Captopril and Renal Failure

[Kluver_Bucy]

---

Members do not see this ad.

Help, how does decreasing AII cause renal failure?

 

[omarsaleh66]

ATII maintains blood flow to the kidneys by its actions on the efferent arteriole. So if u have renal stenosis and u have problems getting blood to the kidneys in the first place, then renin is secreted and u get ATII, aldosterone to maintain adequate blood pressure to your kidneys. That's why ACE inhibitors are contraindicated in renal artery stenosis.

On the flip side, if u are a diabetic and u are peeing out all this albumin, then u want to give ACEI so efferent arterioles are relaxed and u can decrease proteinuria. (I think this is right? I forgot??)

Also, if u give ACEI to a pregnant woman, the fetal kidneys dont develop and u get oligohydramnios and Potters syndrome (this might show up on step 1? )

later

 

[12R34Y]

Help, how does decreasing AII cause renal failure?

in renal artery stenosis the GFR is dependant on the angiotensin mediated vasoconstriction of the efferent arterioles in the kidney. this constriction maintains adequate GFR. If you lose that by giving an ACE you could theoretically/potentially dramatically and suddenly decrease GFR causing oliguric renal failure.

later

 

[HiddenTruth]

On the flip side, if u are a diabetic and u are peeing out all this albumin, then u want to give ACEI so efferent arterioles are relaxed and u can decrease proteinuria. (I think this is right? I forgot??)

Yea, pretty much you are right. Just to fill in the spaces, and for sake of its entirety, in DM, you develop hyaline arteriolosclerosis of both afferent and efferent arterioles, (efferents worse, and occur first) due to nonenzymatic glycosylation, rendering BM permeable and resulting in leakage of plasma components across vascular endothelium and increased ECM production by sm mm cells. This leads to narrowing of the lumen, and progressive renal ischemia. So, you have significant increases in GFR over time, due to the arterioloscl and the ATII mediated VC of efferent arterioles in response to the decreased blood flow to the kidney. So, your kidneys are just being hammered with the increased GFR and decreased blood flow. And eventually, after 10 years or so, you end up getting microalbuminuria, (this is why in HTN pts, who can develop similar vascular damnage, you check annual Urine microalbumin/Cr levels, and likewise in DM pts), and this is usually the first sign of nephropathy. A lot of this proteinuria is the combination of the increased GFR (as a result ATII and narrowed lumen--which is indirectly as a a result of the nonenz glycos), and the nonenz glycos directly rendering the BM perm to proteins. So, you can see, that the glucose levels are crtical here, becuase the nonenz glycos has a pretty significant impact on the capill.

So, to put this in context with ACE-I, you always read that they "slow the onset and the progression of nephropathy", well all this means is that they let off some of the pressure on the glomer. by inhibiting ATII formation. You still have the narrowed hyalinized arterioles, and the nonenz glycosylation, etc...but u just inhibit the ATII effect (VC) on the efferents, and thus, can decrease the GFR a bit. Pretty much, ACE-I aint gonna do jack if the sugar levels remain uncontrolled (as explained above). Well, anyways, I'm done blabbing-sorry for my fragmented verbage.

 

[Kluver_Bucy]

ATII maintains blood flow to the kidneys by its actions on the efferent arteriole. So if u have renal stenosis and u have problems getting blood to the kidneys in the first place, then renin is secreted and u get ATII, aldosterone to maintain adequate blood pressure to your kidneys. That's why ACE inhibitors are contraindicated in renal artery stenosis.

On the flip side, if u are a diabetic and u are peeing out all this albumin, then u want to give ACEI so efferent arterioles are relaxed and u can decrease proteinuria. (I think this is right? I forgot??)

Also, if u give ACEI to a pregnant woman, the fetal kidneys dont develop and u get oligohydramnios and Potters syndrome (this might show up on step 1? )

later

Thanks Omar. What book did you use for pharmacology during the school year, and what is your study technique for pharmacology for the boards.

 

[omarsaleh66]

I didnt really use any pharm books that instensly during the year cuz our pharm lecture notes were sufficient. Pharm Recall is a good book if u are studying for the boards and u are running out of time. I think that when u study pharm u really gotta think of the physiology behind how the drug works. Dont really memmorize the drug, think more about the drug class and how it works, side effects, and how it interacts with other drugs.

I have step 1 next week, I might not even get to pharm. I have a lot of weak areas I need to address before pharm but if i have time, I definietly will look at Pharm Recall really quick to see everything once or fly thru my class powerpoints (not for learnign but just recall so it can be done in a couple of hours). And also First Aid. Just holler at me if u need anything. later

 

[omarsaleh66]

Some more thoughts:

Another thing that helps is to lump eveyrhting together. Like we were talking about ATII right? So we discussed ATII and renal artery stenosis and diabetes. See how they work differently on the efferent arterioloe. The next thing I think about is the afferent arteriole? That is controlled by Prostaglandins and NSAIDS hit that so a lady thats taking NSAIDS might get renal problems from that.
By lumping all this stuff together u can remember it. Goljan teaches this as a way to learn and it works I think.

The Appleton Lange Pharmacology section is really good. So are the comprehensive exams.

If u are really weak in certain pharm subjects, u might wanna do those specific sections in Pretest. Thats up to u.

But everyone says, including my frend who just took step 1 that everything is in First Aid and its pretty much all drug-drug interactions.

Ill tell u more next monday, LOL.

later