Hypoperfusion in RAS results in ↓GFR and activation of the RAAS: ↑ plasma renin, aldosterone (leads to hypokalemia & metabolic-alkalosis) and AT-II.

AT-II leads to constriction of efferent arterioles to ↑GFR and ↑systemic BP to ↑renal perfusion. This response is necessary to maintain renal function (↑FF).

ACE inhibitors ↓AT-ii which ↓perfusion/GFR leading to ↑renin.

I thought that it was essential hypertension, because when one gives ACE inh, Renin can Increase, due to loss of negative feedback.

However know that I know the answer I guess that it is Renal Artery stenosis because Renin and Aldosterone are increased (in essential htn they can be increased too but I guess not to the point where it causes metabolic derangements).

I'll appreciate if anyone can comment on this one.

Look, whenever the NBME describes a situation in which RAAS gets activated in response to NSAID or ACE/ARB, they are talking about renal artery stenosis.

NSAID leads to afferent arteriole constriction (blunted effect of prostaglandins)

ACE/ARB leads to efferent dilation (blunted effect of Ang II)