-2-190
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This excerpt has been provided in the absence of an abstract.

Renal failure may precipitate or exacerbate hepatic encephalopathy in patients with liver disease (1, 2). One postulated mechanism is the excessive production of ammonia by the bacterial flora of the gastrointestinal tract as a result of high blood urea nitrogen levels. Others (2) postulate that there is underexcretion of potentially toxic, but as yet unidentified, metabolites that accumulate in patients with severe liver disease. Hyperammonemic encephalopathy recently has been described in a patient with normal liver function and excessive ammonia production secondary to infection in a neurogenic bladder (3).

Standard hemodialysis (1, 2, 4) and modifications such as the use

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