This transcript has been edited for clarity.
Hello. This is Ileana Piña. I'm a professor of medicine at Wayne State University, and this is my blog. We're going to talk about potassium.
We have talked about potassium before. If you look at the literature, potassium is a very interesting ion that accumulates when patients are in renal dysfunction. We don't have great biomarkers in renal dysfunction for what I call true acute kidney injury. Regardless, as the creatinine goes up, the potassium goes up.
What is the knee reflex reaction of most clinicians when they see that? First of all, they become very scared because we were told in medical school that high potassium can produce arrhythmias and affect the EKG.
However, that response is attributed to really sudden rises in potassium rather than chronic rises in potassium. I personally have always run the potassium levels in my patients around 5 mmol/L because I think that a slightly higher level of potassium is actually protective against arrhythmias.
What does the average clinician do? Many nephrologists will tell you to remove the RAAS inhibitors. If you have heard any of my blogs before, you know that I am an ardent supporter of RAAS inhibition, particularly in heart failure with reduced ejection fraction (HFrEF), because they have been proven to improve survival and to decrease hospitalizations.
Then came the mineralocorticoid receptor antagonists, such as spironolactone and eplerenone. What do they do? They increase potassium. Now you have two types of drugs that are both increasing potassium.
Here's the dilemma: Do you keep the good drugs on and try to facilitate it with something to control the potassium? Doctors don't really like to facilitate a drug with another drug.
Let's look at our oncologists, though. They facilitate chemotherapy all the time by giving patients nausea medicine—antiemetics. We've been doing this for a long time too. I've been giving ACE inhibitors and cutting back the diuretic so that I can get the ACE inhibitor on board. So we've been doing it, but we just haven't called it that.
Now we have some choices because, to date, what we have had is SPS or Kayexalate, which has a black box warning from the FDA for colonic ulcers. It is a very unpleasant drug that is mixed in sorbitol and can actually increase volume.
We have two potassium binders on the market. One is called patiromer, which is a ligand that binds potassium primarily in the colon and lowers potassium levels within approximately 6 hours. It comes in doses of 8.4, 16.8, and 25.2 g.
I've been using that drug for a while and I've only really needed to give the lower dose along with the other drugs that I want the patients to have. It keeps the potassium around 4.6 mmol/L. There are data showing 52 weeks of potassium being very stable with patiromer.
The second potassium binder on the market is called ZS-9 or [sodium zirconium cyclosilicate]. That drug is very different because it's a chemical cage that cages potassium inside. It binds the potassium, but it trades it for sodium.
One of the concerns that people have had is, based on trading potassium for sodium, whether you are actually going to increase sodium absorption and fluid, which is something we're always trying to get rid of in our patients. However, if you look at the data very critically, it only happens at very high doses.
At least we have two choices. Now, the question comes as to whether the other drugs that increase potassium work because they increase potassium. In other words, is the higher potassium a protector of mortality and hospitalizations? If you lower the potassium, are you changing the effect of the drug?
What do we need when we have questions? You've heard me say this. If we have a question, then we need to do the study. And that's, in fact, what we are doing.
The study is called DIAMOND. This is a patiromer withdrawal study that is going to include patients who have been hyperkalemic in their history or are currently hyperkalemic, and we're going to randomize them to either continue patiromer or switch to placebo.
Then we're going to compare how many patients are able to stay on the RAAS inhibition with patiromer, and we're going to track outcomes. You need outcomes for this. Outcomes can include hospitalization in general, hospitalizations for heart failure, and mortality.
I leave you with those thoughts. I hope you consider that before you remove the good drugs that your patients need. Thank you for being with me today. This is Ileana Piña, signing off.
Ileana L. Piña, MD, MPH, is a heart failure and cardiac transplantation expert. She serves as an advisor/consultant to the FDA's Center for Devices and Radiological Health and has been a volunteer for the American Heart Association since 1982. Originally from Havana, Cuba, she is passionate about enrolling more women and minorities in clinical trials. She also enjoys cooking and taking spin classes.
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Any views expressed above are the author's own and do not necessarily reflect the views of WebMD or Medscape.
Cite this: Ileana L. Piña. Is Hyperkalemia Always Bad in Patients With Heart Failure? - Medscape - Mar 12, 2020.
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