Metastatic calcification describes the abnormal deposition of calcium salts into otherwise healthy tissues throughout the body. This occurs when elevated calcium levels in the bloodstream, known as hypercalcemia, lead to calcium precipitation in various soft tissues. In contrast, dystrophic calcification involves calcium deposition in tissues that are already damaged, necrotic, or degenerated, regardless of normal blood calcium levels. Both types of calcification involve the formation of calcium phosphate crystals, but their underlying causes and tissue characteristics differ significantly.
Underlying Causes of Calcium Imbalance
A frequent cause is chronic kidney failure, where the kidneys cannot adequately excrete phosphate. This leads to an imbalance in the calcium-phosphate product in the blood, which, when elevated, promotes the precipitation of calcium salts in soft tissues. For instance, a calcium-phosphate product exceeding 55 mg²/dL² often leads to crystal formation and deposition.
Another common cause is hyperparathyroidism, where overactive parathyroid glands release excessive amounts of parathyroid hormone (PTH). PTH then draws calcium from the bones into the bloodstream, increasing serum calcium levels.
Vitamin D-related disorders can also contribute to metastatic calcification. This includes excessive intake of vitamin D supplements, which enhances the absorption of calcium from the gastrointestinal tract. Certain diseases like sarcoidosis can also cause increased production of active vitamin D by immune cells.
Conditions involving extensive bone destruction, such as multiple myeloma or other cancers that have spread to the bone, release large amounts of calcium into the bloodstream. The resulting high calcium levels can overwhelm the body’s regulatory mechanisms, leading to widespread calcification.
Commonly Affected Organs and Tissues
Metastatic calcification frequently affects specific organs and tissues. These include the kidneys, lungs, the lining of the stomach (gastric mucosa), and blood vessels. These sites are particularly susceptible due to their internal environment.
The localized alkaline environment within these organs contributes to this susceptibility. Tissues like the lungs, kidneys, and stomach actively excrete acid, which makes their internal interstitial fluid relatively alkaline. This higher pH creates conditions favorable for calcium phosphate to precipitate out of the bloodstream and form deposits.
Calcium salts are often deposited in the alveolar walls of the lungs and the tubules of the kidneys. In the stomach, deposits tend to occur around the fundic glands. The vasculature, particularly systemic arteries, also commonly shows these calcifications.
Health Implications and Diagnosis
In the kidneys, metastatic calcification can cause nephrocalcinosis, potentially worsening kidney dysfunction or contributing to kidney stone formation. When the lungs are affected, it can result in restrictive lung disease, leading to symptoms such as shortness of breath and a persistent cough, though many patients may remain asymptomatic.
Calcification in blood vessels contributes to arteriosclerosis, or hardening of the arteries, which can increase the risk of cardiovascular problems. Calcium deposits in the stomach lining may cause pain or discomfort, though these symptoms are often overshadowed by the underlying condition causing the hypercalcemia. Symptoms of metastatic calcification are frequently subtle and may only become apparent in advanced stages of the underlying disease.
Diagnosis often involves a combination of laboratory tests and imaging studies. Blood tests measure serum calcium and phosphate levels, confirming hypercalcemia and an elevated calcium-phosphate product. Imaging techniques like X-rays or computed tomography (CT) scans visualize calcium deposits in various organs and tissues. Bone scintigraphy using technetium-99m methylene diphosphonate (99mTc-MDP) can also detect widespread calcium accumulation in soft tissues, as technetium seeks calcium.
Management and Treatment Approaches
The primary strategy for managing metastatic calcification involves addressing the underlying cause of elevated blood calcium levels. Directly removing calcium deposits from affected tissues is generally not the focus of treatment. For patients with chronic kidney disease, management may include dialysis to excrete excess phosphate and calcium, or medications like phosphate binders to reduce phosphate absorption.
If hyperparathyroidism is the cause, surgical removal of overactive parathyroid glands can significantly lower parathyroid hormone and calcium levels. In cases of vitamin D toxicity, adjusting or discontinuing vitamin D supplement intake is necessary to reduce calcium absorption. For cancers causing bone destruction and hypercalcemia, treating the specific malignancy through chemotherapy or other targeted therapies is the main approach.
Supportive measures also lower blood calcium directly while the primary condition is addressed. These can include intravenous hydration to promote calcium excretion through the kidneys and bisphosphonates, which reduce calcium release from bones. Medications like calcitonin can also be used for a rapid, albeit temporary, reduction in calcium levels.