title: Electrophysiological response to dialysis: the role of dialysate potassium content and profiling.
abstract: The task of dialysis therapy is, amongst other things, to remove excess potassium (K+) from the body. The need to achieve an adequate K+ removal with the risk of cardiac arrhythmias due to sudden intra-extracellular K+ gradient advises the distribution of the removal throughout the dialysis session instead of just in the first half. The aim of the study was to investigate the electrical behavior of two different K+ removal rates on myocardial cells (risk of arrhythmia and ECG alterations). Constant acetate-free biofiltration (AFB) and profiled K+ (decreasing during the treatment) AFB (AFBK) were used in a patient sample to understand, first of all, the effect on premature ventricular contraction (PVC) and on repolarization indices [QT dispersion (QTd) and principal component analysis (PCA)]. The study was divided into two phases: phase 1 was a pilot study to evaluate K+ kinetics and to test the effect on the electrophysiological response of the two procedures. The second phase was set up as an extended cross-over multicenter trial in patient subsets prone to arrhythmias during dialysis. Phase 1: PVC increased during both AFB and AFBK but less in the latter in the middle of dialysis (298 in AFB vs. 200 in AFBK). The PVC/h in a subset of arrhythmic patients was 404 +/- 145 in AFB and 309 +/- 116 in AFBK (p = 0.0028). QT interval (QTc) prolongation was less pronounced in AFBK than in AFB. Phase 2: The PVC again increased in both AFB and AFBK but less in the latter mid-way through dialysis (79 +/- 19 AFB vs. 53 +/- 13 AFBK). Moreover, in the most arrhythmic patients the benefit accruing from the smooth K+ removal rate was more pronounced (103 +/- 19 in AFB vs. 78 +/- 13 in AFBK).
  
  
  CONCLUSIONS
  It is not the K+ dialysis removal alone that can be destabilizing from an electrophysiological standpoint, but rather its removal dynamics. This is all the more evident in patients with arrhythmias who benefit from the K+ profiling during their dialysis treatment.
authors.affiliation: Malpighi Nephrology Division, Policlinico S. Orsola-Malpighi, Bologna, Italy.
authors.forename: A
authors.initials: A
authors.lastname: Santoro
authors.forename: E
authors.initials: E
authors.lastname: Mancini
authors.forename: R
authors.initials: R
authors.lastname: Gaggi
authors.forename: S
authors.initials: S
authors.lastname: Cavalcanti
authors.forename: S
authors.initials: S
authors.lastname: Severi
authors.forename: L
authors.initials: L
authors.lastname: Cagnoli
authors.forename: F
authors.initials: F
authors.lastname: Badiali
authors.forename: B
authors.initials: B
authors.lastname: Perrone
authors.forename: G
authors.initials: G
authors.lastname: London
authors.forename: H
authors.initials: H
authors.lastname: Fessy
authors.forename: L
authors.initials: L
authors.lastname: Mercadal
authors.forename: F
authors.initials: F
authors.lastname: Grandi
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001145:Arrhythmias, Cardiac / Q000209:etiology; D018592:Cross-Over Studies; D015314:Dialysis Solutions / Q000737:chemistry*; D004198:Disease Susceptibility; D004305:Dose-Response Relationship, Drug; D004562:Electrocardiography; D004594:Electrophysiology; D006801:Humans; D007674:Kidney Diseases / Q000503:physiopathology* / Q000628:therapy*; D007700:Kinetics; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism; D010865:Pilot Projects; D011188:Potassium / Q000032:analysis* / Q000378:metabolism*; D006435:Renal Dialysis / Q000009:adverse effects / Q000379:methods*; D018879:Ventricular Premature Complexes / Q000503:physiopathology
chemical_list: D015314:Dialysis Solutions; D011188:Potassium