Guest guest Posted April 27, 2012 Report Share Posted April 27, 2012 I took the liberty of changing the name of this thread. Hope it better describes what we are talking about. Dr. Grim, I would like to respectfully suggest that there is a lot going on in the advancement of diagnosing and treating hyperaldosteronism. I know from spending 2 weeks at NIH that " the air is electric " and the " best Endocrinologists in the World " are working on it, I even had the privilege of talking with a couple of them. I suspect the following, note it was published 2 weeks ago, may be part of it but my Team is not available this week so I have not verified it. We have talked about the " KCNJ5 " gene and I understand they are very interested in dissecting my right adrenal! (I'm still waiting for their complete ideas!) They are also very interested in getting DNA from me and my three children! (Three or III is an interesting number isn't it!) Suggest you pubmed KCNJ5 and pay particular attention to the dates of publiction! You can also see where the work is being done! With that information and the following you might begin to see why I say low K may never be an issue for me, have a look: http://www.ncbi.nlm.nih.gov/pubmed/22508439 " Advances in WNK Signaling of Salt and Potassium Metabolism: Clinical Implications. " Abstract Recent evidence due to the discovery of a family of kinases implicated in arterial hypertension now points to the underlying molecular mechanisms that dictate Na(+), K(+) and water handling in the nephron. These new key players need to be understood in order to fully comprehend the pathophysiology, manifestations, and treatment of common clinical entities such as hypovolemic shock, congestive heart failure, primary hyperaldosteronism, nephrotic syndrome and hypertension. It is through the analysis of the volume status and electrolyte abnormalities that commonly present with these diseases that we can begin to create a link between the abstract concept of a kinase regulation and how a patient will respond to a particular treatment. This review is an attempt to bridge that gap. Copyright © 2012 S. Karger AG, Basel. Maybe it will soon be time to update your evolution article! .... > > > > > > > > > > A K of 3.7 could be a poor blood draw. If they use a > > tourniquet,, and I have never seen a nurse in an ER or floor NOT use > > a tourniquet except for someone who is very brittle or very > > dehydrated, and usually only after they have tried the tourniquet > > first. And many slap the vein/arm and can be a little rough about > > it, falsely increasing the K. When I ask them now, most act like > > they knew this about elevating K, but you can tell by their look > > they didn't know this nor were taught this. > > > > >  > > > > > I had the lab a while back draw my blood and I asked her not > > to use a tourniquet due to the potassium - she did anyway saying she > > draws it " fast " and so I let her (because the nurses always know > > more than anyone).  It came back 4.0, I didn't take my K for a few > > days and I could tell, absolutely no doubt, that my K was low. So I > > started taking it again and felt 100 times better. The lab was > > wrong. My follow up, after taking the K and with no tourniquet was 3.4 > > > > > > > > > > > > > > > > > Quote Link to comment Share on other sites More sharing options...
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