Renal osteomalacia

Introduction Renal osteopathy, also known as renal rickets, is not an independent disease, but a long-term renal dysfunction, a complication of bone disease caused by chronic uremia. Osteoporosis is affected by congenital and acquired factors. Congenital factors refer to race, gender, age, and family history; acquired factors include drugs, illness, nutrition, and lifestyle. Old age, female menopause, and male sexual dysfunction are the causes of osteoporosis.

Cause

This type of bone softening is excretory bone softening. Due to poor kidney function, vitamin D3 is a metabolic disorder. The lack of 1.25-(OH)2-D3 reduces intestinal calcium absorption and low calcium. Hypocalcemia promotes hypertrophy of parathyroid hyperplasia and increased secretion of parathyroid hormone; in addition, metabolic acidosis, decreased urinary phosphorus excretion, and elevated blood phosphorus. Hypocalcemia, hyperphosphatemia and secondary hyperparathyroidism together constitute renal osteodystrophy, and the type of development of renal osteopathy is determined according to the relationship between the three. Vitamin D3 metabolic disorder, hypocalcemia can cause bone lesions of adult rickets type, although secondary hyperparathyroidism, under the influence of hypocalcemia, can not make parathyroid hormones fully play their active bone tissue The role of reshaping. Osteoclast dissolving activity and osteoblast production activities are at a low tide. Bone resorption and bone formation are limited to the range of activity of the original osteoclast population and osteoblast group, and there is a certain amount of calcified or decalcified bone. Quality layer. When hypocalcemia, hyperphosphatemia and secondary hyperparathyroidism develop further, the cellular activity of bone tissue changes greatly. Osteoclast proliferation, osteolytic absorption process strengthens, due to high blood phosphorus, from breaking The transformation process from bone cells to osteoblasts is strengthened, osteogenic activity is also strengthened, blood alkaline phosphatase is proliferated, bone tissue is reshaped and active with fibroplasia, and reticular hyperplasia is typical fibrotic osteitis. When it reaches extremes, there will be metastatic calcification in the bone marrow cavity, resulting in osteosclerosis. At the same time, extra-bone soft tissue metastasis calcification occurs.

an examination

Related inspection

Urinary hydroxyproline urinary hydroxyproline (HYP) super imaging bone and joint soft tissue CT examination

1. A history of renal insufficiency caused by chronic and progressive kidney disease.

2. The earliest symptoms of the patient are pain in the lower back and legs, muscle weakness, and then bone tenderness and inconvenient walking. The pain of a long-term patient spreads from the waist and legs to the chest and upper limbs. The nature of the disease is mostly sore or stinging and cannot be turned over automatically. It can cause deformation or pathological fracture of the spine, thorax, pelvis and lower limbs. There are still symptoms such as lack of appetite, indigestion, and hands and feet.

3. Laboratory examination: serum calcium decreased or normal, serum phosphorus increased, blood alkaline phosphatase increased, urinary calcium and phosphorus decreased.

4. X-ray film has general osteoporosis, irregular reticular decalcification, thinning and stratification of the cortex, widening of the medullary cavity, bone bending in the later stage, pathological fracture on the convex side, false appearance of the femur and pubis Fracture line (Looser band).

Differential diagnosis

Patellar softening is a degenerative change caused by cartilage damage of the tibia, including a series of symptoms caused by swelling, fragmentation, shedding and corrosion of cartilage. Finally, the same changes occur in the articular surface of the femur and the tibia, and the reactive hyperplasia of the patellofemoral joint is gradually formed, and osteoarthritis will be formed later. There is often a history of trauma. The performance is "front knee pain", "squatting pain" and "post-sorrow pain". The pain is obvious after going downstairs, climbing, squatting, squatting and sedentary, and it is aggravated after strenuous exercise. The tibia, periorbital, temporal bone and posterior tibial tenderness are obvious, and there may be joint effusion. In severe cases, knee flexion and extension activities are limited and cannot stand on one leg. The fear test is often positive; the squat test is positive. A small number of knee joint "false lock" and "soft leg" symptoms, late can appear tibia friction sounds and limp.

Osteomalacia and rickets (osteopenic softening in adults) are a bone disease characterized by newly formed bone mineralization disorders. As a result, non-mineralized bone-like tissue (osteoid) accumulates, bones soften, and a series of clinical symptoms and signs such as bone pain, bone deformity, and fracture occur. As the bone softening worsens, the muscles are deformed during long-term weight-bearing or active muscles, or the sensory nerve terminals that reach the periosteum cause significant bone pain. Start or discontinuity occurs, obvious in winter and spring, and intensified in late pregnancy and lactation. After a few months or a few years, it gradually becomes persistent, and it develops into severe and severe body pain. When activities and walking are aggravated, there may be lameness and duck gait, and it is difficult to bend, comb, and turn over. In severe cases, the bones are further softened, and the thoracic invagination and sternal lordosis can form, and the chicken breast can be formed, which affects the heart and lung function. Long-term bed rest, sitting position can make the cervical spine shorter, lumbar lordosis, thoracic kyphosis, leading to scoliosis deformity, hunchback, shortened height. The bones become soft and long-term weight-bearing, so that the sacral sag is bulging, the pubis is prematurely bird-like, the two acetabular sacs are invaginated, the pubic arch is acute, and the pelvis is chicken heart or trilobal deformity, which can lead to dystocia. Myasthenia gravis is also a prominent symptom, especially in patients with significant hypophosphatemia.

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