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Serum calcium concentrations are normally tightly controlled within a narrow range, usually 8.5–10.5 mg/dL. However, the serum calcium concentration comprises less than 1% of the total body calcium content and is a poor reflection of overall total body calcium. The remainder of total body calcium is stored in bone. Serum calcium concentration comprises ionized calcium (approximately 40%), which is physiologically active, while the remainder of the calcium is bound predominantly to albumin (approximately 45%) and to a much lesser extent to anions (approximately 15%) such as citrate, bicarbonate, and phosphate. In the presence of acidosis, there is a relative increase in the ionized calcium component of the total serum calcium. Serum levels of ionized calcium are maintained in the normal range by the secretion of parathyroid hormone.

In normal individuals, the net calcium balance (intake–output) varies with age. Children and young adults are usually in a slightly positive net calcium balance to enhance linear growth; beyond age 25–35, when bones stop growing, the calcium balance tends to be neutral. Normal individuals have protection against calcium overload by virtue of their ability to increase renal excretion of calcium and reduce intestinal absorption of calcium by actions of parathyroid hormone and the activated form of vitamin D (calcitriol). However, in chronic kidney disease, the ability to maintain normal calcium homeostasis, including a normal serum ionized calcium level and appropriate calcium balance for age is lost.

Calcium absorption across the intestine occurs via a vitamin D dependent, saturable (transcellular) and independent, nonsaturable (paracellular) pathway. In states of adequate dietary calcium, the paracellular mechanism prevails, but the vitamin D dependent pathways are critical in calcium deficient states. In general, 15–25% of ingested calcium is absorbed. Normal ionized serum calcium is maintained by the secretion of parathyroid hormone which will increase bone resorption to release calcium into the circulation as well as to enhance calcium reabsorption by the kidneys. Parathyroid hormone also has an indirect effect by increasing the production of calcitriol by the kidney, which will act to increase the transcellular gastrointestinal absorption of calcium.


Essentials of Diagnosis

  • Decreased ionized serum calcium concentration or a decreased albumin corrected serum calcium concentration.

  • Defect or deficiency in the parathyroid hormone and/or vitamin D axis, resulting in decreased GI absorption or inability to mobilize calcium from bone.

  • Excessive tissue deposition such as occurs with massive tissue death or trauma, such as in rhabdomyolysis, tumor lysis, or acute pancreatitis.

  • Hyperphosphatemia results in complexation with high phosphate load, which may occur with excessive oral phosphate ingestion, phosphate enemas, or chronic kidney disease.

  • Excessive deposition of calcium in bone in patients with osteoblastic metastasis, such as prostate cancer.

  • May occur transiently in patients with severe sepsis or other serious illnesses.

General Considerations

The incidence of hypocalcemia is difficult to quantify as there have been very few studies. ...

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