Tag: potassium

Posted on

Hyperkalemia or not

A patient came to the hospital with a swollen arm. The ED suspected a DVT and ordered a doppler ultrasound which confirmed their suspicion. The admission labs included a chem-7 which revealed a potassium of 7. Her creatinine was 1 and she wasn’t taking an ACEi, ARB, aldactone, ketoconazole, or potassium supplements. The ER was surprised and repeated the study and checked an EKG:

Narrow QRS and unimpressive T-waves

The EKG gave no hint of hyperkalemia, though EKG changes are not a sensitive marker for hyperkalemia. The ED gave insulin, glucose and Kayexalate for the lab finding of hyperkalemia. We were consulted to determine the cause of the hyperkalemia. The patient’s past medical history was significant for primary thrombocytosis and during the hospital stay her platelet count rose to over a million.

dats a lot o’platelets

We presumed that his hyperkalemia was actually pseudohyperkalemia due to the high platelet count. Platelets release potassium when they clot and the risk of pseudohyperkalemia rises as the platelet count approaches a million.

You remember this classic NEJM article from 1962. 

We then sent the patients blood to the ABG lab in a heparinized syringe rather than a red top and the potassium normalized. Platelets release potassium when they are activated. By measuring the potassium in whole blood rather than serum, the contribution of platelet activation is prevented. The ABG results are the electrolytes to the far left in the screen-grab below (click to enlarge).

– Posted using BlogPress from my iPad

Posted on

Highest TTKG with hypokalemia

Patient with a lifelong history of hypokalemia. He came to me for a second opinion, his previous nephrologist had been nudging up his potassium dose on every visit and the patient was now on 70 mEq of KCl daily and was getting uncomfortable with endlessly increasing doses of potassium.

At the time I saw him these were his labs (he had decreased his potassium supplementation to 20 mEq/day):

  • Blood
    • sodium: 128
    • glucose: 90
    • potassium: 2.8
    • Creatinine: 0.9
    • BUN: 11
    • Magnesium: 1.8
    • Calculated osmolality: 265
  • Urine 
    • sodium: 135
    • potassium: >100
    • Osmolality: 637
Trans-tubular potassium gradient: 14.9. That’s crazy high for a patient with hypokalemia, one should expect it to be less than 2 for hypokalemia of extra-renal origin, and only 7 or 8 for hypokalemia from hyperaldosteronism. Halperin et al. were not able to get the TTKG that high even when they took normokalemic patients and doped them with fludrocortisone and 50 mEq of oral potassium. 
And that 14.9 is assuming the urine potassium is 100, our lab doesn’t do serial dilutions so who knows what the actual potassium is? 120? 140?
I’m still waiting for the renin and aldo but I smell some Bartter’s
Posted on

Pregnant Gitelman Patient follow-up

Last week I posted on my pregnant patient who has Gitelman’s Syndrome. I am managing her with amiloride and a mixture of oral potassium and a mixture of oral and IV magnesium.

I received the following letter from a reader who went through a similar experience:

I am not a doctor, but I have Gitelman’s, and 16 years ago, was pregnant and ended up having to go on amiloride at the start of my second trimester, because my potassium and magnesium levels just tanked.   Being part of proving the track record on the viability of amiloride in pregnancy was a scary time, I tell you what.  Your patient’s experiences are similar to mine, though I did not require the magnesium IVs she apparently does during gestation. 

The great news is my son turned out healthy, and without any sign of potassium disorders of any sort, so far as we can tell at nearly 16.  He’s healthy, bright, nearly 6 ft – no indication at this time  that he was harmed in any way by the fetal exposure to amiloride. 

And another point to pass along – after he was born, I had my breast milk checked for traces of amiloride, and it passed whatever screens were applied. Therefore I nursed him for about 9 months, though I supplemented with formula.  It was an acceptable risk for me – since I know the literature does not record any data on nursing while on amiloride, I thought I’d pass along one uncontrolled anecdote for you to ponder. [Note: on further communication the patient clarified that she did not take amiloride during breast feeding] 

Anyway, please pass this information along to your patient – I am sure it will help her peace of mind to know another successful long term outcome.  It was a scary time for me, and without the widespread use of Internet back in 1995, the only piece of mind I got was by tracking down Dr. Almeida, who wrote the 1989 paper about Gitelman’s in pregnancy.  I spoke to one of his nurses to see if they could give me some info on long term followup on the baby, but the mother had disappeared after giving birth, and they had nothing to report.    

Best of luck to your patient – I know what she’s going through. 

Final note for your patient going forward: Getting my levels back up after the birth was a bit of a challenge, I recall.  But many of the details have been lost to time and the fog of war, I’m afraid – I will just say that the first month post-partum was pretty rough on me.

Posted on

Gitelman syndrome and Pregnancy

One of my Gitelman patients (whom I kidding, “one of my Gitelman patients”, how about “my only Gitelman patient”) finally got pregnant. We had been managing her with amiloride and a truck load of oral potassium and magnesium supplements. I was shocked to find that amiloride is acceptable in pregnancy with a track record of successful births. Prior to starting amiloride the patient was taking twenty-eight 20 mEq pills of KCl a day. She abandoned her prior nephrologists when she was told to further increase her potassium pills.

from UpToDate

We are now using magnesium sulfate infusions 4 grams twice a week to keep her magnesium north of zero. She was able to keep her magnesium around 1.4 with oral supplements and amiloride prior to being pregnant but now, despite 8 grams of weekly IV magnesium her magnesium is sitting around 1.1. This probably represents one of downsides of the up-regulated GFR of pregnancy.

Interestingly, she saw her labs and saw that her sodium was 132. Modest hyponatremia is a normal finding in pregnancy, so she decided to increase her dietary sodium intake. Bad move, increased renal sodium loads increases renal magnesium losses. Her serum mag fell 30% to 0.8.

Posted on

Hyperkalemia as an indication for dialysis

A few weeks ago we admitted a patient who has been approaching ESRD for a number of years. Most of her medical care had been provided in the hospital as she bounced from admission to admission. Though we tried to get her into our CKD clinic she always failed to show up. You can track the progression of her CKD from hospitalization to hospitalization with a gradually increasing baseline creatinine.

On this most recent admission, she came in with the triple 8s:

  • Hemoglobin 8.8
  • Creatinine 8.1
  • Potassium 8.6

Here is her initial EKG with that potassium:

The most remarkable part of the EKG was the profound bradycardia, heart rate of 30. Also she has beautifully peaked T waves. I’m surprised by the lack of a prolonged QRS. She had a great response to medical management with her K falling to the 5s. The repeat EKG was rather unremarkable.
The patient received dialysis on the day of admission and the following day I set her up for chronic dialysis. Whenever a patient progresses to chronic dialysis from CKD I always try to remind myself of how rare this event is. As nephrologists it is too common and seeing that unfortunate outcome alters our perception so that we may overestimate its frequency. End-stage renal disease is an exceptional, not a routine outcome of CKD. The vast majority of patients with CKD ultimatly expire of something other than renal failure. Let’s review three important studies to emphasize this:
Keith et al looked at the five-year outcome of 28,000 patients with chronic kidney disease. He divided them by CKD stage and found that of the 11,278 patients with CKD stage 3, only 1.1% of then received dialysis and 0.2% received a transplant. A quarter of them died (24.3%). The authors summarized the results:

The likelihood of renal replacement therapy, either transplant or dialysis, was near zero (≤1.3%) for patients in all stages except stage 4, where 2.3% ± 1.1% of patients received a transplant and 17.6% ± 2.7% had dialysis initiated.

Eriksen et al found similar results in a 10-year study, with a 4% risk of renal failure for patients with CKD stage three compared to a 51% risk of death.
And lastly, O’Hare, et al’s VA study that looked explicitly at renal failure and the competing outcome of death. They asked, “At what age and GFR is renal failure more likely than death?”. Obviously, at a younger age, when death is a more remote possibility, a higher GFR will have the time to deteriorate to the point of requiring renal replacement therapy. The results showed surprisingly low GFRs:
To read the graph, find your patients age and then line it up with their GFR. If the intersection is in the black, they are more likely to die, if it is in the grey then hello Mr. Fresenius, nice to meet you Ms. Tacrolimus. Note, that in a 75 year old with a GFRas low as 16 mL/min, death is still more likely than ESRD.
So, the next time you see a patient initiating dialysis after a long run of chronic kidney disease don’t be frustrated by the fact that they didn’t do enough to prevent this, be amazed that they survived to this outcome. 
Posted on

Aldosterone escape versus Aldosterone breakthrough

Fluid and electrolyte deity, Robert Schrier,  had an interesting editorial in Feburary’s Nature Reviews: Nephrology (yes, I’ve gotten a little behind in this blogging business).

Escape versus breakthrough refere to completely different and unrelated concepts related to aldosterone.

  • Aldosterone breakthrough occurs following administration of an ACEi or ARB. ACEi block the conversion of angiotensin I to angiotensin II. The decrease in angiotensin II lowers aldosterone. Angiotensin receptor blockers prevent angiotensis II from from binding receptors through out the vasculature but including the adrenal gland where it prevents aldosterone release. At least that is the plan. In reality about 30-40% of patients given ACEi or ARBs have only a temporary decrease in aldosterone and then after a few weeks, aldosterone returns to pre-treatment levels.  

  • Aldosterone escape is a physiologic phenomenon that occurs with hyperaldosteronism. Aldosterone initially decreases urinary sodium increasing sodium retension contributing to hypertension. This does not result in edema because the sodium retention is short lived. After a short time urinary sodium returns to normal through a process called aldosterone escape. There are two processes that account for this:

    1. Pressure natriuresis. Increased blood pressure decreases distal sodium resorption. The exact mechanism of pressure natriuresis is unknown, it is thought to be mediated by hydrostatic forces. Increased blood pressure is transmitted to the peritubular capillaries, so the resorption of solutes must overcome an elevated hydrostatic pressure gradient. In the face of this increased gradient, sodium resorption falls.
    2. Decreased proximal sodium resorption. Volume expansion decreases proximal sodium reabsorption and increases sodium delivery to the distal nephron and overwelms the aldosterone induced sodium resorption.

The implications of aldosterone escape is that primary hyperaldosteronism does not cause edema. It also explains the delay in hypokalemia found with primary hyperaldosteronism. Aldosterone stimulates potassium excretion but hypokalemia is a late finding in primary hyperaldosteronism. The increased potassium excretion occurs with aldosterone escape when the increased sodium delivery (decreased proximal absorption, i.e. escape) occurs with the increased aldosterone levels.

Posted on

Kayexalate: risks and benefits

When I was a fellow I got an opportunity to write the chapter in Intensive Care in Nephrology on Disorders of Potassium Homeostasis.

Dr. Murray, the editor and my fellowship program director, told me that I couldn’t use review articles or text books as references. It was a golden experience. I systematically went through all of the pearls I had collected on potassium and drilled down to the original data.

The primary conclusion I had after months of exploring the stacks of The Crerar was that the wall of knowledge that I had assumed backed up all of our clinical practices was more like a chain link fence with isolated points of solidity but mostly holes. Science could provide a rough outline but too much of medicine is based on conjecture and reasoned guesses.

One of my finds was the near total lack of data showing cation-exchange resins to be effective. In the chapter I wrote:

…Two recent studies have questioned the effectiveness of SPS [sodium polysterene] resins, but until larger studies corroborate these findings, SPS resins remain part of the therapy for acute hyperkalemia. (106, 122, PDF) SPS and sorbitol usage have rarely been associated with intestinal necrosis; whether this is due to sorbital, the resin, or other factors is unclear. (123, 124, 125)

The key table from the Gruy-Kappal article showing the lack of effectiveness of SPS resins

This was actually the revised paragraph. The first draft was much stronger. I railed against the use of kayexylate given the lack demonstrated benefit and the emerging data on the dangers of this medication. I was ready to throw kayexalate on the hyperkalemic trash heep along with bicarbonate. My co-author, John Asplin calmed me down and had me moderated the section. He explained that despite the lack of data, SPS resins have a long history of use and explained that though I have the option of using dialysis, intensivists often find themselves in binds where dialysis is not available and they need an extra-renal method for potassium clearance.

I can appreciate Asplin’s wisdom now. In the last decade I have used SPS resins innumerable times in patients with and without ESRD, though my data is circumstantial I am believer in the effectiveness of this drug. I hope the latest publicity about the purported ineffectiveness of Kayexalate leads to well done large studies rather than a loss of this effective medicine.