AJP - Renal Physiology, Vol 250, Issue 2 181-F188, Copyright © 1986 by American Physiological Society
Roles of urea production, ammonium excretion, and amino acid oxidation in acid-base balance
W. Mackenzie
Atkinson and colleagues recently proposed several concepts that contrast
with traditional views: first, that acid-base balance is regulated chiefly
by the reactions leading to urea production in the liver; second, that
ammonium excretion by the kidney plays no role in acid-base homeostasis;
and third, that ammonium does not stimulate ureagenesis (except
indirectly). To examine these concepts, plasma ions other than bicarbonate
are categorized as 1) fixed cations (Na+, K+, Ca2+, and Mg2+, symbolized
M+) and anions (Cl-), 2) buffer anions (A-), 3) other anions (X-), and 4)
ammonium plus charged amino groups (N+). Since electroneutrality dictates
that M+ + N+ = Cl- + HCO3- + A- + X-, it follows that delta HCO3- =
delta(M+ - Cl-) - delta A- - delta X- + delta N+. Therefore acid-base
disturbances (changes in HCO3-) can be categorized as to how they affect
bodily content and hence plasma concentration of each of these four types
of ions. The stoichiometry of ureagenesis, glutamine hydrolysis, ammonium
and titratable acid excretion, oxidation of neutral, acidic, and basic
amino acids, and oxidation of methionine, phosphoserine, and protein are
examined to see how they alter these quantities. It is concluded that 1)
although ureagenesis is pH dependent and also counteracts a tendency of
amino acid oxidation to cause alkalosis, this tendency is inherently
limited by the hyperammonemia (delta N+) that necessarily accompanies it,
2) ammonium excretion is equivalent to hydrogen excretion in its effects on
acid-base balance if, and only if, it occurs in exchange for sodium or is
accompanied by chloride excretion and only when the glutamate generated by
glutamine hydrolysis is oxidized.(ABSTRACT TRUNCATED AT 250 WORDS)
