Renal bone disease

Introduction to renal osteopathy Renal osteodystrophy is a metabolic disease caused by chronic renal failure. Referred to as renal bone disease. It is characterized by calcium and phosphorus metabolism disorders, acid-base balance disorders, skeletal deformities and can cause secondary hyperparathyroidism. Skeletal manifestations of osteoporosis, osteomalacia, fibrocystic osteitis, osteosclerosis and metastatic calcification. Infants may cause growth and development disorders. The purpose of treatment is to relieve symptoms, prevent bone deformity and fracture, high blood phosphorus and vitamin D deficiency; relieve hyperparathyroidism, prevent soft tissue metastatic calcification, and strengthen bone mineralization. Patients with increased uremia undergo dialysis or kidney transplantation. basic knowledge The proportion of sickness: 0.0031% Susceptible people: no special people Mode of infection: non-infectious Complications: rickets Osteoporosis Osteosclerosis Fractures

Causes of renal osteopathy

Calcium and phosphorus metabolic disorders (25%):

In the early stage of renal failure, there is a disorder of blood phosphorus filtration, urinary phosphorus excretion is reduced, blood phosphorus retention, blood calcium reduction, both cause parathyroid hyperplasia, PTH secretion increases. PTH acts on the bone to release Ca2+ to restore blood calcium levels. When renal failure develops further, compensatory function fails, high blood phosphorus, low blood calcium persists, PTH is also secreted in large quantities, and mobilization of bone calcium is continued, such a vicious circle, and finally leads to fibrotic osteitis.

Vitamin D metabolic disorders (20%):

In renal failure, intracellular phosphorus in cortical renal tubules increased significantly and severely inhibited the synthesis of 1,25(OH)2D3. 1,25(OH)2D3 promotes bone salt deposition and intestinal calcium absorption. When it is reduced in synthesis, plus persistent hypocalcemia and loss of protein-bound vitamin D in peritoneal dialysis patients, it can lead to bone salt deposition. Obstruction causes osteomalacia, while intestinal calcium absorption is reduced, and blood calcium is lowered, which in turn causes parathyroid function and causes fibrotic osteitis.

Hyperparathyroidism (20%):

In the early stage of renal failure, there is hyperparathyroidism and elevated blood PTH, which is consistent with the severity of renal failure. Secondary hyperparathyroidism, in addition to causing the aforementioned bone disease, also caused a series of extra-osseous lesions.

Aluminum poisoning (15%):

Aluminum deposits between the bone progenitor and mineralized bone and forms a cross-linking combination with collagen, which impairs the induction efficiency of bone remodeling, reduces the number of osteoclasts and osteoblasts, acid phosphatase and alkaline phosphatase. Reduced activity, both bone formation and mineralization are inhibited.

Metabolic acidosis (10%):

Acidosis may affect the dissolution of bone salts. Acidosis also interferes with the synthesis of 1,25(OH)2D3, the absorption of intestinal calcium and the resistance of bone to PTH.

Soft tissue calcification (5%):

Renal osteodystrophy manifestations include: bone pain, pseudogout and pathological fractures, mostly with proximal myopathy and muscle weakness. Bone deformities are more common in children, such as rickets, long bones arched, and osteophytes Wide or osteophyte detachment and growth stagnation, adults with spinal curvature, thoracic deformity and sacral deformation of the bone ends. Extra-osseous manifestations are soft tissue calcification.

Renal osteopathy prevention

Actively treat the primary disease.

Prevent phosphorus retention and hyperphosphatemia from reducing phosphorus intake in the diet.

This is the most important measure to prevent and treat uremia secondary to parathyroidism. Meat and dairy products are important sources of phosphorus in food. However, limiting the intake of phosphorus in the diet can cause loss of appetite and malnutrition. Daily phosphorus intake should be controlled at 800 mg.

Renal osteopathic complications Complications Osteoporosis Osteoporosis Fractures

Rickets or osteomalacia, cystic fibrosis, osteoporosis, osteosclerosis and heterotopic ossification, fractures, etc.

Symptoms of renal osteopathy Common symptoms Bone pain in children with repeated fractures of cartilage dysplasia and... Muscular dysplasia "duck step" gait knee valgus valgus or hip varus congenital bone dysplasia

In children or adolescents, the disease manifests as dysplasia and muscle weakness; when walking, it is duck gait, with knee valgus or varus; the humeral or rib cartilage junction is swollen, the upper femur is slippery; the severe femur can cause femur Cervical fibrous osteitis. Adults present with symptoms of osteomalacia and tenderness in the Looser degeneration area.

Renal osteopathy is slow, and it is already late in the onset of symptoms. Clinically, bone pain, fracture, and bone deformation are the main features. One of the symptoms of bone pain, often systemic, occurs in the lower part of the lower body (waist, back, hip, knee joint), increased during exercise or compression, walking and shaking can not even get up. Pathological fractures occur mostly in the ribs, and other parts can also cause fractures due to slight external forces. More common in low-transportation and glucocorticoid-treated kidney transplant patients, high-speed type is rare. Adults are prone to vertebrae, thoracic and pelvic deformation, and severe patients cause height shortening and ventilation disorders, known as retraction syndrome, and children may have delayed growth.

Examination of renal bone disease

(1) Total serum calcium: In patients with osteomalacia, the total amount of serum calcium is generally low; those with fibroostitis are generally normal or high; those with severe renal failure, serum protein-bound calcium and ionized calcium Both are low.

(2) Serum inorganic phosphorus: generally increased, which is extremely high.

(3) Alkaline phosphatase, serum magnesium and blood urea are all elevated; plasma carbonate is reduced by acidosis, with proteinuria and low urinary calcium.

Diagnosis and differential diagnosis of renal osteodystrophy

Bone biopsy

Bone biopsy is one of the most important methods for diagnosing and studying renal bone disease. With the improvement and development of bone biopsy techniques and histology, the application of bone biopsy in clinical diagnosis and treatment is becoming more and more popular. When glomerular filtration rate (GFR) drops below 40 ml/min, renal biopsy can reflect increased PTH activity and bone mineralization disorders. In addition, renal biopsy is the only reliable basis for the diagnosis of aluminum-related bone damage (ARBD). At the same time, bone biopsy has a certain significance for the monitoring of patients taking calcitriol.

Bone X-ray examination

Bone X-ray examination is one of the classic methods for diagnosing renal osteodystrophy. X-ray examination of the bone can be found in subperiosteal absorption, osteoporosis, pathological fractures, rickets and osteomalacia caused by secondary hyperparathyroidism, as well as secondary hyperparathyroidism or 2 microglobulin amyloidosis Bone cystic lesions. However, X-ray examination alone does not clarify the tissue type and bone transport rate of renal osteodystrophy, and is not conducive to the early diagnosis of bone disease.

Bone density determination

The use of bone mineral density to reflect the content of bone minerals can improve the sensitivity of renal bone disease damage assessment, but it is still unable to determine the high transportability, low transportability or aluminum poisoning of kidney damage. Can be used for follow-up observation of the treatment of renal osteopathy.

Nuclear medicine examination

In recent years, with the development of nuclear medicine technology, 99mTC-labeled MDP (methylene diphosphonate) for bone imaging in patients with renal osteodystrophy, localized damage such as fractures and pseudo-fractures can be found, and high-transportation bone diseases It has differential diagnostic value for osteomalacia caused by fibrotic osteitis and low transport bone disease. Renal osteopathy caused by aluminum poisoning has a low concentration of tissue radioactivity in bone imaging, and a hot spot with high concentration of soft tissue. Therefore, the non-invasive examination using nuclear medicine bone imaging has certain value for the diagnosis and classification of renal osteodystrophy.

Biochemical indicators

There are also some biochemical changes in renal osteopathy, including PTH, alkaline phosphatase (AP), osteocalcin (BGP), 2-HS glycoprotein, and insulin growth factor-1 (IGF-1). VII type procollagen extended peptide and the like. The mechanism of some of these indicators in the pathogenesis of renal osteopathy remains unclear, but contributes to the diagnosis and research of renal osteodystrophy.

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