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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