Abstract
A 7.1 kg infant, age 7m, was maintained on TPN (Ca 261mg/24h, P 124mg/24h, D 400 IU/24h), and developed renal calculi and osteopenia. The urinary Ca/creatinine (Ca/Cr) was 1.0 (nl<0.3). The serum Ca was 9.6mg/dl; the P, 2.5mg/dl. Because of the hypophosphatemia, the concentration of P in the TPN fluid was increased to deliver 240mg/24h. After a transient increase in urinary Ca and P, the Ca/Cr decreased to 0.1. However, the serum P increased to only 3.1mg/dl. D metabolites were: 1,25(OH)2D 100pg/m1 (n1 40±10); 24,25(OH)2D <1.0ng/m1 (n1 2.4±1.1); 25(OH)D 35ng/m1 (n1 21±9.4). Following the increase in P concentration in TPN, the renal calculi resolved.
In contrast to other reports of TPN, the osteopenia cannot be attributed to reduced serum 1,25(OH)2D in this patient. The role of the reduced serum 24,25(OH)2D in the bone abnormality deserves consideration since there is evidence that this metabolite exerts an effect on bone formation. The elevated serum 1,25(OH)2D and the depressed serum 24,25(OH)2D may be secondary to the hypophosphatemia. This suggests the possibility that the abnormal levels of circulating vitamin D metabolites, rather than causing the bone disease, are a physiologic response to the macronutrient status produced by prolonged TPN. These results suggest that modification of macronutrient composition of TPN fluid may be necessary to prevent metabolic bone disease.
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Key, L., Anast, C., Sutphen, J. et al. 575 OSTEOPENIA, HYPERCALCIURIA, AND RENAL CALCULI IN A PATIENT RECEIVING PROLONGED TOTAL PARENTERAL NUTRITION. Pediatr Res 15 (Suppl 4), 536 (1981). https://doi.org/10.1203/00006450-198104001-00588
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DOI: https://doi.org/10.1203/00006450-198104001-00588
