Renal osteodystrophy - reason

Its pathogenesis and the following factors :
( 1 ) calcium and phosphorus metabolism disorders: renal failure early phosphorus filter out that there is an obstacle , reduce urinary excretion of phosphorus , phosphorus retention, reduce calcium , both caused by parathyroid hyperplasia , PTH secretion. PTH acts on the bone to release Ca2 + to restore blood calcium levels . When further development of renal failure , failure decompensation , hyperphosphatemia , hypocalcemia persists , PTH secretion also continue to mobilize calcium release , so a vicious cycle , leading to osteitis .
( 2 ) vitamin D metabolism disorders: renal failure , renal tubular cells in the cortex of phosphorus increased significantly, and there is severely inhibited 1,25 (OH) 2D3 synthesis. 1,25 (OH) 2D3 promote bone salt calm and intestinal absorption of calcium , when it decreased synthesis , coupled with persistent hypocalcemia and peritoneal dialysis patients with protein binding of vitamin D can lead to bone loss and other salt calm barriers caused by osteomalacia , while reducing intestinal calcium absorption , reduce calcium , secondary hyperparathyroidism is caused by osteitis .
( 3 ) hyperparathyroidism : Early renal failure that is parathyroid hyperplasia and increased serum PTH , consistent with the degree of renal failure severity. Secondary hyperparathyroidism, in addition to causing the aforementioned bone disease , but also caused a series of bone lesions.
( 4 ) aluminum toxicity : Aluminum between mineralized bone mass and bone deposition before , and with the formation of collagen cross-linking combined damage induction efficacy of bone remodeling , so that the number of osteoclasts and osteoblasts to reduce acid phosphatase enzymes and alkaline phosphatase activity decreased bone formation and mineralization are subject to rejection.
( 5 ) metabolic acidosis : acidosis , may affect bone salt is dissolved , acidosis also interfere with the synthesis of 1,25 (OH) 2D3 , and intestinal calcium absorption and bone resistance to PTH .
( 6 ) Soft tissue calcification : the performance of renal osteodystrophy are: bone pain, pathological fractures and pseudo gout , and more with proximal myopathy and muscle weakness, bone abnormalities were more common in children , such as rickets changes, long bones into a bow , or epiphyseal detachment epiphyseal end widened and growth retardation, adult manifested as curvature of the spine , thoracic deformity and bone ends clubbing . Bone showed soft tissue calcification.