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Effect of diuretics on renal tubular transport of calcium and magnesium #MMPMID28274923
Alexander RT; Dimke H
Am J Physiol Renal Physiol 2017[Jun]; 312 (6): F998-F1015 PMID28274923show ga
Calcium (Ca(2+)) and Magnesium (Mg(2+)) reabsorption along the renal tubule is dependent on distinct trans- and paracellular pathways. Our understanding of the molecular machinery involved is increasing. Ca(2+) and Mg(2+) reclamation in kidney is dependent on a diverse array of proteins, which are important for both forming divalent cation-permeable pores and channels, but also for generating the necessary driving forces for Ca(2+) and Mg(2+) transport. Alterations in these molecular constituents can have profound effects on tubular Ca(2+) and Mg(2+) handling. Diuretics are used to treat a large range of clinical conditions, but most commonly for the management of blood pressure and fluid balance. The pharmacological targets of diuretics generally directly facilitate sodium (Na(+)) transport, but also indirectly affect renal Ca(2+) and Mg(2+) handling, i.e., by establishing a prerequisite electrochemical gradient. It is therefore not surprising that substantial alterations in divalent cation handling can be observed following diuretic treatment. The effects of diuretics on renal Ca(2+) and Mg(2+) handling are reviewed in the context of the present understanding of basal molecular mechanisms of Ca(2+) and Mg(2+) transport. Acetazolamide, osmotic diuretics, Na(+)/H(+) exchanger (NHE3) inhibitors, and antidiabetic Na(+)/glucose cotransporter type 2 (SGLT) blocking compounds, target the proximal tubule, where paracellular Ca(2+) transport predominates. Loop diuretics and renal outer medullary K(+) (ROMK) inhibitors block thick ascending limb transport, a segment with significant paracellular Ca(2+) and Mg(2+) transport. Thiazides target the distal convoluted tubule; however, their effect on divalent cation transport is not limited to that segment. Finally, potassium-sparing diuretics, which inhibit electrogenic Na(+) transport at distal sites, can also affect divalent cation transport.
Am+J+Physiol+Renal+Physiol 2017 ; 312 (6): F998-F1015
