Laboratory Studies
Laboratory analysis by atomic absorbance spectrophotometry (AAS) is the most specific technique available for measuring total serum magnesium in patients with suspected hypermagnesemia.
Although ion-selective electrodes for measuring free magnesium have been developed, their use has not been tested rigorously, and they are not readily available on a wide-scale basis.
Hypermagnesemia usually is not found as an isolated electrolyte abnormality; hyperkalemia and hypercalcemia often are present concurrently. Hypermagnesemia may secondarily cause hypocalcemia by suppressing parathyroid hormone (PTH) and by directly suppressing non–PTH-mediated renal tubular calcium reabsorption.
Obtain BUN and creatinine levels to determine the presence of renal insufficiency, as serum magnesium levels rise when the creatinine clearance is less than 30 mL/min.
Check creatine phosphokinase (CPK) or urine myoglobin in patients with suspected rhabdomyolysis.
Because hypothyroidism and adrenal insufficiency are rare causes of hypermagnesemia, perform thyroid function tests and at least an early morning serum cortisol test in recurrent or refractory cases of hypermagnesemia.
Other Tests
An ECG and cardiac monitor may demonstrate prolongation of the P-R interval, intraventricular conduction delay, or other nonspecific findings. [13]
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(A) Magnesium reabsorption in the thick ascending limb of the loop of Henle. The driving force for the reabsorption against a concentration gradient is a lumen-positive voltage gradient generated by the reabsorption of NaCl. FHHNC = Familial hypomagnesemia with hypercalciuria and nephrocalcinosis. ADH = autosomal dominant hypocalcemia. FHH/NSHPT = Familial hypomagnesemia/neonatal severe hyperparathyroidism. (B) Magnesium reabsorption in the distal convoluted tubule. Active transcellular transport is mediated by an apical entry through a magnesium channel and a basolateral exit, presumably via a Na+/Mg2+ exchange mechanism. HSH = Hypomagnesemia with secondary hypocalcemia. GS = Gitelman syndrome. IDH = Isolated dominant hypomagnesemia. Source: Konrad M, Schlingmann KP, Gudermann T: Insights into the molecular nature of magnesium homeostasis. Am J Physiol Renal Physiol 2004; 286: F599-F605.
