1. The serum oxalate concentration rises in chronic renal failure and it is only partially eliminated by regular dialysis treatment. However, the recent literature is not conclusive on whether progressive oxalate retention and secondary oxalosis should be expected in patients on regular dialysis treatment.

2. To further investigate this, we have estimated the state of saturation with respect to calcium oxalate mono-hydrate in plasma ultrafiltrates from 28 patients on maintenance haemodialysis and eight healthy control subjects, matched for sex and age. Five patients had type I primary hyperoxaluria and histologically proven oxalosis, whereas 23 had oxalosis-unrelated renal diseases. Dialysis efficiency was quantified as the KdTd/V of urea. Samples were obtained from each patient before, immediately after and 48 h after a dialysis session. Fasting samples were obtained from the control subjects. Oxalate was determined in both plasma ultrafiltrates and the whole dialysate by ion-exchange chromatography, after a non-delayed and [14C]oxalate-recovery-controlled procedure. The state of saturation with calcium oxalate monohydrate was estimated by means of a computer system which solved the interactions among 45 complex species.

3. The fasting plasma oxalate concentration (means ± sd) in ultrafiltrates from healthy subjects was 3.8 ± 1.5 (range 1.4–5.8) μmol/l, and the state of saturation with calcium oxalate monohydrate was 0.096 ± 0.04. The 23 patients with oxalosis-unrelated chronic renal failure had a pre-dialysis plasma oxalate concentration of 49.8 ± 14.0 μmol/l, which yielded a state of saturation with calcium oxalate monohydrate of 1.0 ± 0.3; dialysis produced a steep decrease in the state of saturation with calcium oxalate monohydrate and the samples remained undersaturated at 48 h from the end of the session. The pre-dialysis oxalate concentration in plasma ultrafiltrates from patients with primary oxalosis was 170 ± 21 μmol/l, so as to exceed saturation by more than threefold. The samples remained above saturation even at the end of dialysis.

4. In 116 ultrafiltrates the state of saturation with calcium oxalate monohydrate was closely dependent on the plasma oxalate concentration but not on the plasma calcium concentration. The pre-dialysis state of saturation with calcium oxalate monohydrate was poorly influenced by the residual renal function and was independent of the sex, age, body weight or time on dialysis.

5. The results of the present study suggest that, unless chronic renal failure is due to primary hyperoxaluria, the extracellular body fluid of patients on current dialysis is often undersaturated with calcium oxalate and this is inconsistent with progressive oxalate accumulation and secondary systemic oxalosis. However, since some tissues may generate or selectively accumulate oxalate, local formation of crystalline deposits may still occur on regular haemodialysis.

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