CONTRIBUTION OF DIALYSIS TO ENDOGENOUS OXALATE PRODUCTION IN PATIENTSWITH CHRONIC-RENAL-FAILURE

We tested the possibility that the buffering agents in dialysis bath f luid might contribute to increased endogenous oxalate production in di alyzed patients. Using stable isotope dilution mass spectrometry, we o btained oxalate production rates and pool sizes directly for 10 patien ts in chronic renal failure, 5 of whom were undergoing continuous ambu latory peritoneal dialysis (lactate-buffered fluid). All peritoneal di alysis patients had either increased oxalate production rates or expan ded oxalate pools when compared with undialyzed patients in renal fail ure. From a further four patients receiving maintenance hemodialysis w e took blood samples immediately before and after three consecutive di alysis sessions in which the bath-fluid buffering agent (bicarbonate o r acetate) was alternated; we analyzed these samples for oxalate and k ey precursors by capillary gas chromatography. Plasma glycine and seri ne concentrations remained within the physiological range. Glycolate a nd oxalate concentrations decreased, but the oxalate remained above no rmal after dialysis. All changes were independent of the bath-fluid bu ffering agent. We suggest that dialysis might stimulate the formation of oxalate by removing product inhibition of a late catabolic step.