Figure 1

In healthy controls the excretion of ammonia is mediated by two mechanisms: liver detoxification and renal excretion. Renal excretion is modulated by angiotensin II (ATII) at the level of the proximal tubule. In our patient the hepatic mechanism is impaired, due to the liver cirrhosis, making the renal route essential for elimination of ammonia. Suppression of ATII activity through a combination of angiotensin-converting enzyme inhibitors and angiotensin II receptor blockers prevented adequate renal excretion, leading to an abrupt rise in serum ammonia concentration and the described neurological complications.