title: Evidence for a causal relationship between hyperkalaemia and axonal dysfunction in end-stage kidney disease.
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.
  
  
  CONCLUSIONS
  From a clinical perspective, strict K(+) control may help improve nerve function in ESKD.
authors.affiliation: Translational Neuroscience Facility, School of Medical Sciences, University of New South Wales, Sydney, Australia.
authors.forename: Ria
authors.initials: R
authors.lastname: Arnold
authors.affiliation: Department of Nephrology, Prince of Wales Hospital Randwick, Sydney, Australia; Prince of Wales Clinical School, University of New South Wales, Sydney, Australia.
authors.forename: Bruce A
authors.initials: BA
authors.lastname: Pussell
authors.affiliation: Institute of Clinical Neurosciences, Royal Prince Alfred Hospital and The University of Sydney, Sydney, Australia.
authors.forename: James
authors.initials: J
authors.lastname: Howells
authors.affiliation: Department of Nephrology, Prince of Wales Hospital Randwick, Sydney, Australia.
authors.forename: Virginija
authors.initials: V
authors.lastname: Grinius
authors.affiliation: Neuroscience Research Australia, University of New South Wales, Sydney, Australia; Prince of Wales Clinical School, University of New South Wales, Sydney, Australia.
authors.forename: Matthew C
authors.initials: MC
authors.lastname: Kiernan
authors.affiliation: Translational Neuroscience Facility, School of Medical Sciences, University of New South Wales, Sydney, Australia.
authors.forename: Cindy S-Y
authors.initials: CS
authors.lastname: Lin
authors.affiliation: Translational Neuroscience Facility, School of Medical Sciences, University of New South Wales, Sydney, Australia. Electronic address: arun.krishnan@unsw.edu.au.
authors.forename: Arun V
authors.initials: AV
authors.lastname: Krishnan
mesh_terms: D001369:Axons / Q000502:physiology*; D005260:Female; D006801:Humans; D006947:Hyperkalemia / Q000150:complications / Q000503:physiopathology*; D007676:Kidney Failure, Chronic / Q000097:blood / Q000150:complications / Q000503:physiopathology*; D008297:Male; D008475:Median Nerve / Q000503:physiopathology; D010523:Peripheral Nervous System Diseases / Q000209:etiology / Q000503:physiopathology*; D011188:Potassium / Q000097:blood; D006435:Renal Dialysis / Q000009:adverse effects; D014511:Uremia / Q000150:complications
chemical_list: D011188:Potassium
keywords: Dialysis; Membrane potential; Nerve excitability; Potassium; Uraemic neuropathy