The secondary causes of rickets and osteomalacia that result from vitamin D deficiency are illustrated in Figure 1. For example, in liver disease, serum concentrations of 25(OH)D3 are invariably too low, and in renal disease too little of the hormonal form of vitamin D, 1,25(OH)2D3, is produced. Other causes relate to reduced cell receptor responsiveness to the hormone because of genetic mutations and, hence, inappropriate adaptations that normally contribute to conservation of calcium and/or phosphate ions.
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