Calcium Regulation

Calcium disorders are not diagnosed from a calcium value in isolation. Start by deciding whether the biologically active calcium is low or high, then ask whether the parathyroid hormone (PTH) response is appropriate for that calcium level. A high PTH in hypercalcaemia is abnormal even if it falls within the laboratory reference range; a low or merely normal PTH during hypocalcaemia is an inadequate response. The kidney is both a regulator and a target organ. PTH and calcitriol alter renal calcium and phosphate handling, while chronic kidney disease changes vitamin D activation, phosphate balance, bone turnover and the safety of calcium-based treatment. The practical consequences are substantial: hypocalcaemia can produce tetany, seizures and ventricular arrhythmia, whereas excessive calcium replacement can cause hypercalciuria, nephrolithiasis, vascular calcification or acute kidney injury. A useful clinical sequence is therefore: verify the calcium measurement, interpret PTH with phosphate and magnesium, identify the source of the disorder, assess ECG and neuromuscular danger, and choose treatment that corrects the immediate problem without creating renal or skeletal harm.