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

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• 作者：Ria Arnold ; Bruce A. Pussell ; James Howells ; Virginija Grinius ; Matthew C. Kiernan ; Cindy S.-Y. Lin ; Arun V. Krishnan
• 关键词：Dialysis ; Potassium ; Membrane potential ; Nerve excitability ; Uraemic neuropathy
• 刊名：Clinical Neurophysiology
• 出版年：January, 2014
• 年：2014
• 卷：125
• 期：1
• 页码：179-185
• 全文大小：838 K

文摘

class="h4">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).

class="h4">Methods

Median motor nerve excitability studies were undertaken in four haemodialysis patients during a modified dialysis session. The serum K⁺ level was 鈥渃lamped鈥?(fixed) for the first 3 h 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.

class="h4">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.

class="h4">Conclusions

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

class="h4">Significance

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