THE CASE is presented of a child with lead poisoning who developed biochemical disturbances similar to those seen in the congenital metabolic defect known as the de Toni-Fanconi syndrome. The most important aspects of the disturbance demonstrated in the child were amino-aciduria, glycosuria, hypophosphatemia, and the skeletal changes of acute rickets.
The occurrence of transient glycosuria and of anatomic renal tubular lesions in human lead poisoning has long been known, although the nature of the biochemical disturbance involved remains obscure. This case provides new information on this point and may indicate a new avenue of approach in the study of lead poisoning.
Recently, Wilson and co-workers1 reported coincident glycosuria and gross amino-aciduria in a child with lead poisoning. In their case, however, there was no roentgenologic evidence of rickets and no emphasis was laid upon changes in serum phosphorus concentration. In 1938, Caffey2 reported the occurrence of active
CHISOLM JJ, HARRISON HC, EBERLEIN WR, HARRISON HE, Mohr FC. AMINO-ACIDURIA, HYPOPHOSPHATEMIA, AND RICKETS IN LEAD POISONING: Study of a Case. AMA Am J Dis Child. 1955;89(2):159–168. doi:10.1001/archpedi.1955.02050110201004
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