Effect of chloride dialysate concentration on metabolic acidosis in aintenance hemodialysis patients

F.O Marques,E.F Daher,A.B Libório

doi:10.1590/s0100-879x2010007500094

Abstract

Hyperchloremia is one of the multiple etiologies of metabolic acidosis in hemodialysis (HD) patients. The aim of the present study was to determine the influence of chloride dialysate on metabolic acidosis control in this population. We enrolled 30 patients in maintenance HD program with a standard base excess (SBE) ≤2 mEq/L and urine output of less than 100 mL/24 h. The patients underwent dialysis three times per week with a chloride dialysate concentration of 111 mEq/L for 4 weeks, and thereafter with a chloride dialysate concentration of 107 mEq/L for the next 4 weeks. Arterial blood was drawn immediately before the second dialysis session of the week at the end of each phase, and the Stewart physicochemical approach was applied. The strong ion gap (SIG) decreased (from 7.5 ± 2.0 to 6.2 ± 1.9 mEq/L, P = 0.006) and the standard base excess (SBE) increased after the use of 107 mEq/L chloride dialysate (from -6.64 ± 1.7 to -4.73 ± 1.9 mEq/L, P < 0.0001). ∆SBE was inversely correlated with ∆SIG during the phases of the study (Pearson r = -0.684, P < 0.0001) and there was no correlation with ∆chloride. When we applied the Stewart model, we demonstrated that the lower concentration of chloride dialysate interfered with the control of metabolic acidosis in HD patients, surprisingly, through the effect on unmeasured anions.

Highlights

Metabolic acidosis is a common feature of chronic kidney disease (CKD), worsening progressively with renal function decline [1]
It was difficult to demonstrate which factors affected by dialysis had the most influence on acidosis
Regardless of bicarbonate diffusion has been the center of acidosis correction, it is necessary to remove the anions resulting from metabolism, while bicarbonate is being replaced

Summary

Introduction

Metabolic acidosis is a common feature of chronic kidney disease (CKD), worsening progressively with renal function decline [1]. One-third to one-half of patients on maintenance hemodialysis (HD) have a predialysis serum bicarbonate level below 22 mEq/L, in contrast to a serum level at or above 22 mEq/L as suggested by the K/DOQI statement guidelines [2]. In these patients, metabolic acidosis has detrimental effects such as renal osteodystrophy, inflammation and impaired nutritional status [3,4,5,6,7]. Serum pH is determined by three independent variables: partial carbon dioxide tension (pCO2), the difference in charge between strong cations and strong anions (“strong ion difference” or SID) in plasma, and the total plasma concentration of nonvolatile weak acid buffers, mainly albumin and inorganic phosphate, with bicarbonate being a dependent variable [8,9]

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Methods

Conclusion