Along with the development and progress of blood purification technology, survival and quality of life of uremic patients improved significantly. Renal osteodystrophy (renaloseodystrophy, ROD, referred to as renal osteodystrophy) the incidence rate was increased with the time of dialysis.
The clinical symptoms of ROD, bone histology and imaging findings are not consistent between. Early diagnosis mainly depends on bone biopsy and serological markers. According to the ROD histological classification, X-ray examination, biochemical changes and pathogenesis, as follows.
1. high turnover bone disease is common in severe hyperparathyroidism (HPT) patients. Bone biopsy showed osteitis fibrosa, active osteoblasts and osteoclast proliferation, increase bone remodeling, accelerate mineralization, small beam shape and irregular arrangement, lamellar structure of bone tissue lost its rules, and even the formation of grain shape bone; bone area increased, the fiber hyperplasia induced by trabecular area and bone marrow fibrosis. Biochemical changes including serum calcium decreased and serum phosphorus, alkaline phosphatase, osteocalcin, parathyroid hormone (iPTH) levels were significantly increased. The bone line X examination can discover subperiosteal resorption, bone sclerosis and characteristic changes.
2. low transformation bone disease is characterized by reduced bone formation and bone mineral dysfunction, which can be pided into two types according to the changes of bone biopsy
(1): rickets impaired bone mineralization are prominent. Bone biopsy showed the osteoblast and osteoclast number and activity decreased, bone formation, absorption, calcification area reduced, matrix increased. Biochemical examination showed normal serum calcium, serum phosphorus, aluminum levels, alkaline phosphatase, osteocalcin and iPTH levels decreased. X-ray mainly showed pseudo fracture.
(2) dynamic disorder osteopathy: bone formation was significantly reduced for the performance of aluminum and aluminum non correlation relationship between two forms. Non aluminum associated motility disorders of bone proportion has increased, accounting for about half of that often occurs in the elderly, following the treatment of HPT inappropriate medication iPTH secretion insufficiency, lack of bone growth factor, low phosphorus conditions. Bone histological changes of bone cell activity decreased, osteoblasts and bone formation area reduced bone formation and mineralization matter before inhibition, decreased trabecular area. Blood biochemical examination showed normal calcium, phosphorus, alkaline phosphatase, osteocalcin and iPTH were normal or slightly reduced. In addition, bone formation obstacles but also related to iron overload.
More than 3. mixed osteodystrophy two factors are present, as has more than two mixed osteodystrophy bone damage characteristics. Histology showed osteitis fibrosa and osteomalacia coexist, the majority of dialysis patients (45% ~ 80%) end osteodystrophy in patients with end-stage kidney failure is the variable type and non dialysis.
4. bone and soft tissue calcification due to persistent calcium phosphorus product were caused by severe cases can form giant tumor calcification and the influence of joint activities around the joints, were found to be ahead of the skeletal lesions, can affect the long-term prognosis of patients than bone lesions.
5.. Growth retardation in children has recently been found to be related to HPT in children, but simply correcting HPT does not correct growth retardation, suggesting that there are other factors too. Growth hormone seems to be more effective