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Can anybody tell me why do we have decreased GFR (decreased uptake) after giving captopril in patients with renal artery stenosis?

Isn't it that we actually give captopril for patients with renal artery stenosis as a mode of medical therapy!

Please explain for me :rolleyes:
 

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About Captopril and Renal Artery Stenosis

The kidney in renal artery stenosis is hypoperfused and it depends much on angiotensin to maintain it's GFR by constricting the efferent. When you remove the effect of Angiotensin by giving an ACE inhibitor you'll take from the kidney it's precious way of preserving the GFR and therefore you diminish the GFR.

The effect of ACE inhibitors on the kidney is transient as the kidney eventually will overcome the problem by local metabolites therefore on the long term ACE inhibitors not only they don't affect renal function but in fact they are protective against further renal damage (by decreasing the intra-glomerular hypertension and thence decreasing proteinuria and glomerular damage). That's why ACE inhibitors are perfect for diabetic hypertensives as it will postpone the onset of diabetic nephropathy.

In renal artery stenosis, you don't jump right away to Captopril but rather the first choice is percutaneous angioplasty and if that fails then surgery and if that fails then you go to Captopril.

When you give Captopril to these patients, OK you'll reduce the renal function for a while but as I said that's temporary and not permanent. But Captopril is absolutely contraindicated in bilateral renal artery stenosis as it risks a serious renal shut down in the acute phase.
 
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