Acid-base balance in peritoneal dialysis patients: a Stewart-Fencl analysis

Evaluation of acid-base disorders using the Stewart-Fencl principle is based on assessment of independent factors: strong ion difference (SID) and the total concentration of non-volatile weak acids (Atot). This approach allows for a more detailed evaluation of the cause of acid-base imbalance than the conventional bicarbonate-centered approach based on the Henderson-Hasselbalch principle, which is a necessary yet insufficient condition to describe the state of the system. The aim of our study was to assess acid-base disorders in peritoneal dialysis (PD) patients using both of these principles.

A total of 17 patients with chronic renal failure (10 men), aged 60.7 (22-84) years, treated by PD for 25.7 (1-147) months were examined. A control group included 17 healthy volunteers (HV) (8 males), with a mean age of 42.7 (22-77) years and normal renal function. Patients were treated with a solution containing bicarbonate (25 mmol/L) and lactate (15 mmol/L) as buffers; eleven of them used, during the nighttime dwell, a solution with icodextrin buffered by lactate at a concentration of 40 mmol/L. The following equations were employed for calculations of acid-base parameters according to the Stewart-Fencl principle. The first is SID = [Na+] + [K+] + 2[Ca(2+)] + 2[Mg(2+)] - [Cl-] - [UA-], where SID is the strong ion difference and [UA-] is the concentration of undetermined anions. For practical calculation of SID, the second equation, SID = [HCO3-] + [Alb-] + [Pi-], was used, where [Alb-] and [Pi-] are the charges carried by albumin and phosphates. The third is Atot, the total concentration of weak non-volatile acids, albumin [Alb] and phosphates [Pi].

The capillary blood pH in PD group was 7.41 (7.27-7.48), [HCO3-] levels 23.7 (17.6-29.5) mmol/L, SID 36.3 (29.5-41.3) mmol/L, sodium-chloride difference 39.0 (31.0-44.0) mmol/L, [Pi] 1.60 (0.83-2.54) mmol/L, and [Alb] 39.7 (28.8-43.4) g/L (median, min-max). Bicarbonate in blood correlated positively with SID (Rho = 0.823; p < 0.001), with the sodium-chloride difference (Rho = 0.649; p < 0.01) and pH (Rho = 0.754; p < 0.001), and negatively with residual renal function (Rho = -0.517; p < 0.05). Moreover, the sodium-chloride difference was also found to correlate with SID (Rho = 0.653; p < 0.01). While the groups of PD and HV patients did not differ in median bicarbonate levels, significantly lower median value of SID were observed in PD patients, 36.3 vs. 39.3 mmol/L (p < 0.01); additionally, PD patients were shown to have significantly lower mean value of serum sodium levels, 138 vs. 141 mmol/L (p < 0.01), and serum chlorides levels, 100 vs. 104 mmol/L (p < 0.001). Despite the higher [UA-] levels in PD patients, 9.1 vs. 5.4 mmol/L (p < 0.001), this parameter was not found to correlate with bicarbonate levels.

The results suggest that the decreased bicarbonate in PD patients results from a combination of decreased sodium-chloride difference and mildly increased unmeasured anions.