Renal bone disease is a complex complication that emerges as kidney function declines. This condition affects the skeletal system and the body’s management of key minerals like calcium and phosphorus. It is a progressive disorder that can lead to weakened bones, increased fracture risk, and serious systemic issues, including cardiovascular problems.
Defining Chronic Kidney Disease–Mineral and Bone Disorder
The term “Renal Bone Disease” is now considered an outdated description for a far more extensive health problem. The modern, comprehensive name for this complication of chronic kidney disease (CKD) is Chronic Kidney Disease–Mineral and Bone Disorder (CKD-MBD). CKD-MBD is formally defined as a systemic disorder of mineral and bone metabolism that develops as a consequence of CKD.
This systemic disorder is characterized by three main issues: abnormalities in the metabolism of calcium, phosphorus, parathyroid hormone (PTH), and Vitamin D; defects in bone structure, strength, and mineralization; and the development of vascular or soft-tissue calcification. CKD-MBD impacts not only the skeleton but also the circulatory system, highlighting its potential to affect overall health and longevity.
The Biological Mechanism of Bone Damage
The damage to bone health begins when the kidneys lose their ability to properly balance minerals and hormones. A key step is the kidneys’ inability to convert inactive Vitamin D into its active form, calcitriol (1,25-dihydroxyvitamin D). This deficiency of active Vitamin D leads to poor absorption of calcium from the gut, resulting in low calcium levels in the bloodstream.
Failing kidneys cannot excrete phosphorus effectively, causing phosphate levels in the blood to rise. This phosphate retention, called hyperphosphatemia, can begin to occur as early as CKD stage 3. High phosphate levels contribute to low calcium levels and directly stimulate the production of Fibroblast Growth Factor 23 (FGF-23), which suppresses active Vitamin D production.
These imbalances—low calcium and low active Vitamin D—trigger the parathyroid glands to overproduce parathyroid hormone (PTH). This excessive secretion is known as secondary hyperparathyroidism, a compensatory mechanism to restore calcium levels. PTH achieves this by signaling the release of calcium and phosphate directly from the bones, a process called bone resorption.
While this action temporarily raises blood calcium, the continuous pull of minerals severely weakens the skeleton, leading to a condition known as renal osteodystrophy. Persistently high PTH levels can cause a high-turnover bone disease, where bone is broken down and reformed too quickly. Conversely, over-suppression of PTH can lead to adynamic bone disease, a low-turnover state where bone rebuilding is too slow.
Recognising Symptoms and Confirming Diagnosis
The physical effects of CKD-MBD often remain subtle until the condition is moderately advanced. Patients may experience persistent bone and joint pain, particularly in the hips, back, and legs, which may be mistaken for general aging or arthritis. Muscle weakness, especially in the muscles closest to the center of the body, is also a common complaint that can affect mobility.
The underlying bone weakness increases the likelihood of fractures from minimal trauma, known as fragility fractures. High levels of calcium and phosphate can lead to soft-tissue calcification, where minerals are deposited in blood vessel walls. This hardening of the arteries raises the risk of heart attacks and strokes, making CKD-MBD a contributor to cardiovascular mortality in CKD patients.
Diagnosing CKD-MBD involves assessment by healthcare professionals, beginning with specific blood tests. These tests monitor the levels of key biochemical markers, including calcium, phosphorus, and parathyroid hormone (PTH). Active Vitamin D levels are also checked.
Imaging studies and scans are used to evaluate the skeletal component of the disease. While bone mineral density scans are sometimes used, the gold standard for characterizing the type of bone disease is a bone biopsy. Doctors typically rely on the trends and patterns of the blood markers over time to guide diagnosis and treatment decisions.
Treatment and Management Strategies
The goal in managing CKD-MBD is to restore the balance of mineral and hormone levels to prevent further damage to the skeleton and cardiovascular system. Treatment involves dietary management, specifically controlling the intake of phosphorus. Patients are often referred to a dietitian to help identify and limit high-phosphate foods, such as processed meats, dairy products, and certain beverages.
Medications are required to manage the biochemical abnormalities. Phosphate binders are taken with meals to limit the absorption of phosphorus from the gut, reducing the amount that enters the bloodstream. These binders can be calcium-based or non-calcium-based, with the choice depending on the patient’s existing calcium levels and risk of vascular calcification.
To address the lack of active Vitamin D, patients may be prescribed nutritional Vitamin D supplements or activated Vitamin D analogs, such as calcitriol. Activated Vitamin D helps to improve calcium absorption and regulate PTH production. New classes of drugs, known as calcimimetics, work by making the parathyroid glands more sensitive to calcium, helping to suppress excessive PTH secretion.
In rare and severe cases of hyperparathyroidism that do not respond to medication, a surgical procedure called a parathyroidectomy may be necessary. This surgery involves removing some or all of the overactive parathyroid glands to stop the uncontrolled production of PTH. Management requires continuous monitoring of mineral and hormone levels to tailor the approach to the patient’s specific metabolic profile.