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.
Keywords: Dialysis; Membrane potential; Nerve excitability; Potassium; Uraemic neuropathy.
Copyright © 2013 International Federation of Clinical Neurophysiology. Published by Elsevier Ireland Ltd. All rights reserved.