204 - Osteomalacia, rickets, and renal osteodystrophy

Abstract

Osteomalacia is caused by a defect in the mineralization of osteoid laid down by mature osteoblasts. The most common causes of osteomalacia and rickets are vitamin D deficiency and calcium deficiency. Any acquired or inherited disorder that alters absorption of phosphorus in the intestine and enhances excretion of phosphorus via the kidneys will also cause osteomalacia and rickets. Treatment of vitamin D deficiency and correction of calcium and phosphorus intake results in complete resolution of osteomalacia or rickets when caused by these nutritional deficiencies. Several hereditary and acquired disorders affect both calcium and phosphorus metabolism and lead to rickets and osteomalacia. Management of these disorders depends on the cause and should be based on treating the mechanism resulting in osteomalacia or rickets or removing the offending agent that may be precipitating the mineralization defect. Renal osteodystrophy is an acquired defect in bone mineralization and bone turnover that occurs as a result of chronic kidney disease. It is associated with abnormalities in calcium and phosphate balance, parathyroid hormone, and active vitamin D and results in bone fracture, deformities, and delayed growth. Within patients with chronic kidney disease, an interaction between the skeletal and cardiovascular systems results in premature vascular calcifications and early cardiovascular mortality. Current treatment is aimed at addressing defects in bone mineralization and turnover while minimizing the adverse impact on the cardiovascular system.