To examine erythrocyte band III transport protein (SLC4A1), erythrocyte oxalate flux, and plasmatic, cellular, and urine oxalate concentrations and blood gas analyses in calcium oxalate monohydrate stone–forming patients (COM) in comparison with normal controls (NC).

Isolated red cells from 51 NC and 25 COM cases were divided for cellular oxalate measurement and for measurement of transcellular erythrocyte oxalate flux (pH 7.48-8.24). SLC4A1 protein levels were determined by Western blot analyses. Plasmatic and urinary oxalate levels and the venous blood gas analysis were measured simultaneously.

SLC4A1 protein levels were significantly higher in COM (8.76 ± 2.12) than in NC (4.17 ± 0.61; P < .02). Cellular oxalate and venous HCO₃^- were significantly lower in COM (2.35 ± 0.26 μmol/L) and (24.06 ± 0.24 mmo/l) than in NC (4.03 ± 0.49 μmol/L; P < .05) and (24.93 ± 0.17 mmol/L; P < .01). Urinary oxalate was significantly higher in COM (0.31 ± 0.02 mmol/L) than in NC (0.25 ± 0.01 mmol/L; P < .04). The erythrocyte transmembrane oxalate flux correlated with the pH value and with the urinary oxalate in both groups (r = .25-.55; P = .01). With increased pH values, the oxalate flux showed inverse effects in both groups.

SLC4A1 associated changes of HCO₃⁻ and pH levels influenced the cellular oxalate levels and urinary oxalate clearance. Under normal conditions (pH 7.55) the oxalate efflux in COM was comparable with the acid stimulated oxalate efflux in NC. The addition of HCO₃⁻ compensated the flux of COM stone formers to the levels of normal controls.