Background: Advanced glycation end products (AGE) accumulate in uremia and
represent an important etiopathogenetic cause of morbidity in dialyzed pati
ents. Conventional hemodialysis treatment seems to be ineffective in loweri
ng AGE levels. We wished to investigate whether daily hemodialysis (DHD), a
treatment that seems to result in better clinical condition in end-stage r
enal disease patients, is effective in the reduction of these compounds.
Methods: We evaluated 10 non-diabetic patients on standard hemodialysis (SH
D = 3 x 4h/week) for more than 6 months by a crossover study. These patient
s were assigned randomly to 6 months of DHD (6 x 2h/week) or 6 months of SH
D. Then, they were switched to 6 months of the alternative treatment. At th
e end of these two periods, we studied pentosidine-like AGE compounds by me
asuring the total fluorescence at a wavelength characteristic for these sub
stances: Ex: 335nm / Em:385nm; we also measured protein-linked pentosidine
at the same time points. Finally we determined the AGE-related total fluore
scence in the deproteinized serum of 13 uremic patients on peritoneal dialy
sis (CAPD) and of 10 healthy controls.
Results: Pre-HD AGE-related total fluorescence obtained after 6 months of D
HD was significantly lower than that obtained with standard HD (DHD = 201.3
+/- 36.4 AU/ml vs. SHD = 267.5 +/- 141.4 AU/ml, p=0.03). The extraction ra
te per minute of dialysis was slightly, but not significantly higher during
DHD than SHD (0.29 +/- 0.11% vs. 0.23 +/- 0.04, p = 0.07). AGE-related tot
al fluorescence pre-HD values in patients treated by SHD and DHD were about
20-fold higher than in control subjects. They did not differ from CAPD pat
ients. The pre-dialysis level of protein-linked pentosidine was significant
ly lower in DHD than in SHD (DHD = 16.12 +/- 4.71 pmol/mg protein, SHD = 22
.64 +/- 6.86 pmol/mg protein, p < 0.01).
Conclusions: DHD showed a reduction in AGE-related total fluorescence, alth
ough the mean value remained higher than in control subjects. DHD is also a
ccompanied by a decrease in protein-linked pentosidine.