ACEi and Kidney

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qw098

zyzzbrah
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Confused as ****.

ACEi and kidney.. I thought ACEi could cause acute renal failure... but ACEi is used in chronic renal failure..?

I'm confused. Could anyone elaborate please?
 
http://circ.ahajournals.org/content/104/16/1985.full

think about the physiology of ace inhibitors and how they block the effects of angiotensin 2 at efferent arterioles. ace inhibitors decrease gfr by increasing flow past the renal tubules instead of through the glomeruli into the tubules. so you'd expect to see a rise in creatinine. but in chronic renal failure, you have renal tubules getting messed up by sugar, high pressure, etc. ace inhibitors decrease the negative hemodynamic effects of chronic hypertension on the glomeruli (remember that the kidneys get somewhere around 25% of co) and block remodeling of the heart as well
 
http://circ.ahajournals.org/content/104/16/1985.full

think about the physiology of ace inhibitors and how they block the effects of angiotensin 2 at efferent arterioles. ace inhibitors decrease gfr by increasing flow past the renal tubules instead of through the glomeruli into the tubules. so you'd expect to see a rise in creatinine. but in chronic renal failure, you have renal tubules getting messed up by sugar, high pressure, etc. ace inhibitors decrease the negative hemodynamic effects of chronic hypertension on the glomeruli (remember that the kidneys get somewhere around 25% of co) and block remodeling of the heart as well

ok sweet, that's exactly what I thought. But I guess if you're in renal failure it's odd that you would be willing to decrease your gfr... but i guess decreasing the sugar in your tubules and decreasing your high pressure is more beneficial than decreasing the gfr...

thanks psai
 
I think it depends on the aetiology of the CKD. An ACE inhibitor would be indicated in something like diabetic kidney disease and in instances of proteinuria where the ACEi will help lower blood pressure, reduce proteinuria etc. It's not really a straight forward relationship where decreasing GFR = Bad for your kidneys under any circumstance. While a decreased GFR is an extremely common cause of AKI, a high GFR can also be an indirect cause of AKI, or more commonly CKD.
 
ACEi are good for CKD for a variety of reasons:
1) overall systemic blood pressure control
2) decreases hydrostatic pressure in the glomerulus leading to lower single nephron GFR and (varying degrees) of overall GFR which reduces maladaptive hyper filtration in diabetic kidney disease and virtually all other renal diseases
3) biologic effects that aren't completely understood but AngII is a bad player in the genesis of renal fibrosis by directly stimulating TGF-B production in the kidney and heart and probably other organs, these are probably the most important effects as CKD patients don't die from renal disease per se, rather cardiovascular complications

ACEi are bad in situations that stress renal auto regulation: volume contraction, coexisting diuretics and NSAIDs, CNIs, systemic hypotension. Though the effects may be mild or negligable in patients without renal issues who can auto regulate RBF well, in a patient who is "stressed" with a chronic disease at baseline: renovascular disease (hyalin arteriosclerosis of afferent arterioles), advanced CKD (lower reserve), HF, cirrhosis, and nephrosis (chronic prerenal state), the effect can be dramatic and ACEi can help precipitate ischemic tubular injury.
 
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