Renal osteodystrophy is an important complication in patients with chronic kidney disease and dialysis, treatment should be emphasized in the early prevention and early kidney damage can be used in small doses of 1,25- (OH) 2D3 and oral calcium, to prevent severe hyperparathyroidism and parathyroid hyperplasia; and comprehensive treatment measures reasonably according to the type of bone disease. So, early the prevention of renal osteodystrophy and we still have what method? We may wish to take a look.
The pathogenesis is related to the following factors:
(1): early renal failure, metabolic disorder of calcium and phosphorus phosphorus filter is disorder, urinary phosphorus excretion decreased, blood phosphorus retention, blood calcium decreased, both caused by parathyroid hyperplasia, increased secretion of PTH.PTH to release Ca2+ to restore the blood calcium level of bone. When the further development of renal failure, compensatory function failure, hyperphosphorus hypocalcemia, persistent, PTH will continue to mobilize a large number of secretion, bone calcium release, so finally lead to vicious spiral, osteitis fibrosa.
(2) vitamin D metabolic disorders: renal failure, renal cortex cells P were significantly increased, and there is a severe inhibition of 1,25 (OH).1,25 2D3 synthesis (OH) 2D3 can promote bone salt pigmentation and intestinal calcium absorption, when it reduced the synthesis of vitamin D, the loss can be coupled with persistent hypocalcemia and peritoneal dialysis patients and protein binding leads to bone pigmentation disorders caused by osteomalacia, and reduced intestinal calcium absorption, calcium decreased, while secondary hyperparathyroidism caused by osteitis fibrosa.
(3) hyperparathyroidism: renal failure in early stage of parathyroid hyperplasia and increased blood PTH, the degree of renal failure and the severity of secondary hyperparathyroidism. In addition, due to the disease, but also caused a series of bone lesions.
(4): aluminum aluminum poisoning on bone quality and bone mineralization between pre deposition, and the formation of cross-linking in combination with collagen, damage the inductive effectiveness of bone remodeling, the osteoblast and osteoclast number decreased, reduce the acid phosphatase and alkaline phosphatase activity, and mineralization of bone formation was suppressed.
(5) metabolic acidosis: acidosis may affect the dissolution of bone salts, acidosis also interfere with the synthesis of 1,25 (OH) 2D3, intestinal calcium absorption and the resistance of bone to PTH
(6) soft tissue calcification: manifestations of renal osteodystrophy are: pain, pseudogout and pathological fracture, with proximal myopathy and muscle weakness, bone deformities in children were more common, such as rickets change, long arched, epiphyseal widened epiphyses and growth or stagnation, adult performance curvature of the spine, thoracic deformity and bone clubbing. Bone showed soft tissue calcification.
Keep normal calcium and phosphorus as much as possible;
Prevention and correction of hyperparathyroidism and parathyroid hyperplasia;
Prevention and reverse of bone calcification;
Prevent deposition of aluminum and other poisons;
Avoid adverse factors associated with treatment
In the past ten years, many scholars use 1,25 (OH) 2 D3 intravenous injection or oral pulse therapy to treat renal osteodystrophy, achieved good clinical efficacy. Treatment is currently used: 4 g/ time, 2 times a week. It can significantly improve hypocalcemia and hyperphosphatemia; histological changes of bone significantly organization; clinical symptoms; fewer side effects; the impact of oral treatment can achieve the same effect with intravenous administration. But in the process of using still need to pay attention to: firstly, to control hyperphosphatemia, lest the calcium phosphorus product resulting in high metastatic ossification difficult to reverse; try to avoid the combination of aluminum, aluminum to avoid retention the regular detection; calcium concentration, when calcium >2.75mol/L should be promptly discontinued.
Secondly, active treatment of primary disease, prevent phosphorus retention and hyperphosphatemia in reducing the intake of dietary phosphate, which is the prevention and treatment of uremic patients with secondary hyperparathyroidism. The most important measures of meat and dairy products are important sources of phosphorus in food. But limit the intake of phosphorus in the diet will lead to loss of appetite and malnutrition. Daily intake of phosphorus should be controlled at 800mg.
Again, during the application of active vitamin D treatment should be closely monitored, blood calcium, blood phosphorus and IPTH levels, avoid hypercalcemia, hyperphosphatemia, metastatic calcification and adynamic bone disease.