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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Vitamin B6 (B6) is a coenzyme essential for collagen cross-linking in bone and for regulating cytokine synthesis. Although B6 deficiency has been frequently reported in chronic kidney disease (CKD), its mechanism remains unclear. We re-evaluated our previously unassessed data from studies on B-vitamin metabolism in CKD to investigate the potential mechanisms of B6 deficiency.
We re-analyzed data from a study in which hemodialysis (HD) patients were randomly assigned to receive either B6 (60 mg/day orally), methylcobalamin (500 μg intravenously at each dialysis), and folic acid (15 mg/day orally) (Group A: n=5, female/male=2/3, age: 59.3 ± 18.2 y), or methylcobalamin and folic acid without B6 (Group B: n=5, female/male=2/3, age: 48.3 ± 19.4 y). Plasma concentrations of homocysteine (Hcy), cysteine (Cys), and B6 were measured before and after treatment. Healthy volunteers served as controls (Group C: n=5, female/male=1/4, age: 32.3 ± 5.8 y). We also re-evaluated results from a separate study measuring plasma S-adenosylmethionine (SAM) levels in 40 HD patients (age: 61.9 ± 12.3 y).
Baseline B6 levels (ng/mL) were significantly lower in HD patients than in controls (2.9 ± 1.1 vs 20.1 ± 10.8, p<0.01). Baseline Hcy levels (nmol/mL) were significantly higher in HD patients (A: 21.1 ± 8.9, B: 20.5 ± 6.9) than in controls (8.8 ± 2.0, p<0.01), but normalized after treatment in both groups (A: 8.2 ± 2.3, B: 8.2 ± 1.7). Cys levels (nmol/mL) were elevated in HD patients (A: 310.6 ± 34.1, B: 369.1 ± 104.3) compared with controls (240.2 ± 15.6, p<0.01) and remained elevated after treatment, with no effect of B6 supplementation (A: 327.3 ± 49.7, B: 332.2 ± 76.1). Plasma SAM in 40 HD patients was markedly elevated (373.6 ± 119.7 nmol/L) compared with reference values. In CKD, B6 levels were markedly reduced. Despite the normalization of Hcy, Cys remained elevated, suggesting persistent activation of the B6-dependent transsulfuration pathway by an unknown mechanism, leading to B6 depletion. SAM, which accumulated in HD patients, is known to activate the transsulfuration pathway, but is also an intermediate of Hcy synthesis and may accumulate due to Hcy metabolic abnormalities.
Our findings suggest that persistent activation of the transsulfuration pathway is a key cause of B6 deficiency in CKD, with SAM accumulation being a likely driver of this activation. Impaired Hcy metabolism may underlie this pathophysiology.
