Chronic Kidney Disease and Osteoporosis: Treatment and New Insights
Update Date：2025/11/04，
Views：128
Nephrology Division, Dr. Wang Rui-Lin, Dr. Xu Shun-Neng
Ⅰ. Renal Bone Disease
Chronic kidney disease with mineral and bone disorder (CKD-MBD) is a common and important complication in patients with chronic kidney disease (CKD). Its main cause is the decline in kidney function, which leads to imbalances in the regulation of calcium, phosphorus, vitamin D, and parathyroid hormone (PTH), resulting in abnormal bone metabolism and vascular calcification, among other pathological changes.
Normally, the kidneys are responsible for excreting excess phosphorus, converting vitamin D into its active form (calcitriol), and maintaining stable calcium levels in the blood. However, as kidney function deteriorates, these regulatory mechanisms become disrupted, leading to increased blood phosphorus and decreased calcium levels. To compensate for low calcium and high phosphorus, the parathyroid gland secretes excessive PTH, leading to secondary hyperparathyroidism. If left uncontrolled for a prolonged period, excessive PTH stimulation causes renal bone disease and promotes vascular calcification, increasing cardiovascular risk and creating a "bone-vascular-heart" vicious cycle.
Epidemiological data shows that in stage 3 CKD patients, approximately 40%-50% exhibit abnormalities in calcium, phosphorus, or PTH levels. By stage 4, this rate increases to 60%-70%, and by stage 5 (including dialysis patients), 80%-90% of patients experience hypocalcemia and hyperphosphatemia. Chronic imbalances in calcium-phosphorus metabolism, elevated PTH, and the accumulation of uremic toxins ultimately lead to renal bone disease. Furthermore, the prevalence of osteoporosis in CKD patients is significantly higher than in the general population, with 30%-60% of CKD stage 3-5 patients meeting the diagnostic criteria for osteoporosis (T-score ≤ -2.5). Studies indicate that the fracture risk in CKD patients is 3-10 times higher than in the general population. According to data from Tri-Service General Hospital, the 10-year mortality rate for dialysis patients with hip fractures can reach 100%, highlighting the critical importance of bone health in CKD care.
Ⅱ. Clinical Symptoms and Abnormal Findings in Laboratory Tests
Symptoms of renal bone disease may not always be prominent, but as the condition progresses, several issues may arise. Symptoms include bone pain, increased fracture risk, joint stiffness and pain, muscle weakness, decreased endurance, arteriosclerosis, valve calcification leading to an increased risk of heart failure, and in severe cases, intermittent claudication or arrhythmia.
Laboratory abnormalities include elevated phosphorus levels (>4.5 mg/dL), decreased or unstable calcium levels, increased PTH, and elevated alkaline phosphatase.
Ⅲ. Diagnosis and Evaluation of CKD with Mineral Bone Disease and Osteoporosis
Clinically, doctors combine blood tests, imaging examinations, and clinical history to determine whether CKD patients have mineral metabolism abnormalities or bone disease, and further assess osteoporosis and fracture risk.
1. Blood Tests: Common tests include calcium, phosphorus, PTH, vitamin D, and alkaline phosphatase. Bone turnover markers (BTMs), such as β-CTX (reflecting bone resorption) and P1NP (reflecting bone formation), can help assess bone turnover dynamics.
2. Imaging Tests: X-rays can detect vascular calcification or obvious bone abnormalities. Dual-energy X-ray absorptiometry (DXA) is the standard tool for assessing bone mineral density (BMD). Cardiac ultrasound or CT scans can further assess valve or vascular calcification to understand cardiovascular complications. In addition, Tri-Service General Hospital’s AI-CXR can use chest X-rays to estimate bone density and osteoporosis risk, serving as an early screening tool for timely intervention.
3. Fracture Risk Assessment Tools: The FRAX score calculates the 10-year probability of major fractures and hip fractures based on age, gender, weight, height, bone mineral density (T-score), history of previous fractures, smoking, alcohol consumption, and steroid use. The FRAX score can be used in all stages of CKD, though adjustments for advanced CKD may require more evidence.
4. Bone Biopsy: When diagnosing is difficult or differentiation between "high turnover vs. low turnover/apathetic bone" is required, a bone biopsy may be considered to guide treatment.
Ⅳ. Prevention and Treatment Methods
The core of treating CKD-MBD and osteoporosis lies in controlling blood phosphorus, maintaining calcium balance, adjusting PTH levels, correcting vitamin D deficiency, and simultaneously reducing vascular calcification and fracture risk.
1. Lifestyle and Dietary Control: Limit high-phosphorus foods (processed meats, nuts, dairy products) and avoid excessive animal protein intake, which can increase phosphorus load. Ensure adequate calcium and vitamin D intake, engage in regular weight-bearing exercise and strength training, quit smoking, limit alcohol consumption, and prevent falls.
2. Traditional Medications: Phosphate binders reduce intestinal phosphorus absorption; active vitamin D and analogs promote calcium absorption and suppress PTH secretion; calcimimetics activate the calcium-sensing receptor (CaSR) on the parathyroid gland, effectively reducing PTH secretion and improving calcium-phosphorus metabolism.
3. New Osteoporosis Medications: Starting from March 2025, the National Health Insurance (NHI) in Taiwan expanded coverage for osteoporosis protection and treatment. Denosumab (Prolia) is a RANKL inhibitor that reduces bone loss and is suitable for patients with a T-score ≤ -2.5 and high fracture risk factors (such as rheumatoid arthritis, diabetes with insulin use, long-term steroid use, previous vertebral or hip fractures). Romosozumab (Evenity) is a sclerostin inhibitor that both promotes bone formation and inhibits bone resorption, suitable for high-risk postmenopausal women with a T-score ≤ -3 and fractures in at least two sites (such as distal radius, proximal humerus, spine, or hip).
4. Dialysis Treatment: Adjusting calcium concentration in dialysis fluid and ensuring adequate dialysis can help with phosphorus clearance and maintain calcium-phosphorus balance.
5. Surgical Treatment: For patients with severe and uncontrolled secondary hyperparathyroidism, parathyroidectomy may be recommended.
Ⅴ. Coexistence: Self-management and Lifestyle Adjustments for Patients
CKD with mineral bone disease and osteoporosis is a chronic, progressive condition that requires long-term collaboration between patients and healthcare teams with continuous monitoring. Through dietary adjustments, medication therapy, individualized dialysis prescriptions, surgical interventions, and the establishment of self-care habits, the risk of fractures, vascular calcification, and other complications can be significantly reduced. Personalized precision medicine, combined with AI-assisted detection, blood biomarker monitoring, and new osteoporosis medications (such as Denosumab and Romosozumab), can help dialysis patients improve from the challenges of osteoporosis and fractures, restore mobility, reduce mortality, and enhance quality of life.