How Does KCNJ5 affeet K & Na?

[Guest guest]

, I'm not smart enough to know WHAT is going on but I am smart enough to

know SOMETHING IS going on! You keep talking about K and I think this may be a

large part of the alteration of both K and Na. (If I read this correctly it may

affect almost half w/adenomas!, who knows how many w/o!)

How about a $10 blood test (okay $250 with handling and government) and a pill

that addresses that specific issue!

I asked dr. Moriatis If KCNJ5 was likely issue for me and here is his answer,

" We can find out if the adenoma harbors the mutation after we take the right

adrenal out. Your AVS showed that the dominant gland is on the right side. "

Src: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3289329/pdf/pnas.201121407.pdf

Title: " Hypertension with or without adrenal hyperplasia due to different

inherited mutations in the potassium channel KCNJ5 "

The demonstration of increased cell lethality with both G151R and G151E

mutations has potential implications for the molecular diagnosis of APAs. With

only two mutations in KCNJ5 (G151R and L168R) accounting for ~45% of APAs, it

might be possible to develop specific tests for these somatic mutations in DNA

released from dying cells in APAs into the circulation. Identification of these

mutations in plasma could be used as a simple noninvasive diagnostic test in

patients in whom APA is suspected. The increased turnover of cells harboring

these mutations increases the likelihood that these mutations might be of

sufficient prevalence in plasma to be detected. This test could be used to

identify individuals with high likelihood of APA. Alternatively, it might be

possible to develop selective inhibitors of mutant KCNJ5 that would be highly

selective and effective in the treatment of patients with these mutations.

Lastly, these findings also have implications for other patients with primary

aldosteronism who do not have APA or hyperplasia. The ability of G151E mutations

to cause aldosteronism without hyperplasia or APA raises the question of whether

somatic, rather than inherited, G151E mutations might frequently contribute to

development of hypertension featuring high aldosterone:renin ratios and/or

primary aldosteronism in the absence of APA or hyperplasia.

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