Molecular and pathophysiologic mechanisms of hyperkalemic metabolic acidosis.
In summary, hyperkalemia may have a dramatic impact on ammonium production and excretion. Chronic hyperkalemia decreases ammonium production in the proximal tubule and whole kidney, inhibits absorption of NH4+ in the mTALH, reduces medullary interstitial concentrations of NH4+ and NH3, and decreases entry of NH4+ and NH3 into the medullary collecting duct. The potential for development of a hyperchloremic metabolic acidosis is greatly augmented when renal insufficiency with associated reduction in functional renal mass coexists with the hyperkalemia, or in the presence of aldosterone deficiency or resistance. Such a cascade of events helps to explain, in part, the hyperchloremic metabolic acidosis and reduction in net acid excretion characteristic of several experimental models of hyperkalemic-hyperchloremic metabolic acidosis including: obstructive nephropathy, selective aldosterone deficiency, and chronic amiloride administration (7.9).
DuBose
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TD
Department of Internal Medicine, University of Texas Medical School-Houston, USA.
D000138:Acidosis / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology*; D000450:Aldosterone / Q000172:deficiency / Q000378:metabolism; D000641:Ammonia / Q000378:metabolism; D002713:Chlorine / Q000097:blood; D005799:Genes, Dominant; D005808:Genes, Recessive; D006801:Humans; D006947:Hyperkalemia / Q000150:complications* / Q000188:drug therapy / Q000503:physiopathology*; D007684:Kidney Tubules / Q000187:drug effects / Q000378:metabolism; D007685:Kidney Tubules, Collecting / Q000378:metabolism; D008564:Membrane Potentials; D011546:Pseudohypoaldosteronism / Q000235:genetics / Q000503:physiopathology; D012083:Renin / Q000097:blood / Q000172:deficiency / Q000378:metabolism
D000450:Aldosterone; D002713:Chlorine; D000641:Ammonia; D012083:Renin