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  #1  
Old 04-22-2012
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Kidney Bartter syndrome Hypokalemia and renal effects

Hi guys,
In Goljan RR 3rd edition page 65, on Bartter syndrome is said that:
hypokalemia stimulates increased prostaglandin synthesis in the kidney, which then stimulates hyperplasia of JG apparatus.
Can anyone explain me how all this happens?

Thanks
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Old 06-07-2012
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Originally Posted by sol1411 View Post
Hi guys,
In Goljan RR 3rd edition page 65, on Bartter syndrome is said that:
hypokalemia stimulates increased prostaglandin synthesis in the kidney, which then stimulates hyperplasia of JG apparatus.
Can anyone explain me how all this happens?

Thanks
Well man... to answer this Q... first you have to realize what is the function of the JGA. It detects renal perfusion pressure (RPP) (detected directly by the granular cells) and detects NaCl reabsorption in the Macula Densa (2nd to changes GFR).

High tubular concentrations of CaCl or a decrease in RPP---> increase renin secretion from JGP = improves CaCl reabsorption (via decreased GFR) and increased RPP (via vasoconstriction of afferent arteriole ), all of this leads to a low GFR/lower RBP (afferent arteriole vasoconstriction) = Increase FF ---> increase NaCl reabsorption. Now, having said all this...

in Batter's disease, there's an increases in Na, K, and Cl concentrations in the tubular lumen secondary to a defect in Cl reabsorption which has a "loop diuretics-like action" that leads to hypokalemia and metabolic alkalosis (secondary to increased HCO3 reabsorption due to the increased H excretion that couples K loss) Still with me??? I know, that last part was sort of a mix... (Review RR again if you got lost there )

Now.... (Here comes the trick)... Hypokalemia leads to increase PGE2 ---> afferent arteriole dilation ---> decreased RPP ---> JGA senses the high tubular Na, K, Cl concentrations plus the decrease RPP = renin secretion, but because PGE2 overcomes this reaction, there is a persistent vasodilation of the afferent arteriole (= decreased RPP) which in turn increases renin secretion (Also, the high tubular concentration of Na, K, Cl keeps stimulating the macula densa cells).

So at the end... and to summarize... chronic renin secretion with no effect on GFR, RPP, Na, Cl, K reabsorption = JGA hypertrophy due to exces of work.

Well... there you go... Any corrections or comments are more than welcome...
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  #3  
Old 06-08-2012
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Originally Posted by Dr. Mexito View Post
Well man... to answer this Q... first you have to realize what is the function of the JGA. It detects renal perfusion pressure (RPP) (detected directly by the granular cells) and detects NaCl reabsorption in the Macula Densa (2nd to changes GFR).

High tubular concentrations of CaCl or a decrease in RPP---> increase renin secretion from JGP = improves CaCl reabsorption (via decreased GFR) and increased RPP (via vasoconstriction of afferent arteriole ), all of this leads to a low GFR/lower RBP (afferent arteriole vasoconstriction) = Increase FF ---> increase NaCl reabsorption. Now, having said all this...

in Batter's disease, there's an increases in Na, K, and Cl concentrations in the tubular lumen secondary to a defect in Cl reabsorption which has a "loop diuretics-like action" that leads to hypokalemia and metabolic alkalosis (secondary to increased HCO3 reabsorption due to the increased H excretion that couples K loss) Still with me??? I know, that last part was sort of a mix... (Review RR again if you got lost there )

Now.... (Here comes the trick)... Hypokalemia leads to increase PGE2 ---> afferent arteriole dilation ---> decreased RPP ---> JGA senses the high tubular Na, K, Cl concentrations plus the decrease RPP = renin secretion, but because PGE2 overcomes this reaction, there is a persistent vasodilation of the afferent arteriole (= decreased RPP) which in turn increases renin secretion (Also, the high tubular concentration of Na, K, Cl keeps stimulating the macula densa cells).

So at the end... and to summarize... chronic renin secretion with no effect on GFR, RPP, Na, Cl, K reabsorption = JGA hypertrophy due to exces of work.

Well... there you go... Any corrections or comments are more than welcome...
uhh is this barter's syndrome thing hi yield?? i skipped it coz i hated it
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  #4  
Old 06-08-2012
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uhh is this barter's syndrome thing hi yield?? i skipped it coz i hated it

Not sure ... but he wanted to know ... Actually, I think is not big deal (is not that I am a genus or anything closer to one)... I just wanted to understand it because I was having some problems with fluids and electrolytes, plus, if it happens to be in step 1... I think I'll able to answer it
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