Chronic Kidney Disease (CKD) describes a condition where the kidneys progressively lose their function. Calcium is necessary for strong bones, muscle function, and nerve signaling. When kidneys fail, the system that stabilizes blood calcium is disturbed, which can lead to health issues if not addressed.
The Kidney’s Role in Mineral and Bone Metabolism
Healthy kidneys are important for maintaining mineral balance. One of their jobs is to convert vitamin D into an active form, calcitriol. Active vitamin D is necessary for the intestines to absorb calcium from food. Without it, the body cannot effectively obtain the calcium it needs.
The kidneys also regulate the balance of calcium and phosphorus in the bloodstream by filtering out and removing excess phosphorus. Phosphorus and calcium have an inverse relationship; when phosphorus levels are high, they can bind with calcium, lowering the amount of usable calcium in the blood. Healthy kidneys maintain this balance by excreting unneeded phosphorus in the urine.
This balance is further managed by the parathyroid glands. When these glands detect that blood calcium levels are low, they release parathyroid hormone (PTH). PTH signals the bones to release calcium into the bloodstream. It also acts on the kidneys to increase calcium reabsorption and stimulate the activation of vitamin D.
With the onset of CKD, these regulatory mechanisms begin to fail. Damaged kidneys become less efficient at activating vitamin D and excreting phosphorus, leading to low active vitamin D and high phosphorus in the blood. The elevated phosphorus binds with calcium, causing blood calcium levels to drop. In response, the parathyroid glands work overtime, releasing excessive PTH to raise calcium levels, a condition known as secondary hyperparathyroidism. This process is known as CKD-Mineral and Bone Disorder (CKD-MBD).
Hypocalcemia and Hypercalcemia in CKD
The disruption of mineral metabolism in CKD can lead to two conditions related to calcium levels: hypocalcemia and hypercalcemia. Hypocalcemia, or low blood calcium, is often seen in the earlier stages of CKD as a consequence of the mechanisms described above. Symptoms of hypocalcemia can include muscle cramps and spasms, numbness, and tingling in the hands, feet, or face.
Conversely, hypercalcemia, or high blood calcium, can also occur, particularly in later stages of CKD or as an unintended result of treatment. Prolonged secondary hyperparathyroidism can cause the parathyroid glands to draw large amounts of calcium from the bones into the blood. Additionally, treatments like high doses of calcium-based phosphate binders or certain vitamin D supplements can inadvertently raise blood calcium to unsafe levels. Symptoms of hypercalcemia include nausea, vomiting, constipation, increased thirst and urination, fatigue, and confusion.
Health Complications of Unregulated Calcium
The imbalance of calcium and other minerals in CKD can lead to long-term health problems. The overproduction of PTH places a demand on the bones to release their calcium stores. This process, if left unchecked, weakens the skeletal system, leading to a condition called renal osteodystrophy. Bones become brittle, painful, and more susceptible to fractures, impacting a person’s mobility and quality of life.
A dangerous consequence of unregulated calcium and phosphorus is vascular and soft tissue calcification. When there is an excess of both minerals in the bloodstream, they can combine to form hard, crystal-like deposits. These deposits can lodge in the walls of blood vessels, heart valves, and other soft tissues. Calcification of the arteries makes them stiff and narrow, which can elevate blood pressure and reduce blood flow. This process increases the risk for cardiovascular events like heart attacks and strokes, a leading cause of mortality for individuals with CKD.
Monitoring and Management Strategies
Managing mineral imbalances in CKD requires monitoring. Healthcare providers regularly order blood tests to track levels of calcium, phosphorus, PTH, and vitamin D. These tests allow the medical team to observe trends and make timely adjustments to the treatment plan, helping to prevent the progression of CKD-Mineral and Bone Disorder.
Dietary modification is a component of management. A renal dietitian often works with patients to create a plan that limits the intake of dietary phosphorus. High-phosphorus foods that are often restricted include:
- Dairy products
- Nuts
- Beans
- Dark-colored sodas
Calcium intake may also need to be adjusted based on blood test results and the types of medications being used. The goal is to control mineral intake to lessen the burden on the kidneys.
Medications help control mineral levels. Phosphate binders are a common prescription and are taken with meals to bind to phosphorus in the gut, preventing its absorption into the bloodstream. These binders come in calcium-based and non-calcium-based forms, and the choice depends on the patient’s specific blood calcium levels.
To address issues with vitamin D and PTH, other medications are used. Activated forms of vitamin D, such as calcitriol, may be prescribed to help control PTH levels. Another class of drugs, called calcimimetics, works by mimicking the action of calcium in the blood. This tricks the parathyroid glands into thinking calcium levels are adequate, reducing their production of PTH.