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在终末期肾病中,高钾血症与轴突功能障碍之间存在因果关系的证据。

Evidence for a causal relationship between hyperkalaemia and axonal dysfunction in end-stage kidney disease.

机构信息

Translational Neuroscience Facility, School of Medical Sciences, University of New South Wales, Sydney, Australia.

Department of Nephrology, Prince of Wales Hospital Randwick, Sydney, Australia; Prince of Wales Clinical School, University of New South Wales, Sydney, Australia.

出版信息

Clin Neurophysiol. 2014 Jan;125(1):179-85. doi: 10.1016/j.clinph.2013.06.022. Epub 2013 Jul 16.

DOI:10.1016/j.clinph.2013.06.022
PMID:23867066
Abstract

OBJECTIVE

Potassium (K(+)) has been implicated as a factor in the development of uraemic neuropathy. This study was undertaken to investigate whether hyperkalaemia plays a causal role in axonal dysfunction in end-stage kidney disease (ESKD).

METHODS

Median motor nerve excitability studies were undertaken in four haemodialysis patients during a modified dialysis session. The serum K(+) level was "clamped" (fixed) for the first 3h of dialysis, whilst allowing all other solutes to be removed, this was followed by dialysis against low dialysate K(+) for a further 4 h. Blood chemistry and nerve excitability studies were undertaken prior to, during and following dialysis. Results were compared to results from the same patients during routine dialysis sessions.

RESULTS

All patients demonstrated significant nerve excitability abnormalities reflective of nerve membrane depolarization in pre-dialysis recordings (p<0.01). After the 3 h clamp period, serum K(+) remained elevated (5.0 mmol/L) and nerve excitability remained highly abnormal, despite the significant clearance of other uraemic toxins. In contrast, studies undertaken during routine dialysis sessions demonstrated significant improvement in both serum K(+) and nerve function after 3 h.

CONCLUSIONS

The current study has established a causal relationship between serum K(+) and axonal membrane depolarization in haemodialysis patients.

SIGNIFICANCE

From a clinical perspective, strict K(+) control may help improve nerve function in ESKD.

摘要

目的

钾(K(+))被认为是尿毒症性神经病发展的一个因素。本研究旨在探讨高钾血症是否在终末期肾病(ESKD)中轴突功能障碍中起因果作用。

方法

在改良透析期间,对 4 名血液透析患者进行了中位运动神经兴奋性研究。在透析的前 3 小时“固定”(固定)血清 K(+)水平,同时允许去除所有其他溶质,然后用低透析液 K(+)进行另外 4 小时透析。在透析前、透析中和透析后进行血液化学和神经兴奋性研究。将结果与相同患者在常规透析期间的结果进行比较。

结果

所有患者在透析前记录中均表现出明显的神经兴奋性异常,反映出神经膜去极化(p<0.01)。在 3 小时夹闭期后,血清 K(+)仍升高(5.0 mmol/L),神经兴奋性仍高度异常,尽管其他尿毒症毒素的清除显著。相比之下,在常规透析期间进行的研究表明,在 3 小时后,血清 K(+)和神经功能均显著改善。

结论

本研究确立了血清 K(+)与血液透析患者轴突膜去极化之间的因果关系。

意义

从临床角度来看,严格的 K(+)控制可能有助于改善 ESKD 中的神经功能。

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