πͺ¨ Metastatic calcification is the deposition of calcium salts in normal tissues, unlike dystrophic calcification which occurs in damaged tissue.
Commonest causes: 𦴠Hyperparathyroidism, π« Sarcoidosis, π¦ Malignancy (myeloma, mets), βοΈ Vitamin D excess.
It may also occur in patients with hypermetabolic states and prolonged bed rest.
βΉοΈ About
- Deposition of calcium salts in previously normal tissue. π§¬
𧬠Aetiology
- Occurs when the calcium Γ phosphate product is increased β precipitation of amorphous calcium phosphate in organs, vessels, and soft tissues.
π Causes
- β¬οΈ PTH (primary or secondary hyperparathyroidism) β hypercalcemia.
- Renal failure (secondary hyperparathyroidism, phosphate retention). π§
- Malignancy: multiple myeloma, breast Ca, squamous cell Ca (PTHrP). ποΈ
- Vitamin D intoxication or sarcoidosis (β calcitriol). βοΈ
- Granulomatous disease (TB, histoplasmosis, toxoplasmosis).
- Amyloidosis, Addisonβs disease (adrenal calcification).
- Endocrine tumours (e.g. gastrinoma).
- Nephrocalcinosis, ossifying metastases (osteosarcoma, ovarian mets).
π Common Causes (High Yield)
- Hyperparathyroidism: β bone resorption & β renal Ca reabsorption.
- Renal failure: β¬οΈ phosphate + secondary HPT β Ca-P imbalance.
- Malignancy: Osteolysis or PTHrP secretion.
- Vitamin D intoxication: β intestinal Ca absorption.
- Granulomatous disease (e.g. sarcoidosis, TB): β calcitriol production.
π§« Pathology
- Deposits both intracellular & extracellular. π¬
- Favoured sites: kidneys, lungs (alveolar walls), gastric mucosa, cornea, conjunctiva, arteries (media & intima).
βοΈ Pathophysiology
- Occurs when Ca Γ phosphate > solubility threshold β Ca salts precipitate.
- Unlike dystrophic calcification, this occurs in absence of tissue injury.
- Favourable environments: alkaline tissues (lungs, kidney, stomach, vessels).
π― Commonly Affected Sites
- π« Lungs: Alveolar walls & bronchi β dyspnea, restrictive changes.
- π§ Kidneys: Tubules/parenchyma β nephrocalcinosis, renal impairment.
- π½οΈ Stomach: Gastric mucosa β gastritis, β acid secretion.
- β€οΈ Heart/vessels: Valves, myocardium, arteries β HTN, arrhythmias.
π©ββοΈ Clinical Presentation
- Symptoms depend on affected organs + severity.
- π« Dyspnoea, chronic cough, β lung capacity (pulmonary calcification).
- π§ Polyuria, polydipsia, renal insufficiency (nephrocalcinosis).
- π½οΈ Nausea, vomiting, epigastric pain (stomach calcification).
- β€οΈ HTN, arrhythmias, heart failure (cardiac involvement).
π Diagnosis
- π§ͺ Bloods: β calcium, phosphate, PTH Β± vitamin D abnormalities.
- π©» Imaging: X-ray/CT/MRI β tissue calcifications.
- π¬ Biopsy: Confirms Ca deposits in normal tissue.
- π§Ύ Renal function & metabolic workup.
π Treatment
- π― Treat underlying cause of hypercalcemia.
- Hydration + loop diuretics (furosemide) to enhance Ca excretion.
- Bisphosphonates & calcitonin to lower Ca. π
- Parathyroidectomy if refractory hyperparathyroidism.
- Dialysis in renal failure cases. π§
- Ongoing monitoring: renal, lung, and cardiac function.
π Prognosis
Depends on underlying cause & extent of organ involvement.
π©Ί Early recognition + calcium control prevents irreversible organ damage.