Niwa T, Miyazaki T, Momoi T, Ogawa H, Saito A, Maeda K
3-deoxyglucosone accumulating in uremic serum modified beta-2-
microglobulin with age as observed in dialysis related
amyloidosis
33rd Congress of the Eur Dial Transplant Assoc
Nephrol Dial Transplant
(Jun) 11:A232 1996
Advanced glycation end products (AGEs) have been demonstrated into
amyloid deposits in dialysis-related amyloidosis. 3-deoxyglucosone (3
DG) is a potent protein-crosslinking intermediate of the Maillard
reaction which may modify beta2 microglobulin amyloid (beta2-m).
Serum 3 DG was markedly increased in uremic patients on
conservative treatment as well as in HD patients. The serum
concentration of 3-DG decreased after hemodialysis (- 67%) but
remained significantly higher than in normal subjects. Incubation of
beta2-m with 3-DG at 37 C emitted fluorescence characteristic
for AGE, and caused dimer formation of beta2-m. The AGE-modified
dimer of beta2-m could be extracted from the amyloid tissue of a
patient with dialysis related amyloid.3-deoxyglucosone showed more
intense and faster reactivity with beta2-microglobulin to form AGE and dimer
as compared to glucose. Interestingly, aminoguanidine suppressed the
AGE and dimer formation of beta2-microglobulin induced by 3DG.
Comment: Accumulation of 3-deoxyglucosone in uremic
patients is likely involved in the pathogenesis
of beta 2-microglobulin-amyloid in these patients (Carlo Basile,
M.D., Taranta, Italy).
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33rd Congress of the Eur Dial Transplant Assoc
CRF by organ system :
Joint disease, beta-2 microglobulin