Re: How Does KCNJ5 affeet K & Na?

[Guest guest]

Note that most genetic causes of HTN only manifest if there is excess of salt (sodium) in the diet. So one good cheap test would be to DASH and see if BP gets better. If it does problem solved if it gets better enough. If not then do further testing or meds. But too easy I think. Well easy in concept, difficult in implementation.Just started trying Indian foods from a cook book with salt content or receipes. Salt can be lowered markedly by leaving salt out of recipe. Also looked at salt content of Indian breads and most are very high. But did find one Sanabel pita bread with only 25 mg per large slice. Made in Chicago.RE adrenal bumps: As most adenomas/hyperplasia are not detectable with current imaging methods this poses a problem as well. So must rely on their signature: low renin, not low aldo.On May 6, 2012, at 11:54 AM, wrote: , 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. ....

[Guest guest]

Is the problem solved or averted? And if it is averted is it likely to creep

back over time so it becomes a reoccuring problem? (You tell many to loose

weight and some do and some keep it off but many do not!) Is the same likely to

happen with DASH and NA?

If your roof leaks do you keep patching it and finally give up and replace it or

do you fix it (replace it) before it starts leaking? With a roof we use age as

a factor. With the human body we use good testing and proper tretment, IMHO!

Scans have progressed over the years and an experienced individual can tell a

lot from what I learned at NIH. I understand contrast can really help but some

don't believe in using it!

>

> > , 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.

> >

> > ....

> >

> >

>