Automated individualization of dialysate sodium concentration reduces intradialytic plasma sodium changes in hemodialysis.

In standard care, hemodialysis patients are often treated with a center-specific fixed dialysate sodium concentration, potentially resulting in diffusive sodium changes for patients with plasma sodium concentrations below or above this level. While diffusive sodium load may be associated with thirst and higher interdialytic weight gain, excessive diffusive sodium removal may cause intradialytic symptoms. In contrast, the new hemodialysis machine option "Na control" provides automated individualization of dialysate sodium during treatment with the aim to reduce such intradialytic sodium changes without the need to determine the plasma sodium concentration. This proof-of-principle study on sodium control was designed as a monocentric randomized controlled crossover trial: 32 patients with residual diuresis of ≤1000 mL/day were enrolled to be treated by high-volume post-dilution hemodiafiltration (HDF) for 2 weeks each with "Na control" (individually and automatically adjusted dialysate sodium concentration) versus "standard fixed Na" (fixed dialysate sodium 138 mmol/L), in randomized order. Pre- and post-dialytic plasma sodium concentrations were determined at bedside by direct potentiometry. The study hypothesis consisted of 2 components: the mean plasma sodium change between the start and end of the treatment being within ±1.0 mmol/L for sodium-controlled treatments, and a lower variability of the plasma sodium changes for "Na control" than for "standard fixed Na" treatments. Three hundred seventy-two treatments of 31 adult chronic hemodialysis patients (intention-to-treat population) were analyzed. The estimate for the mean plasma sodium change was -0.53 mmol/L (95% confidence interval: [-1.04; -0.02] mmol/L) for "Na control" treatments and -0.95 mmol/L (95% CI: [-1.76; -0.15] mmol/L) for "standard fixed Na" treatments. The standard deviation of the plasma sodium changes was 1.39 mmol/L for "Na control" versus 2.19 mmol/L for "standard fixed Na" treatments (P = 0.0004). Whereas the 95% CI for the estimate for the mean plasma sodium change during "Na control" treatments marginally overlapped the lower border of the predefined margin ±1.0 mmol/L, the variability of intradialytic plasma sodium changes was lower during "Na control" versus "standard fixed Na" treatments. Thus, automated dialysate sodium individualization by "Na control" approaches isonatremic dialysis in the clinical setting.

Acid-base disorders associated with serum electrolyte patterns in patients on hemodiafiltration.

BACKGROUND: Metabolic acidosis (MAC) is a common aspect of dialysis-dependent patients. It is definitely caused by acid retention; however, the influence of other plasma ions is unclear. Understanding the mechanism of MAC and its correction is important when choosing the dialysis solution. Therefore, we assessed the relationship between intradialytic change of acid-base status and serum electrolytes. METHODS: We studied 68 patients on post-dilution hemodiafiltration, using dialysate bicarbonate concentration 32mmol/L. The acid-base disorders were evaluated by the traditional Siggaard-Anderson and modern Stewart approaches. RESULTS: The mean pre-dialysis pH was 7.38, standard base excess (SBE) -1.5, undetermined anions (UA(-)) 7.5, sodium-chloride difference (Diff(NaCl)) 36.2mmol/L. MAC was present in 34% of patients, of which 83% had an increased UA(-) as a major cause of MAC. The mean nPCR was 0.99g/kg/day and correlated negatively with SBE. After dialysis, metabolic alkalosis predominated in 81%. The mean post-dialysis pH was 7.45, SBE 4, UA(-) 2.6, Diff(NaCl) 36.9mmol/L. ΔSBE significantly correlated with ΔUA(-), but not with ΔDiff(NaCl) or ΔCl(-). CONCLUSIONS: MAC in patients on hemodiafiltration is mainly caused by acid retention and is associated with higher protein intake. We did not prove the effect of sodium or chloride on acid-base balance. Even though we used a relatively low concentration of dialysate bicarbonate, we recorded a high proportion of post-dialysis alkalosis caused by the excessive decrease of undetermined anions, which had been completely replaced by bicarbonate and indicated the elimination of undesirable anions, as well as of normal endogenous anions.

Determination of dialysis dose: a clinical comparison of methods.

BACKGROUND: Guidelines recommend regular measurements of the delivered hemodialysis dose Kt/V. Nowadays, automatic non-invasive online measurements are available as alternatives to the conventional method with blood sampling, laboratory analysis, and calculation. METHODS: In a prospective clinical trial, three different methods determining dialysis dose were simultaneously applied: Kt/V(Dau) (conventional method with Daugirdas' formula), Kt/V(OCM) [online clearance measurement (OCM) with urea distribution volume V based on anthropometric estimate], and Kt/V(BCM) [OCM measurement with V measured by bioimpedance analysis (Body Composition Monitor)]. RESULTS: 1,076 hemodialysis patients were analyzed. The dialysis dose was measured as Kt/V(Dau) = 1.74 ± 0.45, Kt/V(OCM) = 1.47 ± 0.34, and Kt/V(BCM) = 1.65 ± 0.42. The difference between Kt/V(OCM) and Kt/V(BCM) was due to the difference between anthropometric estimated V(Watson) and measured V(BCM). Compared to Kt/V(Dau), Kt/V(OCM) was 15% lower and Kt/V(BCM) 5% lower. Kt/V(Dau) was incidentally prone to falsely high values due to operative errors, whereas in these cases OCM-based measurements Kt/V(OCM) and Kt/V(BCM) delivered realistic values. CONCLUSIONS: The automated OCM Kt/V(OCM) with anthropometric estimation of urea distribution volume was the easiest method to use, but Kt/V(BCM) with measured urea distribution volume was closer to the conventional method.