Rickets Tables and Figures

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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