What are the causes of renal osteodystrophy?

Renal osteodystrophy is a kind of vitamin D and calcium phosphorus metabolism disorder, it belongs to a kind of disease. If you suffer from renal osteodystrophy, there may be anemia and itching and other symptoms, then cause renal osteodystrophy what? How to treat renal osteodystrophy? Take a look through the following right.

Renal osteopathy

Renal osteodystrophy and renal osteodystrophy, CRF is due to calcium, phosphorus and vitamin D metabolism, secondary hyperparathyroidism osteopathy, acid-base balance disorders and other factors caused. More common in children with congenital malformation of kidney and renal disease. Patients with slow progress

Renal osteodystrophy is renal insufficiency group from excessive parathyroid hormone (PTH) and mineral metabolism disorder to low conversion damage associated with normal or low blood levels of the deleted high conversion damage caused. Almost all the secretion of patients with end-stage renal failure. Renal osteodystrophy can cause serious damage to the bone, as bone softening, osteitis fibrosa, osteoarthritis, osteoporosis, bone sclerosis, bone and rickets, can increase the calcium and phosphorus metabolism, cause skin itching, anemia, nervous system and cardiovascular system damage.

The causes of renal osteopathy

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.

Classification of renal osteopathy

According to the rate of bone turnover, renal osteopathy can be pided into 4 types

A high turnover bone disease: pathology called osteitis fibrosa, to hyperparathyroidism, osteoblast, osteoclast proliferation characteristics around the active and trabecular fibrosis.

Two, low turnover bone disease: including bone softening and non dynamic osteopathy two. The former refers to the formation of the new class of defective bone mineralization, often made of aluminum deposition caused by bone formation. The latter is reduced, and hypercalcemia, using 1,25 (OH) D3 excessive inhibition of PTH secretion and diabetes mellitus.

Three, mixed bone disease, which is characterized by high transformation and low transformation bone disease, is caused by hyperparathyroidism and bone mineralization disorder, characterized by increased bone formation and coexistence of medullary fibrosis, and the rate of bone turnover varies

Four, beta 2- microglobulin amyloidosis osteoarthrosis edit this section of renal osteopathy bone symptoms: renal osteodystrophy was slow, symptoms are advanced, clinically with bone pain, bone fracture, deformation is the main feature. One of the sudden pain symptoms, often systemic, occur in the lower part of the body discreet parts (waist, back, hip, knee), aggravated movement or compression, swaying walk can't even get up. Pathological fracture of multiple ribs, other parts can also be due to a slight force caused by fracture. In low transport and renal transplant patients received glucocorticoid therapy, high type rare. Adult prone vertebrae, thoracic and pelvic deformation caused by height and ventilation in patients with severe disorders, known as the shrinking man syndrome can occur in children, growth delay.

Diagnosis of renal osteopathy

Bone biopsy

Bone biopsy is one of the basic methods for the diagnosis and study of renal osteodystrophy is important. With the improvement and development of bone biopsy and histology, bone biopsy in clinical diagnosis and treatment more and more popular. When the glomerular filtration rate (GFR) decreased to below 40ml/min, renal biopsy to reflect the increase of PTH activity and bone the mineralization of obstacles. In addition, renal biopsy or diagnostic aluminum related bone damage (ARBD) diagnosis only reliable. At the same time, also has a certain significance for monitoring bone biopsy taking calcium three alcohol drugs in patients.

X-ray examination of bone

The classic bone X-ray examination method in the diagnosis of renal osteodystrophy. X-ray examination can be found in secondary hyperparathyroidism caused by subperiosteal resorption, pathological fracture, osteoporosis, rickets and osteomalacia, and secondary hyperparathyroidism or beta 2 microglobulin amyloidosis caused by bone cystic lesions. The type of tissue and bone transport by X-ray examination can not clear the renal osteodystrophy rate, is not conducive to the early diagnosis of bone disease.

Bone mineral density measurement

The application of bone mineral density measurement to reflect the content of bone mineral, can improve the sensitivity of renal osteodystrophy damage evaluation, but it is still not clear edge of renal damage in high transport, low transport or aluminum poisoning. So it can be used to observe the treatment of renal osteopathy follow-up.

Nuclear medicine examination

In recent years, with the development of nuclear medicine technology, using 99mTC labeled MDP (methylene diphosphonate) bone imaging in patients with renal osteodystrophy, can be found in fracture, false fracture local damage, and the high turnover bone disease caused by osteitis fibrosa and low transport osteopathy induced osteomalacia has the differential diagnosis value of aluminum poisoning. Renal osteodystrophy in bone imaging with low concentration of radioactive tissue, and soft tissue of high concentrated focus. Therefore, the use of nuclear medicine bone imaging this non traumatic examination is valuable for the diagnosis of renal osteodystrophy and typing.

Biochemical index

Renal osteodystrophy also change, some biochemical indexes in clinic including PTH, alkaline phosphatase (AP), osteocalcin (BGP), 2-HS glycoprotein, insulin-like growth factor -1 (IGF-1), type VII procollagen peptide. The mechanism of expansion of some indicators in the pathogenesis of renal osteodystrophy in is still unclear. But, there is research on the diagnosis and contribute to renal osteodystrophy.

Treatment of renal osteodystrophy

The target of clinical treatment of renal osteopathy is:

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

Prevent phosphorus retention and hyperphosphatemia, and reduce phosphorus intake in the diet

This is the prevention and treatment of uremic patients with secondary hyperparathyroidism. The most important measure of meat and dairy products are important sources of phosphorus in food. But limit the intake of phosphorus in the diet will cause a loss of appetite and malnutrition. Daily intake of phosphorus should be controlled at 800mg.

Phosphorus adsorbent is used to prevent phosphorus absorption

Aluminum hydroxide and carbonate is very efficient phosphorus adsorbent, but because in patients with renal insufficiency occurred in the bone deposition, solid long-term use should pay attention to detect the concentration of aluminum, to prevent the occurrence of aluminum poisoning. Recently, calcium salt gradually replace aluminum salt as the main clinical phosphorus adsorbent including calcium carbonate. Calcium citrate and calcium acetate, calcium acetate, the strongest adsorption. Due to the use of calcium salt treatment may cause hypercalcemia and metastatic ossification. Therefore, in the use of conventional doses of calcium (4-12g/d), the low calcium dialysate (calciumion concentration 2.5mmol/L).

Removal of phosphorus was enhanced by effective dialysis treatment

The clearance of phosphorus by dialysis is limited, and the clearance rate of phosphorus in dialysis is equivalent to 40-50%. of the normal renal clearance rate

Treatment of active derivatives of vitamin D in recent ten years, vitamin D active derivatives, has opened up a new path for our treatment of renal osteodystrophy. Active derivatives of vitamin D 1 alpha (OH) D3,25 (OH) 2 D3,1,25 (OH) 2 D3, double hydrogen tachysterol (DHT), 22- oxygen - cholecalciferol (OCT), especially 1,25 (OH) 2 D significantly increased the serum calcium concentration, inhibition of parathyroid hormone gene transcription, thereby inhibiting the light, moderate primary hyperparathyroidism, correct bone tissue resistance to PTH, to a great extent improve bone disease.

But at present the use of clinical is still limited as follows: 1. In the treatment of hypercalcemia: often after a few weeks or 3 months after the occurrence of high PTH hyperlipidemia; the hard to correct: This is due to chronic renal failure patients on parathyroid calcium feedback inhibition caused by decreased sensitivity; for severe osteitis fibrosa or symptomatic secondary hyperparathyroidism in patients with poor effect; the transfer of ossification and renal function may decline. The use of 1,25 (OH) 2 D3 should pay attention to detection of calcium phosphorus product.

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.

The treatment direction of renal osteopathy

RenaGel (poly-allylamine hydrochloride, poly allylamine hydrochloride) cross-linked RenaGel is a cationic polymer, it can be through the ion exchange adsorption and hydrogen adsorption to phosphorus anions. In maintenance hemodialysis patients in a 8 week double-blind trials, RenaGel has demonstrated that phosphorus adsorption agent is more traditional than effective and safe.

NPSR-568 is a new compound with calcium receptor agonist. It can inhibit the PTH release and intermittent stimulation of calcitonin secretion in experimental animal model of uremia cat has proved, NPSR-568 in inhibition of PTH secretion and improve bone histological changes obviously, and the side effect is small. So NPS, R-568 is likely to be a new therapeutic method in treatment of secondary hyperparathyroidism.

Bisphosphonates can not only inhibit the inflammatory cytokines (IL-1, IL-6, TNF- alpha) which can inhibit the generation of NO, but also has proved the concentration of NO in uremic patients is increased. Therefore, bisphosphonates may become a new method for treatment of uremic osteopathy.

Conclusion: This article mainly expounds the methods for everyone about renal osteodystrophy and the etiology of symptoms and treatment, through reasonable treatment, can be alleviated and control of the disease, because there is no way to completely cure, so ease become very necessary.