What is renal osteodystrophy? Renal osteodystrophy can be pided into generalized renal osteodystrophy and narrow renal osteodystrophy in two categories. The generalized "renal osteodystrophy" refers to all related bone disease or cause kidney and kidney related bone disease, such as renal tubular acidosis associated with rickets, nephrotic syndrome occurs when bone disease the narrow sense ". Renal osteodystrophy" also known as renal osteodystrophy, refers to occur in chronic renal failure and metabolic bone disease all the time, can be regarded as an important complication of chronic renal insufficiency, severe cases may be associated with multiple system lesions. According to the dynamic changes of bone tissue to Yun and can be pided into high transport type, low transport type and mixed type. Since 1960s to carry out dialysis treatment, with the increase of our dialysis population, prolong the life of dialysis patients dialysis technology improvements, the incidence of renal osteodystrophy is also more and more high, and the treatment effect is not science Yes, it seriously affects the quality of life of the patients.
How renal osteodystrophy occurs?:
1. obstacles of calcium and phosphorus metabolism: renal dysfunction early blood phosphorus leaching disorder, urinary P excretion decreased, serum phosphorus retention, blood calcium decrease caused by parathyroid hyperplasia, parathyroid hormone (PTH) secretion, to release Ca2+ to restore skeletal calcium level. When renal insufficiency further development, 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 insufficiency of kidney active vitamin D (L, 25 (OH) 2D3).1,25 (OH) reduced the synthesis of 2D3 can promote bone salt pigmentation and intestinal calcium absorption, synthesis resulted in a decrease in bone salt pigmentation disorders caused by osteomalacia, and reduced intestinal calcium absorption, calcium decreased, promote secondary hyperparathyroidism caused by osteitis fibrosa hyperparathyroidism:
3.. Renal function All secondary hyperparathyroidism caused by the disease, in addition, it causes a series of bone lesions.
4. metabolic acidosis: acidosis, may affect bone salt dissolution, acidosis also interfere with 1,25 (OH) 2D3 synthesis, intestinal calcium absorption and bone resistance to PTH.