Rustom R, Costigan M, Shenkin A, Critchley M, Bone JM
Oral sodium bicarbonate suppresses renal tubular peptide
catabolism, ammoniagenesis and reduces renal tubular injury in
renal patients
33rd Congress of the Eur Dial Transplant Assoc
Nephrol Dial Transplant
(Jun) 11:A141 1996
In a previous study in patients with nephrotic range proteinuria these
authors showed that proximal tubular catabolism (estimated by measuring the
renal degradation of 99mTc-Aprotinin) is markedly enhanced in these patients
and that increased tubular catabolism is associated with raised NH3
excretion rate suggesting that increased tubular metabolism of filtered
proteins may have deleterious effects on the tubule.
This study evaluates the effects of reducing ammoniagenesis by oral sodium
bicarbonate supplements
(for six weeks) on proximal renal tubular protein
catabolism and tubular injury in patients with mild/moderate renal failure
and nephrotic range proteinuria. Tubular injury was evaluated by measuring
the tubulo-specific A2 isoenzyme of N-acetyl-glucose-aminidase (A2 NAG).
Bicarbonate supplementation produced the expected fall in NH3 excretion rate
(-72%) and caused a significant reduction in renal Aprotinin degradation (-
33%) and in A2 NAG excretion rate (-56%). The authors conclude that oral
bicarbonate may have a protective effect on the proximal renal tubule and
help
to delay progression of renal disease.
Comment: Although of great potential interest, these data do
not fit with the notion that patients with more pronounced acidosis (e.g.
those with interstitial nephropathies) do not have an accelerated progression
as compared with patients with other nephropathies. On the other hand,
remnant rats do not show a slower progression of renal failure after
bicarbonate supplements (Bruno Cianciaruso, M.D., University of Naples,
Italy).
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33rd Congress of the Eur Dial Transplant Assoc
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