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

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

Author information

1
Translational Neuroscience Facility, School of Medical Sciences, University of New South Wales, Sydney, Australia.
2
Department of Nephrology, Prince of Wales Hospital Randwick, Sydney, Australia; Prince of Wales Clinical School, University of New South Wales, Sydney, Australia.
3
Institute of Clinical Neurosciences, Royal Prince Alfred Hospital and The University of Sydney, Sydney, Australia.
4
Department of Nephrology, Prince of Wales Hospital Randwick, Sydney, Australia.
5
Neuroscience Research Australia, University of New South Wales, Sydney, Australia; Prince of Wales Clinical School, University of New South Wales, Sydney, Australia.
6
Translational Neuroscience Facility, School of Medical Sciences, University of New South Wales, Sydney, Australia. Electronic address: arun.krishnan@unsw.edu.au.

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.

KEYWORDS:

Dialysis; Membrane potential; Nerve excitability; Potassium; Uraemic neuropathy

PMID:
23867066
DOI:
10.1016/j.clinph.2013.06.022
[Indexed for MEDLINE]

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