NDT Advance Access originally published online on February 19, 2004
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Nephrol Dial Transplant (2004) 19: 1054-1057
Nephrol Dial Transplant Vol. 19 No. 5 © ERA-EDTA 2004; all rights reserved
Hypothesis
Has potassium been prematurely discarded as a contributing factor to the development of uraemic neuropathy?
1Sobell Department of Neurophysiology, Institute of Neurology and 2Department of Clinical Neurophysiology, National Hospital for Neurology and Neurosurgery, London, 4Department of Renal Medicine, St Mary's Hospital, London, UK, 3Department of Clinical Neurophysiology, Glostrup Hospital, University of Copenhagen, Glostrup, Denmark, 5Prince of Wales Medical Research Institute, University of New South Wales and the Institute of Neurological Sciences, Prince of Wales Hospital, Sydney, Australia
Correspondence and offprint requests to: Dr M. C. Kiernan, Prince of Wales Medical Research Institute, Barker Street, Randwick, NSW 2031, Australia. Email: M.kiernan@unsw.edu.au
Keywords: hyperkalaemia; nerve excitability; uraemic neuropathy
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Introduction
Renal failure results in neurological dysfunction due to uraemia, the accumulation of urea and other substances in the blood [1]. This dysfunction may be manifest in the central, autonomic or peripheral nervous systems, with the incidence of peripheral neuropathy estimated to be 60–65% in patients beginning dialysis [2]. Uraemic neuropathy is a distal, symmetric, mixed sensorimotor, predominantly axonal polyneuropathy, affecting legs more than arms [2,3]. The pathological findings are similar to those in other toxic neuropathies and the mechanism of nerve damage is unknown.
The observation that most neurological complications of renal failure can be improved by adequate haemodialysis led to the conclusion that there is a dialysable uraemic neurotoxin, or toxins [4]. The further observation that haemodialysis regimes sufficient to control urea may be inadequate to prevent neuropathy led to the ‘middle molecule’ hypothesis: uraemic neurotoxins have molecular weights
The ‘potassium hypothesis’ of uraemic neurotoxicity
Potassium meets the criteria for a uraemic neurotoxin
Theoretical dependence of resting membrane potential on potassium ions
Testing the potassium hypothesis
Conclusion
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