Literature DB >> 16543542

Sensory nerve excitability and neuropathy in end stage kidney disease.

A V Krishnan1, R K S Phoon, B A Pussell, J A Charlesworth, M C Kiernan.   

Abstract

BACKGROUND: Peripheral neuropathy is present in 65% of patients with end stage kidney disease (ESKD) starting dialysis. Studies of membrane potential and axonal ion channel function may help explain the pathophysiology.
OBJECTIVES: To follow changes in median sensory axon excitability in patients with ESKD treated with haemodialysis, and correlate them with clinical rating scales and serum levels of potential neurotoxins.
METHODS: Sensory nerve action potentials were recorded from the second digit following stimulation of the median nerve in 12 ESKD patients. Stimulus-response behaviour using two stimulus durations, threshold electrotonus to 100 ms polarising currents, a current-threshold relation, and recovery of excitability following supramaximal stimulation were recorded before, during, and after haemodialysis. Serum concentrations of potential neurotoxins were measured.
RESULTS: Before dialysis, there were changes in nerve excitability consistent with axonal depolarisation: refractoriness was increased; superexcitability and depolarising threshold electrotonus were reduced. Following dialysis there were improvements in all indices, with correlations between excitability abnormalities and serum potassium measurements. Neuropathic symptoms correlated with excitability changes.
CONCLUSIONS: Nerves are depolarised before haemodialysis in ESKD patients. The correlation of excitability abnormalities with potassium indicates that the achievement of normokalaemia should be a priority in treating such patients.

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Year:  2006        PMID: 16543542      PMCID: PMC2077495          DOI: 10.1136/jnnp.2005.079988

Source DB:  PubMed          Journal:  J Neurol Neurosurg Psychiatry        ISSN: 0022-3050            Impact factor:   10.154


  23 in total

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Authors:  M C Kiernan; C S Lin; K V Andersen; N M Murray; H Bostock
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2.  Nerve excitability changes in chronic renal failure indicate membrane depolarization due to hyperkalaemia.

Authors:  Matthew C Kiernan; R Jon L Walters; Kjeld V Andersen; David Taube; Nicholas M F Murray; Hugh Bostock
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4.  Nerve excitability properties in lower-limb motor axons: evidence for a length-dependent gradient.

Authors:  Arun V Krishnan; Cindy S-Y Lin; Matthew C Kiernan
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Review 5.  Has potassium been prematurely discarded as a contributing factor to the development of uraemic neuropathy?

Authors:  Hugh Bostock; Richard J L Walters; Kjeld V Andersen; Nicholas M F Murray; David Taube; Matthew C Kiernan
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6.  Slow actions of hyperpolarization on sodium channels in the membrane of myelinated nerve.

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7.  Sensory conduction of the sural nerve in polyneuropathy.

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  7 in total

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4.  Shear Wave Elastography in the Diagnosis of Peripheral Neuropathy in Patients With Chronic Kidney Disease Stage 5.

Authors:  Xuan Li; Haoqi Sun; Zhaoguang Zhang; Jing Liu; Huiying Xu; Lin Ma; Haibo Zhang; Jialin Li; Qian Luo; Xiangming Wang; Min Guo; Zhentao Guo; Xuexun Chen
Journal:  Front Endocrinol (Lausanne)       Date:  2022-06-23       Impact factor: 6.055

5.  Effects of hemodiafiltration and high flux hemodialysis on nerve excitability in end-stage kidney disease.

Authors:  Ria Arnold; Bruce A Pussell; Timothy J Pianta; Virginija Grinius; Cindy S-Y Lin; Matthew C Kiernan; James Howells; Meg J Jardine; Arun V Krishnan
Journal:  PLoS One       Date:  2013-03-11       Impact factor: 3.240

6.  Potassium and the excitability properties of normal human motor axons in vivo.

Authors:  Delphine Boërio; Hugh Bostock; Romana Spescha; Werner J Z'Graggen
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7.  The role of urea in neuronal degeneration and sensitization: An in vitro model of uremic neuropathy.

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  7 in total

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