Type II RTA and Hypokalemia

[Ihateverbal]

Anyone know the relationship between Type II RTA and Hypokalemia.

Type II RTA is a defect in reabsorption of bicarbonate which would make the urine alkaline but the blood acidic. I would imagine that acidemia, K+ Shifts OUT of the cell and H+ shifts INTO the cell. Wouldn't this make Type II Hyperkalemic?

Please help!

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[AllUpOnYoMama]

whats up dude. hyperkalemia inhibits NH3 synthesis thus produces a decrease in H secretion as NH4.... so hypokalemia must stimulate NH3 synthesis which produces an increase in H secretion. I might be wrong with this thought process here. But I think that in acidosis, there is an adaptive increase in NH3 synthesis due to hypokalemia that occurs aiding in the excretion of the excess H. Its a good question. I'm not too sure about this. Please correct me if Im worng

 

[Ihateverbal]

any other thoughts? i have no idea

Type I --> hypokalemia (makes sense because you inhibit the H/K ATPase)
Type II --> hypokalemia (confused )
Type IV --> hyperkalemia (because hypoaldosteronism due to destruction of JGA, makes sense)

 

[arroser]

any other thoughts? i have no idea

Type I --> hypokalemia (makes sense because you inhibit the H/K ATPase)
Type II --> hypokalemia (confused )
Type IV --> hyperkalemia (because hypoaldosteronism due to destruction of JGA, makes sense)

So, normally carbonic anhydrase makes HCO3 in the lumen, stimulating the Na/H exchanger to secrete protons and reabsorb Na. However, without any stimulus to do so (no functional CA) the protons stay in the body and the Na stays in the urine. As we all know, increased Na delivery to the distal convoluted tubule will increase Na/K exchange via aldosterone.

I'm not quite sure that's right, but it's how I'm going to think about it. Sort of an exaggerated acetazolamide effect.

 

[Ihateverbal]

sigh

oh well...sometimes i feel like we just got to make **** up and just have it make sense to us LOL

 

[stickshift]

So, normally carbonic anhydrase makes HCO3 in the lumen, stimulating the Na/H exchanger to secrete protons and reabsorb Na. However, without any stimulus to do so (no functional CA) the protons stay in the body and the Na stays in the urine. As we all know, increased Na delivery to the distal convoluted tubule will increase Na/K exchange via aldosterone.

I'm not quite sure that's right, but it's how I'm going to think about it. Sort of an exaggerated acetazolamide effect.

The cause of hypokalemia is due to increased Na+ presentation to the collecting ducts. Remember, that whole Na/K exchange via aldosterone occurs in the principal cells of the collecting ducts.

Hyperparathyroidism can also cause type 2 RTA, and hyperparathyroidism would also increase Na+ presentation to the collecting ducts (i.e. inhibiting Na/phosphate co-transport in the proximal tubule and increasing Na/Ca exchange in the distal tubule).

 

[vrentas527]

Urinary K+ wasting and hypokalemia are common in type 2 RTA and are due to persistent hyperaldosteronism, leading to increased K secretion by the distal nephrons. Hyperaldosteronism in these patients is related to the defect in proximal reabsorption of filtered HCO3- which in effect leads to decreased proximal NaCl reabsorption and a tendency for salt wasting.
http://fitsweb.uchc.edu/student/selectives/TimurGraham/RTA2.html

 

[Pons Asinorum]

Strong 4-year RTA bump.

 

[krps85]

Weird, I just got to this thread after googling this exact question... and notice that it was just bumped today

 

[voicesinmyhead]

I read here that the hypokalemia in RTA type II is due to the excess Hco3- in the tubular filtrate binding to the K+, thus precenting its reabsorption.

Some place else states that the hypokalemia is because of hyperaldosteronism due to the volume contraction? (which volume contraction?)

Wonder which one is correct?