Anyone know 3 different mechanism on how ACE inhibitors cause hyperkalemia? My preceptor asked me this question today and I could only come up with 2 reasons being: Inhibition of aldosterone production therefore decreasing Na reabsorbtion and potassium excretion, and dilation of the efferent arteriole causing decreased GFR. Any help would be appreciated.
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Question about ACE-I and hyperkalemia
Started by Pharmer_Andy
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Good question... I'll get back to you on this. I do have another question concerning ACE-I though. Does anyone know how it is nephrotoxic? I had a friend ask me this question while she was on rotation and I couldn't find out the exact mechanism. The insert referenced associated toxicity without an explanation.
Pulling the Insert again to see if I can't answer this question before everyone else lol. Which I'm not having any luck thus far.
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Already been explained in the first post. Efferent arteriole dialiation--> decreased blood pressure in glomerulus--> decreased GFR---> renal insufficiency/ARF.
That does make sense now that I am thinking about it that way. Decreased GFR... didn't relate that to ARF. To think it was that easy.
That does make sense now that I am thinking about it that way. Decreased GFR... didn't relate that to ARF. To think it was that easy.
Apparently this is a popular question on rotations. My preceptor asked me this today. Now why anyone cares about the mechanism behind ACE-I-induced ARF is beyond my knowledge.
So you know don't aggressively dose when initiating therapy. Start low and go slow.
It is an important mechanism, you would be surprised how many PCPs will ask you what is an expected SCr bump with an ACE-I/ARB and when they should worry.
Know the pharmacology and everything else will come to you...
Another mechanisms could be this:
Angiotension II is not only produced in the lung, but also in variety places over the body. ACE Inhibitors will decrease significantly the production of AII mainly in the lung, however, as a result, AII is increasingly synthesized at other places in the body. So, Chronic use of ACEI may cause a significant increasing in AII production in other places of the body. This is just an abstract, I am not 100% sure about it.
Angiotension II is not only produced in the lung, but also in variety places over the body. ACE Inhibitors will decrease significantly the production of AII mainly in the lung, however, as a result, AII is increasingly synthesized at other places in the body. So, Chronic use of ACEI may cause a significant increasing in AII production in other places of the body. This is just an abstract, I am not 100% sure about it.
I was going to guess that it's because people on ACE-I are godless heathens and so they're being smote by The Almighty One for their sinful ways.
True, it could be a right answer.
Uh, knowing the mechanism of ACE-I induced ARF won't give you the answer to that question....
And ditto for the person who said that it somehow teaches you to start ACE-I's at at a low dose and titrate the dose up. Why wouldn't you expect ACE-I's to cause chronic renal insufficiency after you titrate the dose up?
