Hydroelectrolytic equilibrium change in dialysis.

Hydroelectrolytic equilibrium alteration in dialysis patients before dialytic treatment consists in extracellular volume expansion and hyperkalemia. Extracellular volume expansion is due to salt and water retention. Because of the self-regulation phenomenon of cell volume, it is made prevalently at the expense of extracellular volume. Hyperkalemia derives not only from alimentary K+ retention but, above all, from the K+ intracellular transfer into extracellular volume for tamponage of acid load, owing to the same selfregulation of cell volume and to the reduction of Na+/K+ pump activity with a subsequent change in Ki/Ke ratio. Dialysis must reduce expanded extracellular volume without inducing osmolar changes. To do this, salt and water removal must occur by ultrafiltration. Moreover, it is necessary to define Na+ concentration in dialysate or in reinfusion solution able to undo, by diffusion, the plasmatic Na+ increase due to Donnan effect. K+ dialytic removal presents the problem of defining the K+ quantity to be removed: K+ fecal excretion is increased in the uremic patient and there is no correlation between the quantity of K+ removed and successive increase of kalemia. K+ removal occurs by diffusion according to the concentration gradient between plasma and dialysate through dialytic membrane. The reduction of kalemia determines, in its turn, diffusion fluxes according to the concentration gradient of intracellular K+ towards extracellular volume. Because the electrical membrane potential at rest (REMP) is due to K+ fluxes for passive transmembrane diffusion, the increase of these fluxes causes REMP increase. Cardiac activity expresses this change with the appearance of intradialytic arrhythmia. The use of a dialysate with K+ concentration that decreases during dialysis in line with K+ rate (variable K+) reduces the arrhythmias induced by dialysis. The quantity of K+ removed with this procedure is the same as that obtained by using a dialysate with K K+ constant concentration of 3 mEq/l, but the percentage removed from intracellular volume is lower with improvement of Ki/Ke ratio. The influence of intradialytic REMP increase linked to K+ removal also concerns the correction of metabolic acidosis: the acquired bicarbonate during dialysis increases on reducing removal K+ gradient. The Ki/Ke ratio is also dependent on Na+/K+ pump activity which, exchanging intracellular Na+ with extracellular K+, determines intracellular K+ retention and therefore its concentration gradient between intra and extracellular volume. In the uremic patient the retention of nitrogenous catabolites causes the slowing- down in ATP production in Krebs' cycle because of prevalent use of this low -efficiency energetic substrate; ATP supply to Na+/K+ pump, which is ATP-asi- dependent, is reduced and consequently so is pump activity. Thanks to nitrogenous catabolite removal, dialysis recovers the use of other major efficiency energetic substrates, such as carbohydrates and lipids, in Krebs' cycle with an increase of ATP production rate and pump activity. This hypothesis could explain the REMP reduction in end-stage uremia and its correction with dialysis.