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Sudden unexpected hypertension in a young woman with increased renin and no response to regular pharmacotherapy.

Think Renal Artery Stenosis secondary to Fibromuscular dysplasia

Look for abdominal bruits, beaded appearance in angiogrphy, and the treatment of choice is surgery.
 

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Yes, I am wondering about this question too. ARB's should respond? :rolleyes:
Treatment for high BP in FMD is in fact ACE inhibitors and ARB's but often even with management of blood pressure, the disease progresses due to bilateral artery stenosis and resulting ischemia so angioplasty is commonly indicated.

One way that this can be presented is a rise in creatinine or serum potassium shortly after initiation of ACEi or ARB therapy due to bilateral renal artery stenosis (AII normally maintains GFR with decreased blood flow so if this effect is blocked, GFR drops)
 

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Treatment for high BP in FMD is in fact ACE inhibitors and ARB's but often even with management of blood pressure, the disease progresses due to bilateral artery stenosis and resulting ischemia so angioplasty is commonly indicated.

One way that this can be presented is a rise in creatinine or serum potassium shortly after initiation of ACEi or ARB therapy due to bilateral renal artery stenosis (AII normally maintains GFR with decreased blood flow so if this effect is blocked, GFR drops)
Isn't GFR = Creatinine?

So in presense of AII, GFR will increase (constriction of efferent capillary), so if you block AII (by ACE or ARB), will it still be 'rise in creatinine / serum potassium', like you said?

I dont wholy get this :rolleyes::eek:
 

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Isn't GFR = Creatinine?

So in presense of AII, GFR will increase (constriction of efferent capillary), so if you block AII (by ACE or ARB), will it still be 'rise in creatinine / serum potassium', like you said?

I dont wholy get this :rolleyes::eek:
GFR and Creatinine are inversely related. The lower the GFR, the less creatinine is filtered, thus the serum creatinine will rise.

In the setting of bilateral renal artery stenosis, there is decreased blood flow to the glomeruli. In order to compensate and maintain GFR, AII constricts the efferent arteriole.

If you give an ACEi or ARB, this vasoconstriction is blocked so GFR falls to below normal. This leads to increased creatinine in the serum (unfortunately, potassium is a bit more complicated)

Note that if only one renal artery is stenosed, then the other kidney compensates for the decreased GFR in the affected kidney.
 

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GFR and Creatinine are inversely related. The lower the GFR, the less creatinine is filtered, thus the serum creatinine will rise.

In the setting of bilateral renal artery stenosis, there is decreased blood flow to the glomeruli. In order to compensate and maintain GFR, AII constricts the efferent arteriole.

If you give an ACEi or ARB, this vasoconstriction is blocked so GFR falls to below normal. This leads to increased creatinine in the serum (unfortunately, potassium is a bit more complicated)

Note that if only one renal artery is stenosed, then the other kidney compensates for the decreased GFR in the affected kidney.
Oh okay, yea I get what you're saying, that is what I was implying.

What i meant by GFR = Creatinine was that amount of Creatinine cleared = proportionate to GFR.

So if you decrease the GFR (ACEi or ARB), then serum creatinine will rise!

One thing I dont get, if you vasoconstrict (AII), the blood flow will increase (drop in radius), so will the Kidney still be able to extract O2 as compared to vasodilating?
 

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Renovascular hypertension

bilateral renal art stenosis can also be seen in elderly people.
as we know GFR is inversely related to serum creat..meaning an increase in serum creat means a decrease in creat clearance=GFR= renal failure
which is only seen when both kidneys are affected

a patient with bilateral renal art stenosis the GFR is maintained by AII mediated vasoconstriction of efferent arteriole. giving an ACEi/AIIi disregulate this mechanism leading to decreased GFR. further causes deminishing of RAAS leading to decreased aldosterone which promotes the hyperkalemia (also due to ARF).

note that there are more causes of ARF after initiating ACEi : CHF, PKD, bilateral hydronefrose, glomerular disease with intrarenal nefrosclerose.
 
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