Plasma calcium-oxalate saturation in children with renal insufficiency and in children with primary hyperoxaluria

Plasma calcium-oxalate saturation in children with renal insufficiency and in children with primary hyperoxaluria. Calcium-oxalate (CaOx) deposition and systemic oxalosis are uncommon in children with chronic renal failure (CRI), but frequent in children with primary hyperoxaluria type I (PH-1). We hypothesized a difference in plasma CaOx saturation (βCaOx) and its determining factors would explain this discrepancy. Therefore, in addition to common biochemical measurements, plasma-oxalate (POx), citrate (PCit) and sulfate (PSulf) (plasma anions) were measured and βCaOx was calculated in 17 PH-1 patients with normal renal function receiving pyridoxine and citrate therapy, in 54 children with CRI (SCr 0.9 to 5.9mg/dl), and in 50 healthy children (NL). Plasma anions were analyzed by ion-chromatography and βCaOx was calculated using a PC-based program for solution equilibria. Compared to NL, all plasma anion levels and βCaOx were higher in PH-1 and CRI; POx, PCit and βCaOx were higher in PH-1 than in CRI (P < 0.05), but PSulf was higher in CRI (P < 0.01). βCaOx and POx were correlated in all groups (r = 0.63 to 0.95, P < 10-4). POx and βCaOx were both inversely correlated to a decrease in GFR in CRI patients. PCit and PSulf did not influence βCaOx. Although supersaturation (βCaOx > 1) was found in 7 CRI and in 4 PH-1 patients, eye examinations were suspicious for CaOx depositions only in the PH-1 patients, while systemic oxalosis was confirmed in one PH patient because of oxalate osteopathy. In PH-1, POx and βCaOx are elevated even with normal renal function, which increases the likelihood of CaOx crystal deposition. Therefore, more effective therapy to decrease βCaOx is crucial to reduce the risk of systemic oxalosis. In children with CRI unknown, but presumably protective substances, help prevent the risk of systemic oxalosis, despite increased POx and βCaOx levels, often to supersaturation levels.