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Al-related osteomalacia has been reported in young uremic children not yet on dialysis; however, the effect of CAPD on Al metabolism is uncertain. Therefore, we studied 16 children with a mean age of 8.9±1.0 (SE) years and body weight, 24±2.4 kg. Serum (S) Al levels, measured after 8 and 18 mos of CAPD, were 55±11 and 60±10 ug/1, respectively (normal (N) children, 8.2±1.1 ug/1, p<0.001). The estimated oral Al intakes from Al hydroxide gels were 98±20 and 104±32 mg/kg/day at the same times; CAPD fluid Al was <6 ug/1. S-Al correlated with oral Al intake (r=0.86, p<.001) and indirectly with body weight (r=-0.68, p<.01) and age (r=-0.54 p<.01). The youngest patient (2.5 years) had the highest S-Al (174-204 ug/1) and largest Al intake (192-310 mg/kg/day); he failed to respond to calcitriol despite S-Ca of 11.2-13.2 mg/dl. A bone biopsy was characteristic of Al-related bone disease, with marked Al staining, greatly increased osteoid surface, and undetectable bone formation as determined from double tetracycline labelling; findings of 2° hyperparathyroidism were absent. Thus, Al accumulation occurs in young CAPD patients receiving large doses of Al gels despite the removal of significant but small quantities of Al in CAPD fluid. These observations indicate that Al-containing phosphate binders should be used cautiously in young children treated with CAPD.

ALUMINUM-RELATED HONE DISEASE AND SERUM ALUMINUM IN CHILDREN UNDERGOING CAPD