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Brain Advance Access published online on June 9, 2005
Brain, doi:10.1093/brain/awh558
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© The Author (2005). Published by Oxford University Press on behalf of the Guarantors of Brain. All rights reserved. For Permissions, please email: journals.permissions@oupjournals.org
Received February 24, 2005
Revised April 10, 2005
Accepted May 12, 2005

Article

Altered motor nerve excitability in end-stage kidney disease

Arun V. KRISHNAN 1, RICHARD K. S. PHOON 2, BRUCE A. PUSSELL 2, JOHN A. CHARLESWORTH 2, HUGH BOSTOCK 3, and MATTHEW C. KIERNAN 1*

1 Institute of Neurological Sciences, Prince of Wales Hospital, Randwick, Sydney, Australia; Prince of Wales Medical Research Institute and Prince of Wales Clinical School, University of New South Wales, Randwick, Sydney, Australia
2 Department of Nephrology, Prince of Wales Hospital, Randwick, Sydney, Australia
3 Sobell Department of Neurophysiology, Institute of Neurology, Queen Square, London, UK

* To whom correspondence should be addressed.
MATTHEW C. KIERNAN, E-mail: M.kiernan{at}unsw.edu.au


  Abstract

Although multiple toxins have been implicated in the development of uraemic neuropathy, no causative agent has been identified. In the present study, the excitability properties of lower limb motor nerves in patients with end-stage kidney disease treated with haemodialysis were measured before, during and after a standard 5 h haemodialysis session, in an attempt to explore the pathophysiology of uraemic neuropathy. Compound muscle action potentials were recorded from tibialis anterior and extensor digitorum brevis, following stimulation of the common peroneal nerve in 14 patients. Measures of excitability were assessed in relation to changes in serum levels of potential neurotoxins, including potassium, calcium, urea, uric acid, parathyroid hormone and {beta}-2-microglobulin. Before dialysis, measures of nerve excitability were significantly abnormal in the patient group for axons innervating tibialis anterior and extensor digitorum brevis, consistent with axonal depolarization: refractoriness was increased and superexcitability and depolarizing threshold electrotonus were reduced. Pre-dialysis excitability abnormalities were strongly correlated with serum K+. Correlation was also noted between the severity of symptoms and excitability abnormalities. Haemodialysis normalized the majority of nerve excitability parameters. In conclusion, lower limb motor axons in uraemic patients are depolarized before dialysis. The correlation between serum K+ and excitability measures indicates that hyperkalaemia is primarily responsible for uraemic depolarization, and a likely contributing factor to the development of neuropathy.

Keywords: membrane potential; nerve excitability; potassium; threshold electrotonus; uraemic neuropathy.
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