Molecular and pathophysiologic mechanisms of hyperkalemic metabolic acidosis

Trans Am Clin Climatol Assoc. 2000;111:122-33; discussion 133-4.

Abstract

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).

Publication types

  • Research Support, U.S. Gov't, P.H.S.
  • Review

MeSH terms

  • Acidosis / complications*
  • Acidosis / drug therapy
  • Acidosis / physiopathology*
  • Aldosterone / deficiency
  • Aldosterone / metabolism
  • Ammonia / metabolism
  • Chlorine / blood
  • Genes, Dominant
  • Genes, Recessive
  • Humans
  • Hyperkalemia / complications*
  • Hyperkalemia / drug therapy
  • Hyperkalemia / physiopathology*
  • Kidney Tubules / drug effects
  • Kidney Tubules / metabolism
  • Kidney Tubules, Collecting / metabolism
  • Membrane Potentials
  • Pseudohypoaldosteronism / genetics
  • Pseudohypoaldosteronism / physiopathology
  • Renin / blood
  • Renin / deficiency
  • Renin / metabolism

Substances

  • Aldosterone
  • Chlorine
  • Ammonia
  • Renin