title: Mechanisms in hyperkalemic renal tubular acidosis.
abstract: The form of renal tubular acidosis associated with hyperkalemia is usually attributable to real or apparent hypoaldosteronism. It is therefore a common feature in diabetes and a number of other conditions associated with underproduction of renin or aldosterone. In addition, the close relationship between potassium levels and ammonia production dictates that hyperkalemia per se can lead to acidosis. Here I describe the modern relationship between molecular function of the distal portion of the nephron, pathways of ammoniagenesis, and hyperkalemia.
authors.affiliation: Cambridge Institute for Medical Research (Room 4.3), Addenbrooke's Hospital Box 139, Hills Road, Cambridge, CB2 0XY, UK. fek1000@cam.ac.uk
authors.forename: Fiona E
authors.initials: FE
authors.lastname: Karet
mesh_terms: D000138:Acidosis / Q000473:pathology; D000141:Acidosis, Renal Tubular / Q000378:metabolism / Q000503:physiopathology*; D000450:Aldosterone / Q000378:metabolism; D000641:Ammonia / Q000378:metabolism; D000818:Animals; D053503:Epithelial Sodium Channels / Q000378:metabolism; D006801:Humans; D006947:Hyperkalemia / Q000378:metabolism / Q000503:physiopathology*; D007684:Kidney Tubules / Q000473:pathology*; D008954:Models, Biological; D009399:Nephrons / Q000473:pathology; D011188:Potassium / Q000378:metabolism
chemical_list: D053503:Epithelial Sodium Channels; D000450:Aldosterone; D000641:Ammonia; D011188:Potassium