Vitamin b6 and hemodialysis: The impact of high-flux/high-efficiency dialysis and review of the literature

Kasama, Richard; Koch, Terry; Canals-Navas, Carmen; Pitone, Joseph M.

doi:10.1016/s0272-6386(96)90103-1

Cited by 62 publications

(48 citation statements)

References 12 publications

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“…This is in keeping with previous observations [15, 16]which indicated that a substantial percentage of the hemodialysis population probably receives enough pyridoxine in the diet which presumably overrides the above-mentioned proved and theoretical factors acting to deplete pyridoxine body stores. Our study was initiated to examine hematologic response to pyridoxine administration in a segment of hemodialysis patients with apparently normal baseline pyridoxine status.…”

Section: Discussionsupporting

confidence: 92%

“…Previous results assessing body pyridoxine status of patients on chronic hemodialysis were contradictory. Some [14, 15]reported that pyridoxine deficiency is not infrequent, while others were unable to find evidence for such deficiency [3, 16, 17]. In some studies, various disorders found in patients with chronic renal failure or on chronic hemodialysis were attributed to pyridoxine deficiency.…”

Section: Discussionmentioning

confidence: 99%

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Vitamin B6 Therapy Does Not Improve Hematocrit in Hemodialysis Patients Supplemented with Iron and Erythropoietin

Weissgarten¹,

Modai²,

Oz³

et al. 2001

Nephron

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Background/Aim: Pyridoxine deficiency may be the cause of failure to respond appropriately to iron and erythropoietin (EPO) administration in hemodialysis patients. Method: We studied 36 patients on chronic hemodialysis amply supplemented with iron and EPO, who failed to raise hematocrit levels >33%. Patients were divided into three equal groups and evaluated for 6 months as follows: Group A – no additional therapy; group B – supplemented with oral pyridoxine 50 mg/day, and group C received 100 mg/day pyridoxine orally. Results: In all our patients, erythrocyte pyridoxine levels were initially within reference range for a healthy population and did not vary significantly during the study period. Likewise, ferritin levels and iron saturation values remained normal and constant. Hemoglobin and/or hematocrit levels remained practically unchanged in all three groups. Conclusions: The results indicate that in hemodialysis patients with normal pyridoxine status who, despite appropriate supplementation of iron and EPO, fail to reach optimal hematocrit levels, additional pyridoxine treatment does not produce any hematocrit elevation.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 99%

Vitamin B6 Therapy Does Not Improve Hematocrit in Hemodialysis Patients Supplemented with Iron and Erythropoietin

Weissgarten¹,

Modai²,

Oz³

et al. 2001

Nephron

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“…The role of high-flux dialyzers on Hcy clearance has remained inconsistent [27, 28]. However, the introduction of such synthetic membranes may allow a larger loss of small-molecular-weight vitamins as compared to the low-flux dialyzers [29]. In addition, in some studies abnormal methionine loads were noted in ESRD patients [3, 30].…”

Section: Discussionmentioning

confidence: 99%

Polymorphism in Methylenetetrahydrofolate Reductase Gene: Its Impact on Plasma Homocysteine Levels and Carotid Atherosclerosis in ESRD Patients Receiving Hemodialysis

Lim

Hung

Wei³

2001

Nephron

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The methylenetetrahydrofolate reductase (MTHFR) gene polymorphism has been shown to be associated with cardiovascular disease in healthy subjects as well as in patients with end-stage renal disease (ESRD). In this study, we examined the allelic frequency and genotype distribution of the MTHFR gene in 151 Chinese ESRD patients receiving hemodialysis and 135 healthy controls. In addition, we investigated the relationship between the MTHFR gene polymorphism and the plasma homocysteine (Hcy) level as well as the intima-media thickness of common carotid artery (CC-IMT) in these patients. The allelic frequency of the MTHFR gene with the C677T mutation in ESRD patients was 24.5% and that in healthy controls was 23%. Mean plasma Hcy level of the ESRD patients (23.1 ± 7.4 µmol/l) was significantly higher than that of the controls (10.1 ± 5.0 µmol/l), but did not correlate with vitamin B₆ and vitamin B₁₂ status. Moreover, the extent of hyperhomocysteinemia was genetically affected by the C677T mutation of the MTHFR gene. The plasma Hcy levels for the patients with the CC, CT and TT genotypes of the MTHFR gene were 22.3 ± 6.8, 22.8 ± 7.3, and 28.3 ± 2.8 µmol/l, respectively. In addition, we found that the patients bearing the TT genotype had the highest CC-IMT (0.93 ± 0.07 mm), whereas the lowest values (0.79 ± 0.13 mm) were observed in those who had the CC genotype. One-way ANOVA showed that the CC-IMT in the patients with the TT genotype was significantly greater than that of the patients with the CC genotype (p < 0.05). Moreover, the mean CC-IMT of the patients carrying either TT or CT genotype of the MTHFR gene was significantly higher than that of the patients bearing the CC genotype (0.86 ± 0.14 vs. 0.79 ± 0.13 mm, p = 0.002). Multiple regression analysis, in which the change in CC-IMT was used as the dependent variables, identified age, smoking, the MTHFR genotype (CC = 0, CT = 1, TT = 2) and diabetes mellitus as the independent variables significantly associated with the increase of CC-IMT (p < 0.001). These risk factors jointly explained 43.9% of the CC-IMT variation and age explained most of the variation (R² = 0.34). We conclude that both the TT genotype and the T allele of the MTHFR gene are associated with the increase of CC-IMT in hemodialysis patients. The C677T mutation of the MTHFR gene may be an independent risk factor that predicts the development of carotid atherosclerosis in ESRD patients.

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“…These deficiencies are, however, rarely observed in dialysis patients, despite the potential for dialysate losses of these small water-soluble vitamins during both haemodialysis and peritoneal dialysis [2]. Whilst folate deficiency has been demonstrated as a potential cause for epoetin-resistant anaemia in this group [3], there is only one previous report of a dialysis patient showing resistance to epoetin therapy with associated megaloblastic changes and low serum B 12 levels, who subsequently responded to supplementation of vitamin B 12 [4].…”

mentioning

confidence: 99%

Correction of Epoetin-Resistant Megaloblastic Anaemia following Vitamin B12 and Folate Administration

Breen¹,

Macdougall²

1999

Nephron

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Vitamin b6 and hemodialysis: The impact of high-flux/high-efficiency dialysis and review of the literature

Cited by 62 publications

References 12 publications

Vitamin B<sub>6</sub> Therapy Does Not Improve Hematocrit in Hemodialysis Patients Supplemented with Iron and Erythropoietin

Vitamin B<sub>6</sub> Therapy Does Not Improve Hematocrit in Hemodialysis Patients Supplemented with Iron and Erythropoietin

Polymorphism in Methylenetetrahydrofolate Reductase Gene: Its Impact on Plasma Homocysteine Levels and Carotid Atherosclerosis in ESRD Patients Receiving Hemodialysis

Correction of Epoetin-Resistant Megaloblastic Anaemia following Vitamin B<sub>12</sub> and Folate Administration

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