Aldosterone is a bad actor. It is cardiotoxic. It drives a lot of hypertension. It is likely a progression factor in chronic kidney disease. (presentation with a lot of references to the primary data by Adrian Covic can be found here).
This is why aldosterone antagonists are such effective drugs in heart failure, such good antihypertensive agents and have potential in CKD. ACEi and ARB lower aldosterone because one of the two primary stimulants for aldosterone release is angiotensin 2. But about half of patients started on RAAS inhibition experience something called aldosterone escape, where within a few weeks of starting drug therapy, aldosterone levels returns to pre-treatment levels. I suspect a lot of this escape is mediated via increases in potassium.
The addition of patiromer in a situation like this could lower aldosterone levels and result in improved outcomes. So my call for outcome studies beyond changes in serum potassium is not a plot to derail the drug but to give the drug an opportunity to prove how it can actually improve renal and CV outcomes independent of just allowing patients to stay on RAAS inhibition.
The key is that if the studies are not done we will not know.