Renal bone disease, also known as renal osteodystrophy, is a bone disease caused by abnormal calcium and phosphorus metabolism and vitamin D metabolism in chronic renal insufficiency, secondary hyperparathyroidism, disturbance of acid-base balance, etc. The manifestations of abnormal bone metabolism associated with chronic renal insufficiency include hypertransformational bone disease (i.e., hyperparathyroidism), hypotransformational bone disease, and mixed bone disease, with hypertransformational bone disease being the most common. Hypo-transformational bone disease includes osteochondrosis or bone regeneration dysplasia. Hyperparathyroidism, or high-transformation osteopathy, is a bone disease caused by hyperthyroidism and is characterized mainly by a marked increase in bone transformation, massive fibrosis around bone trabeculae, accompanied by increased osteoblast and osteoclast activity, a marked increase in both the number of osteoclasts and resorptive surfaces, and the penetration of osteoclasts into bone trabeculae, creating a large number of resorptive lacunae; hypo-transformation osteopathy, characterized by a decrease in bone transit and Low-transformation bone disease, characterized by reduced bone transport and remodeling, is accompanied by a decrease in the number and activity of osteoclasts and osteoblasts. The two histomorphological manifestations are bone softening and poor bone regeneration. Aluminum-associated bone disease is a specific type of nephropathy in patients with chronic renal insufficiency, mainly due to the high incidence of aluminum toxic bone disease in patients with chronic renal failure until the 1980s, when they mainly took aluminum-containing preparations to reduce blood phosphorus. Afterwards, people gradually recognized the toxicity of aluminum, and after the 1980s, calcium-containing phosphorus-binding agents gradually replaced phosphorus-containing preparations, and the incidence of aluminum toxic bone disease decreased.