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249 mentally severely retarded children were examined for se Ca,P,aminoacid N,alk.P-ase,tubular rejection of P,aminoacid N;urinary aminoacid chromatogram. They had not been treated with vit.D. 170/Group l/did not take anticonvulsants,79/Gr 2/ were on long-term anticonvulsant treatment.Gr 1 showed no abnormal findings,only 6/170 had hyperaminoaciduria.Gr 2 showed first markedly decreased se P,increased a1lc.P-ase,tubular rejection of P and aminoacid N. Hyperaminoaciduria occurred in 25/79. Gr 2 was then subdivided: 39 /Gr 2a/were left without vit.D,&o/Gr 2b/were treated with oral D3,3000 IU/day.Both subgroups continued taking anticonvu1sants.After 3 mos all determinations were repeated.Vit.D3 abolished nearly all abnormalities in Gr 2b,in Gr 2a all deviations got more pronounced,hyperaminoaciduria included.Conclusions : 1.Hyperaminoaciduria in mental retardation is due mostly to anticonvulsant induced vit.D deficiency.2.Measurement of tubular reabsorption of P and aminoacid N is useful in follow-up of patients on anticonvulsant s.

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