What is the aldosterone paradox?
The ability of aldosterone to cause kidney retention of sodium without potassium secretion in states of volume depletion and stimulate kidney potassium secretion without sodium retention in hyperkalemia is called the aldosterone paradox.
During hypovolemia, angiotensin II and aldosterone have a synergistic effect on the sodium chloride cotransporter (NCC) and the ENaCs in the distal nephron, resulting in maximal sodium reabsorption. The resulting decreased distal delivery of sodium, as well as urine flow, reduces the secretion of potassium. In addition, angiotensin II has an inhibitory effect on ROMK, thereby reducing potassium secretion.
Hyperkalemia causes a renin and angiotensin II–independent increase in aldosterone secretion. In the absence of increased angiotensin II levels, NCC inhibition leads to increased sodium delivery to the ENaC. This leads to electrochemical absorption of sodium through ENaC coupled with secretion of potassium through the uninhibited ROMK channels.
