Also, you shouldn't be seeing end-organ damage or increased renin / kidney response with a previously healthy patient that just developed essential HTN. The body doesn't want to increase renin when it has HTN. However, if you have stenosis, the kidneys freak out because they're not getting enough flow and think the whole body isn't either, so they activate the RAAS system. When you give them an ACE-I, the renin is still being produced by the kidney, it just isn't being converted to angiotensin-II.

To eliminate other choices:

• He has increased renin activity so you can eliminate primary aldosteronism. That has inc. aldosterone, dec. renin.
• No signs or sxs of Cushing's so that's eliminated.
• 11-B-hydroxylase deficiency would sxs with the genitalia. You'd have dec. renin activity (aldosterone-like effects still present).
• Essential HTN: explained above

As a rule of thumb, if you give someone an ACE inhibitor and they get a problem, they had renal artery stenosis (usually bilaterally, or so we were taught at our med school). Probably has to do with decreased GFR thanks to decreased Angiotensin II–selective vasoconstriction of the efferent arteriole => decreased sodium delivery to macula densa => increased renin release.

I struggled with why this couldn’t be essential HTN for a while. I think what it comes down to is this, and someone help me out if I’m incomplete/wrong.

In bilateral RAS, ACE inhibitors will decrease the GFR from dilation of efferent arteriole and they can’t increase the GFR further because they’re already maxed out on afferent dilation to keep up GFR in the first place.

In essential HTN, yes ACE inhibitors decrease GFR from dilation of efferent arterioles, however they’re able to maintain GFR through autoregulation because they haven’t touched their afferent arteriole. So this means that renin won’t actually increase.

TL;DR: Bilateral RAS is unable to use autoregulation to correct the decrease in GFR where essential is able to.

FA19 P592: Renovascular disease: Renal impairment due to ischemia from renal artery stenosis or microvascular disease.  renal perfusion (one or both kidneys) Ž INC renin Ž INC angiotensin Ž HTN. Main causes of renal artery stenosis: ƒ Atherosclerotic plaques—proximal 1/3rd of renal artery, usually in older males, smokers. ƒ Fibromuscular dysplasia—distal 2/3rd of renal artery or segmental branches, usually young or middle-aged females. Clinically, patients can have refractory HTN with negative family history of HTN, asymmetric renal size, epigastric/flank bruits. Most common cause of 2° HTN in adults. Other large vessels are often involved

FA19 P 596: Angiotensin- converting enzyme inhibitors Captopril, enalapril, lisinopril, ramipril. mEChANism Inhibit ACE Ž DECR AT II Ž DECR GFR by preventing constriction of efferent arterioles. INCR renin due to loss of negative feedback.