The main cause of familial low phosphorus anti-D rickets: impaired phosphorus reabsorption in the proximal renal tubules and intestine, large amount of phosphorus excretion from the urine, resulting in low blood phosphorus, a calcium-phosphorus product <30, and less calcification of bone, as well as impaired conversion of 25(oh)2d3 to 1,25-(oh)2d3, leading to bone disease. The causative gene is located on X chromosome p22.31-p21.3. Clinical manifestations: (1) Family history. Females are more common with milder disease; males are less affected with more severe disease. (2) Most of the disease develops after 1 year of age, gradually and obviously "O" shaped legs, walking in a duck stance, lower limbs are elbow inversion, knee inversion and knee valgus, and there is slow growth. (3) Pulpal deformation and damage resulting in premature loss of milk teeth, deformation and enamel defects. Laboratory tests: (1) Decreased blood phosphorus: generally shows a moderate decrease of 0.48-0.96 mmol/L,alkaline phosphatase is significantly elevated. Blood calcium is normal and parathyroid hormone levels are normal. (2) Increased urinary phosphorus excretion. (3) X-ray: widening of the long bone epiphysis, brush-like and cup-like changes, osteoporosis and uneven bone density, often secondary to hyperparathyroidism bone lesions.