Bartter Syndome mechanism has lost me

[Imogen]

---

Members do not see this ad.

I've been trying to puzzle out the mechanism for Bartter's for the past 30 mins and clearly I'm doing something wrong. I get that the Na/K/2Cl transporter in the thick ascending limb is blocked, and I understand that this will lead to decreased paracellular reabsorption of Ca (leading to hypercalcicuria). But what I don't get is what causes the hypokalemia and alkalosis.

Initially, I thought that the hypokalemia was simply due to the lack of K reabsorption by the malfunctioning Na/K/2Cl transporter, and that the alkalosis was due to increased H+ secretion (due to more K+ being delivered to the alpha-intercalated cells of the collecting duct and increased activity of the H/K-ATPase there).

Since I was spitballing on these theories, I then went and read this: http://emedicine.medscape.com/article/238670-overview#a3.

I am now totally confused because in the pathophys section of the medscape article, they talk about renin-angiotensin aldosterone system being stimulated... and I have no idea why that would be happening. Blocking the Na/K/2Cl transporter in the thick ascending limb would INCREASE sodium delivery to the distal tubule, which I thought would cause the macula densa to INHIBIT renin output.

I may have just been staring at this little section of the nephron for so long that I've completely thought myself into a loop... so any help would be very very much appreciated!

 

[cs24]

Block of NKCC xporter leaves sodium in the tubule that would have been reabsorbed, prompting your body to recruit aldosterone to try and get back that lost sodium (and water). The excess activity of aldosterone leads to dumping of potassium and H+ --> hypokalemia and alkalosis. At least that's how I think about it all. It's the same way a loop diuretic has its effects.

 

[sliceofbread136]

Block of NKCC xporter leaves sodium in the tubule that would have been reabsorbed, prompting your body to recruit aldosterone to try and get back that lost sodium (and water). The excess activity of aldosterone leads to dumping of potassium and H+ --> hypokalemia and alkalosis. At least that's how I think about it all. It's the same way a loop diuretic has its effects.

Also positive potential in the TAL is lowered, so K+ has less paracellular reabsorbtion

 

[Mkandil]

Block of NKCC xporter leaves sodium in the tubule that would have been reabsorbed, prompting your body to recruit aldosterone to try and get back that lost sodium (and water). The excess activity of aldosterone leads to dumping of potassium and H+ --> hypokalemia and alkalosis. At least that's how I think about it all. It's the same way a loop diuretic has its effects.

I second that

 

[Transposony]

Bartter Syndrome= Loop diuretics
Gitelman syndrome=Thiazide diurectics

"B" comes before "G" so Bartter Syndrome is in PCT and Gitelman syndrome is in DCT.
"B" comes before "G" so Bartter Syndrome is in LOH and Gitelman syndrome is in DCT.

 

[dfib slim]

Bartter Syndrome= Loop diuretics
Gitelman syndrome=Thiazide diurectics

"B" comes before "G" so Bartter Syndrome is in PCT and Gitelman syndrome is in DCT.

Fanconi first, the rest alphabetical in order.

Fanconi - PCT
Bartter - Loop
Gitelman - DCT
Liddle - Collecting tubule

 

[Transposony]

Fanconi first, the rest alphabetical in order.

Fanconi - PCT
Bartter - Loop
Gitelman - DCT
Liddle - Collecting tubule

Exactly. I messed up.

How about this:

"F"irst comes Fanconi (PCT)
"B" comes before "G" so Bartter Syndrome is in Loop of Henle and Gitelman syndrome is in DCT
Liddle is "Late" collecting tubules.

 

[Imogen]

Thanks a ton guys. And Cs24, I completely forgot to consider the overall volume and sodium loss that would result from this, then triggering aldosterone release. I was so caught up in the notion of delivering more NaCl to the macula densa as a result of the initial transporter failure in the TAL.