B. Redaelli et al., EFFECT OF A NEW MODEL OF HEMODIALYSIS POTASSIUM REMOVAL ON THE CONTROL OF VENTRICULAR ARRHYTHMIAS, Kidney international, 50(2), 1996, pp. 609-617
The primary aim of this multicenter, prospective, randomized cross-ove
r study was to clarify whether a new model of hemodialysis (HD) potass
ium (K) removal using a decreasing intra-HD dialysate K concentration
and a constant plasma-dialysate K gradient (treatment B) is capable of
reducing the arrhythmogenic effect of standard HD, which has a consta
nt dialysate K concentration and decreasing plasma-dialysate K gradien
t (treatment A). The secondary aim was to verify whether this new mode
l is clinically safe. In treatment B, the initial dialysate K concentr
ation had to be 1.5 mEq/liter less than the plasma K concentration, an
d exponentially decrease to 2.5 mEq/liter at the end of HD. Forty-two
chronic HD patients with an increase in premature ventricular complexe
s (PVC) during dialysis were enrolled from 18 participating centers, a
nd randomly assigned to either sequence 1 (ABA) or sequence 2 (BAB). A
pool of 333 of 378 expected ECG Holter recordings were checked for si
gnal quality; 269 (71%) from 36 patients (86%) had a satisfactory sign
al quality and 108 were selected for analysis (1 per patient per perio
d). There was a difference in the natural logarithm of the increase in
PVC/hr and PVC couplets/hr during HD between treatments A and B (1.70
+/- 1.59 vs. 1.09 +/- 1.76 and 0.94 +/- 0.86 vs. 0.64 +/- 1.01, a red
uction of 36% and 32%, P = 0.011 and 0.047, respectively) without any
carry over effect (P = 0.61 and 0.24, respectively). The fact that thi
s decrease of one third is due to a lower plasma-dialysate K gradient
is supported by the observation that it was more evident during the fi
rst than the last two hours of HD (a reduction in the natural logarith
m of the increase in PVC/hr and PVC couplets/hr of 60% and 60%, P 0.00
2 and 0.009, vs. 26% and 17%, P = 0.098 and 0.332, respectively): the
initial plasma-dialysate K gradient was 2.3 times lower during treatme
nt B than during treatment A, without adversely affecting pre-HD plasm
a K levels. These results could have a considerably clinical impact no
t only because of the possibility of physiologically decreasing the ar
rhythmogenic effect of HD, but also because this effect can be conside
red a ''marker'' of the electrophysiological derangement induced by th
e administration of standard HD three times a week for years (''electr
ic disequilibrium syndrome'').