systemic sclerosis and renovascular HTN and ACE I's?

[neurotrancer]

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IF ACE I's are contraindicated w/ bilateral renal artery stenosis for fear of precipitating acute renal failure (drop glomerular filtration pressure secondary to efferent arteriolar dilation), then why are ACE I's considered 1st line with CCB's like nifedipine 2nd line in the treatment for renovascular hypertension in systemic sclerosis? isn't the afferent arteriole compromised in a similar way between these two diseases? Obviously there must be some difference, perhaps someone here can enlighten me.

thanks! Good luck on all the interviews!

 

[GreenOne]

cool avatar dude!😎

 

[neurotrancer]

Tnx! Say hello to my little friend!

 

[GreenOne]

Tnx! Say hello to my little friend!

sick man😎

 

[BlackNDecker]

IF ACE I's are contraindicated w/ bilateral renal artery stenosis for fear of precipitating acute renal failure (drop glomerular filtration pressure secondary to efferent arteriolar dilation), then why are ACE I's considered 1st line with CCB's like nifedipine 2nd line in the treatment for renovascular hypertension in systemic sclerosis?

thanks! Good luck on all the interviews!

You probably would have gotten a quicker response in the Clinical roations forum, but nontheless...

In B RAS, ACE is the principle factor maintaing glomerular pressure (by constricting the Efferent artery as you alluded). Giving an ACEI would essentially knockout all renal perfusion and you'd go into acute renal failure because oncotic pressure would be greater than hydrostatic pressure within the vessel in this situation.

Renovascular HTN, when unilateral, results in the secretion of large amounts of ACE from the pathologic kidney. The normal kidney has no choice but to respond to the AII and reabsorb more Na and H2O thus resulting in elevated BP.

isn't the afferent arteriole compromised in a similar way between these two diseases? Obviously there must be some difference, perhaps someone here can enlighten me.

The differece is that Renovascular HTN is more commonly UNILATERAL (not sure the actual %s but you could enlighten us with a search.😉). If the Renovascular HTN was BILATERAL, then the situation would be similar to B RAS.

In this situation you have 1 normal kidney and 1 diseased kidney (the afferent artery is only affected in the diseased kidney). Giving an ACEI will selectively decrease AII production from the diseased kidney and the normal kidney will accomodate the increased workload, eventually resulting in hypertrophy...

What you are essentially doing is finding the right balance b/w inhibiting ACE activity from the diseased kidney as much as possible to alleviate HTN...while at the same time maintaing enough renal perfusion in the normal kidney to prevent renal insufficiency.