Hyperkalemia and NSAIDs

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Dr. Geoff

Mzungu
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Hey, just confused about this mechanism... NSAIDs can cause hyperK through eventual inhibition of renin... I thought with NSAIDs constricting the afferent arteriol, that would reduce kidney flow, and cause an increase in RAAS, and thus lower potassium... Why do they get hyperk? Can someone help me out?
 
I THINK that renin production/secretion is dependent on prostaglandins....

So NSAIDs would inhibit prostaglandins ---> decrease renin levels ---> decrease aldosterone -----> decrease sodium reabsorption and potassium excretion -----> hyperkalemia
 
I THINK that renin production/secretion is dependent on prostaglandins....

So NSAIDs would inhibit prostaglandins ---> decrease renin levels ---> decrease aldosterone -----> decrease sodium reabsorption and potassium excretion -----> hyperkalemia

I know this is late, but for anyone that also has difficulty with this, it helped me to look a little upstream of the situation.
Decreased renal perfusion -> Prostaglandin production -> afferent dilation AND renin stimulation (both beneficial effects of a poorly perfused kidney)

I originally was thinking that the constriction caused by nsaids would be the effect on renin, but when I looked at the reason prostaglandins were there in the first place, it made sense that removing them would decrease renin in addition to (not in response to) afferent constriction.
 
I know this is late, but for anyone that also has difficulty with this, it helped me to look a little upstream of the situation.
Decreased renal perfusion -> Prostaglandin production -> afferent dilation AND renin stimulation (both beneficial effects of a poorly perfused kidney)

I originally was thinking that the constriction caused by nsaids would be the effect on renin, but when I looked at the reason prostaglandins were there in the first place, it made sense that removing them would decrease renin in addition to (not in response to) afferent constriction.

thank you very much
 
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