To pee or not to pee: ammonia hypothesis of hepatic encephalopathy revisited

I.L. Mpabanzi, S. Olde Damink, M.C.G. van de Poll, P.B. Soeters, R.A. Jalan, C.H.C. Dejong

Research output: Contribution to journalArticleAcademicpeer-review

Abstract

Hepatic encephalopathy is a neuropsychiatric syndrome associated with liver failure. Its aetiology has been debated for the past 100 years. Nevertheless, elevated ammonia levels are still believed to play a central role in its pathogenesis. After intestinal production, ammonia is detoxified by the liver. In liver failure, skeletal muscle and brain have been proposed to be alternative, although temporary, ammonia detoxifying organs. However, there is an increasing body of evidence that the kidney, in addition to the gut, is a pivotal organ determining systemic ammonia levels. In the last 20 years, it has been shown that the kidney can switch from an organ of systemic net ammonia production to a net ammonia excretion organ. The kidney plays a central role in the determination of ammonia levels. It is at least as important as the gut and could therefore serve as a target for new treatments for hepatic encephalopathy.
Original languageEnglish
Pages (from-to)449-454
Number of pages6
JournalEuropean Journal of Gastroenterology & Hepatology
Volume23
Issue number6
DOIs
Publication statusPublished - Jun 2011

Keywords

  • ammonia
  • hepatic encephalopathy
  • kidney
  • liver failure
  • ACUTE LIVER-FAILURE
  • AMINO-ACID-METABOLISM
  • INDUCED HYPERAMMONEMIA
  • INTERORGAN AMMONIA
  • SMALL-INTESTINE
  • BLOOD AMMONIA
  • RENAL AMMONIA
  • HUMAN COLON
  • GLUTAMINE
  • CIRRHOSIS

Cite this