Can kidney disease also damage bones? How can kidney disease patients delay the onset of bone disease?

Author: Zuo Li, Chief Physician, Peking University People's Hospital

Reviewer: Mao Yonghui, Chief Physician, Beijing Hospital

When faced with bone pain or fracture symptoms, people often first think of diseases of the bones themselves and tend to seek treatment from orthopedics.

However, it is worth noting that the root cause of these symptoms may sometimes lie in the kidneys, as kidney disease can also cause pathological changes in the bones.

1. How does kidney disease affect bones?

The kidneys have a vital function - the excretion of phosphorus. When kidney function is normal, daily phosphorus intake and excretion maintain a dynamic balance; however, once kidney function is impaired, its ability to excrete phosphorus will decrease, leading to a gradual increase in serum phosphorus levels and the formation of hyperphosphatemia. In order to restore the balance of blood phosphorus, the body triggers the parathyroid glands to secrete parathyroid hormone, which not only acts on the kidneys to promote the excretion of phosphorus, but also acts on the bones to activate osteoblasts and osteoclasts, increasing their activity. If these cells are too active, bone lesions, namely high-transport bone disease, will occur.

In addition, the kidneys are also responsible for activating the inactive substance vitamin D. When kidney function is abnormal, the activation ability of vitamin D is weakened, leading to vitamin D deficiency in the body. Vitamin D plays a key role in promoting the absorption of calcium by the gastrointestinal tract. Its deficiency will weaken the absorption capacity of calcium and thus reduce blood calcium levels. The reduction of blood calcium will also stimulate the parathyroid glands to secrete parathyroid hormone, further affecting the activity of osteoblasts and osteoclasts.

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There are several other ways in which kidney disease can cause bone lesions: first, large amounts of proteinuria may accompany treatment with corticosteroids, which can induce osteoporosis; second, heparin is required for anticoagulation during dialysis, which can also cause osteoporosis; third, vitamin D and calcium are often combined with protein in the blood. Large amounts of proteinuria can cause the loss of vitamin D and calcium, affecting calcium absorption, leading to hypocalcemia, and further stimulating the secretion of parathyroid hormone, exacerbating bone lesions.

In summary, there are three main mechanisms by which kidney disease leads to bone lesions: first, phosphate excretion disorders and vitamin D deficiency caused by impaired kidney function; second, loss of vitamin D and calcium caused by massive proteinuria; and third, side effects caused by the use of drugs (such as hormones and heparin) during treatment.

2. What are the symptoms of renal osteopathy?

Renal osteodystrophy mainly includes three aspects of changes: first, mineral metabolism imbalance, such as hypocalcemia and hyperphosphatemia; second, bone lesions; and third, soft tissue calcification.

In the early stages of renal osteodystrophy, there are usually no obvious clinical symptoms, despite the presence of abnormal calcium and phosphorus metabolism and abnormal parathyroid hormone levels. Once bone lesions occur, patients may experience clinical symptoms such as bone pain or fractures.

Soft tissue calcification can affect nerve endings, causing irritation of sensory nerve fibers, which in turn causes a generalized itching sensation. In most cases, skin calcification is not obvious, and only a few patients can see calcified nodules on the skin surface. If blood vessels calcify, the blood vessel walls will harden, which will cause a significant increase in systolic blood pressure and a relatively low diastolic blood pressure, resulting in an increase in pulse pressure.

3. How to treat renal osteodystrophy?

The risk of renal osteodystrophy increases as kidney disease progresses from stage 1 to stage 5. In stage 1, obvious renal osteodystrophy changes are usually not yet present. However, as the disease progresses to stages 3, 4, and 5, the incidence of bone disease in non-dialysis patients increases. Therefore, when parathyroid hormone levels are elevated, measures should be taken to control phosphorus intake to prevent an increase in blood phosphorus levels, thereby delaying the increase in parathyroid hormone levels and the development of bone disease.

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The incidence of renal osteodystrophy increases further after entering the dialysis stage. Related complications, such as fractures, can be effectively prevented through comprehensive management measures such as diet control, drug therapy, and adequate dialysis.

Medical treatment for renal osteodystrophy requires differentiation between high- and low-turnover bone disease. For low-turnover bone disease, especially in dialysis patients, if the parathyroid hormone level is low, there is currently no routinely used exogenous parathyroid hormone replacement therapy.

For high-transfer bone disease, vitamin D is an important treatment because it can inhibit the secretion of parathyroid hormone. However, vitamin D promotes calcium absorption, thereby increasing the calcium load and aggravating soft tissue calcification. New vitamin D preparations, such as paricalcitol, have the ability to act specifically on the parathyroid glands, reduce gastrointestinal calcium absorption, and do not increase the calcium load. In addition, another drug, cinacalcet, acts directly on the parathyroid glands by simulating the mechanism of action of calcium, inhibiting the secretion of parathyroid hormone. Phosphorus binders are another key class of drugs that can bind to phosphorus in food and then be excreted through the feces, thereby avoiding excessive blood phosphorus levels.

The choice of the above drugs should be determined based on indicators such as blood calcium, blood phosphorus, parathyroid hormone, and bone-specific alkaline phosphatase. The basic treatment method is still diet control, combined with dialysis and drug therapy to maintain a good blood phosphorus level. When the parathyroid hormone level is too high, it often indicates that a parathyroid adenoma has developed and autonomously secretes parathyroid hormone. At this time, drug treatment is not effective, and surgical removal of the parathyroid gland is often required for treatment.