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未透析的尿毒症患者、血液透析患者及非尿毒症肾移植患者中的磷酸吡哆醛5'-磷酸缺乏症

Pyridoxal 5'-phosphate deficiency in uremic undialyzed, hemodialyzed, and non-uremic kidney transplant patients.

作者信息

Lacour B, Parry C, Drüeke T, Touam M, Kreis H, Bailly M, Durand D

出版信息

Clin Chim Acta. 1983 Jan 24;127(2):205-15. doi: 10.1016/s0009-8981(83)80005-9.

Abstract

In this study, we have investigated plasma pyridoxal 5'-phosphate (PLP) concentrations in undialyzed and dialyzed uremic patients and in kidney transplant subjects, using an enzymatic technique with thermal deproteinization to liberate PLP from plasma proteins. The specificity of the reaction indicates no interference with pyridoxal and only 3% interference with pyridoxamine phosphate. In 17 hemodialyzed patients, a deficiency of about 50% of plasma PLP concentration is found as compared to 25 healthy subjects (22.2 +/- 2.47 vs. 48.8 +/- 3.00 nmol . l-1), as mean +/- SEM). In seven undialyzed uremic patients with end-stage renal failure, the plasma PLP concentration is also decreased (29.3 +/- 1.74 nmol . l-1). The absence of PLP in plasma ultrafiltrates demonstrates that no loss of PLP occurs due to hemodialysis. The daily oral supplementation with 250-750 mg pyridoxal induces a supraphysiological increase in plasma PLP concentration in hemodialyzed as well as in undialyzed patients. In 116 non-uremic kidney transplant subjects, the mean plasma PLP concentration was 33.8 +/- 3.50 nmol . l-1). In 65% of these patients, a marked deficit (below 20 nmol . l-1) was observed. In conclusion, uremic patients have a deficient vitamin B6 state. Its correction with pyridoxal to restore physiological plasma PLP concentration necessitates oral supplementation with lower doses that those widely used at present. In kidney transplant patients a similar plasma PLP deficiency is observed in the absence of chronic renal failure.

摘要

在本研究中,我们采用热变性酶法从血浆蛋白中释放磷酸吡哆醛(PLP),调查了未透析和透析的尿毒症患者以及肾移植受者的血浆PLP浓度。该反应的特异性表明其不受吡哆醛干扰,对磷酸吡哆胺的干扰仅为3%。与25名健康受试者相比(均值±标准误,分别为22.2±2.47与48.8±3.00 nmol·l⁻¹),17名血液透析患者的血浆PLP浓度约有50%的缺乏。7名终末期肾衰竭的未透析尿毒症患者,其血浆PLP浓度也降低(29.3±1.74 nmol·l⁻¹)。血浆超滤液中不存在PLP表明血液透析不会导致PLP丢失。每日口服250 - 750 mg吡哆醛可使血液透析患者和未透析患者的血浆PLP浓度出现超生理水平的升高。116名非尿毒症肾移植受者的血浆PLP平均浓度为33.8±3.50 nmol·l⁻¹。在这些患者中,65%观察到明显缺乏(低于20 nmol·l⁻¹)。总之,尿毒症患者存在维生素B6缺乏状态。用吡哆醛纠正以恢复生理血浆PLP浓度需要口服比目前广泛使用剂量更低的补充剂。在肾移植患者中,在无慢性肾衰竭的情况下也观察到类似的血浆PLP缺乏。

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