A potential pathogenic role of oxalate in autism

Abstract

BackgroundAlthough autistic spectrum disorders (ASD) are a strongly genetic condition certain metabolic disturbances may contribute to clinical features. Metabolism of oxalate in children with ASD has not yet been studied. AimThe objective was to determine oxalate levels in plasma and urine in autistic children in relation to other urinary parameters. MethodIn this cross-sectional study, plasma oxalate (using enzymatic method with oxalate oxidase) and spontaneous urinary calcium oxalate (CaOx) crystallization (based on the Bonn-Risk-Index, BRI) were determined in 36 children and adolescents with ASD (26 boys, 10 girls) aged 2–18 years and compared with 60 healthy non-autistic children matched by age, gender and anthropometric traits. ResultsChildren with ASD demonstrated 3-fold greater plasma oxalate levels [5.60 (5th–95th percentile: 3.47–7.51)] compared with reference [(1.84 (5th–95th percentile: 0.50–4.70) μmol/L (p < 0.05)] and 2.5-fold greater urinary oxalate concentrations (p < 0.05). No differences between the two groups were found in urinary pH, citraturia, calciuria or adjusted CaOx crystallization rates based on BRI. Despite significant hyperoxaluria no evidence of kidney stone disease or lithogenic risk was observed in these individuals. ConclusionsHyperoxalemia and hyperoxaluria may be involved in the pathogenesis of ASD in children. Whether this is a result of impaired renal excretion or an extensive intestinal absorption, or both, or whether Ox may cross the blood brain barrier and disturb CNS function in the autistic children remains unclear. This appears to be the first report of plasma and urinary oxalate in childhood autism.