<prompt> What is true of vitamin D resistant rickets?X linked recessiveNo End organ resistance to 1, 25 OH2 D3Defect in proximal tubular reabsorptionHyperphosphatemia and high 1, 25 OH2 D3  <response>: ANSWER: C Defect in proximal tubular reabsorptionREF: Nelsons 18th ed page 2720Familial Hypophosphatemia: Vitamin D-Resistant Rickets, X-Linked HypophosphatemiaThe most commonly encounterednon-nutritional form of rickets is familial hypophosphatemia. The usual mode of inheritance is X-linked dominantPathogenic mechanisms involve defects in the proximal tubular reabsorption of phosphate and in the conversion of 25OHD to l,25OH2 D, The latter defect is evidenced by 1owt- normal serum l,25OH2 D levels despite hypophosphatemia and by the finding that further phosphate depletion of subjects with familial hypophosphatemia does not stimulate 1,25 OH2 D synthesis as it does in normal subjectsPatients have a normal or slightly reduced serum calcium level, a moderately reduced serum phosphate level, elevated alkaline phosphatase activity, and no evidence of secondary hyperparathyroidism. Urinary phosphate excretion Is large, despite hypophosphatemia, indicating a defect in renal tubular phosphate 