It is well known that hypokalemia does not correct easily if
it is accompanied by hypomagnesemia. A
medical student I met looked into this topic and found a “Science in Renal Medicine”
article. According to this article, one of the mechanisms through
which hypokalemia occurs in a hypomagnesemic state is through renal potassium wasting. Several
observations have shown that magnesium infusion decreases renal K secretion in
the distal nephron.
A study from Nature found that ROMK (aka
Kir), one of two potassium channels in the distal nephron, is responsible for the
distal renal K wasting in hypomagnesemia. The mechanism is that the intra-cellular
free Mg blocks the pore of the ROMK channel and limits potassium secretion in a
concentration-dependent manner; therefore low intracellular Mg level increases
potassium secretion.
Some renal Mg wasting disorders (e.g. Mg channel TRPM6
mutation) do not always present with hypokalemia. Why is that? The reason is
that you need 2 components for potassium excretion. One is increased K
permeability of the ROMK, and the other is a driving force to secrete K like increased
distal Na delivery or an elevated aldosterone level (via enhanced Na reabsorption in the distal
nephron). It seems in these disorders you don’t have the second determinant for
K secretion.
Another fascinating renal physiology article! Now we are
still confused but have a better understanding of hypomagnesemia in a case of
hypokalemia.
Posted by Tomoki Tsukahara
A more recent article actually looked at physiologic concentrations of Mg and what affect they have on regulating ROMK currents. It also found extracellular Mg can modulate ROMK activity suggesting that the TRPM6 mutants have low intracellular Mg but could have high extracellular Mg that could block ROMK currents.
ReplyDeletehttp://jasn.asnjournals.org/content/21/12/2109.long