Rickets Tables and Figures

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Assessment of Etiology of Rickets Based on Laboratory Results

Ca Phos Alk phos iPTH 25-(OH)D 1,25-(OH)2D Urine Ca/Cr TRP
Nutritional/insufficient sunlight N or ↓
Malabsorption N or ↓
Renal tubular defects N or ↓ N N or ↓
Altered vitamin D metabolism N or ↓
Genetic forms of rickets
X-linked, AD, and AR hypophosphatemic rickets N N or ↑ N N or ↑ N or ↓
1a-hydroxylase deficiency N
Vitamin D receptor mutations (vitamin D resistance) N
Hereditary hypophosphatemic rickets with hypercalciuria N or ↓ N
Hypophosphatasia N or ↑ N or ↑ N or ↓ N N or ↓ N or ↑ N

Ca, calcium; phos, phosphorus; alk phos, alkaline phosphatase; iPTH, intact parathyroid hormone; 25-(OH)-D, 25-hydroxy vitamin D; 1,25-(OH)2-D, 1,25-dihydroxy vitamin D; Ca/Cr, calcium/creatinine ratio; TRP, tubular reabsorption of phosphorus ([1 − (U phos × P Cr/U Cr × S Phos)] × 100, normal 85–95%); AD, autosomal dominant; AR, autosomal recessive; N, normal.

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