Evaluation of hypomagnesemia: lessons from disorders of tubular transport

Abstract

Hypomagnesemia is a highly prevalent clinical condition affecting a large number of hospitalized patients. A decrease in systemic magnesium concentration may lead to impaired function of both neurologic and cardiovascular systems. The kidney has a pivotal role in magnesium handling by adjusting the urinary excretion of this ion in order to maintain systemic concentrations within a narrow range. As such, the cause of hypomagnesemia can be related to increments in the renal excretion of this cation. Many hypomagnesemic disorders also have characteristic changes in the renal reabsorptive capacity for other electrolytes, leading to symptoms that sometimes obscure the clinical presentation. For instance, changes in serum calcium concentration or its urinary excretion can aid in determining the underlying cause. Moreover, hypokalemia due to renal potassium losses often is associated with hypomagnesemia. Genetic defects in pathways controlling renal electrolyte transport impose the hypomagnesemic condition by facilitating renal losses. The discovery of the causative genes has greatly increased our understanding of how magnesium is transported by the kidney. Such knowledge is integral for the continued improvement of patient care with respect to bettering therapies and diagnosis.

Keywords: Gitelman syndrome; Kidney; inherited renal disorders; transient receptor potential melastin 6 channel (TRPM6).