By 10am we were racing in the second ambulance of the day, leaving behind our small city of 31,465, to the suburban sprawl of London, Ontario’s 383,822. I sat in front with one of the paramedics. In the back was Nicole on a stretcher, a doctor, a nurse and the other paramedic.
As I related in the last three parts of this post, my wife had woken up that morning semi-paralyzed with a low heart rate. Blood work showed it was hyperkalemia, a condition common among those on dialysis. Since Nicole’s kidney have failed potassium she consumes builds up in the blood stream instead of being excreted in urine. In our local ER, the staff had administered an IV cocktail and cortisol gas to stabilize her so she could receive emergency dialysis in London’s ER. They packed more of the IV cocktail and cortisol gas into the ambulance, in case paralysis returned.
At each intersection the sirens blared, cars froze and we’d move into the oncoming traffic lane to pass. Speeding down country roads, 18-wheelers and pick-up trucks all veered to the side. All but one. The driver wouldn’t turn aside. So tho paramedic turned on the “sound gun.” It sounded like a phaser from Star Trek.
“It projects sound straight forward and shakes the entire car,” said the medic gleefully like a kid playing a video game.
Not only did the sound gun shake the car in front of us, it vibrated the entire ambulance.
“Dang!” said the paramedic. “He’s still not moving.”
More rounds of the sound gun were of no avail as we neared his bumper. Finally the paramedic honked the horn. Immediately the driver pulled aside.
Other than that little escapade I didn’t take in much of the the trip. I was trying to figure out how study after study could find no correlation between dietary potassium and potassium overdose.
“Although up to half of severe hyperkalemia episodes in [dialysis] patients are attributed to the consumption of high-potassium foods, the evidence linking high dietary potassium intake to hyperkalemia in [dialysis] patients is virtually non-existent,” concludes the 2016 study from the University of New York.
For example, the 1960 Giovannetti & Maggiore study had the majority of energy coming from low-potassium foods (butter, lard, vegetable oils, sugar, honey, maize and wheat starch). Nonetheless, patients still had high potassium levels.
How high? Probably not as high as Nicole. After several weeks of a diet with a moderate amount of potassium-rich foods Nicole had reached a blood potassium level of 9.1 mEq/L. MedScape defines hyperkalemia as anything above 8.5 mEq/L.
So why did our little experiment result in Nicole almost dying yet all these studies are getting unpredictable results? Why in these studies are those consuming very little potassium ending up with high serum potassium, while those eating four time as much are having a lower potassium level? Here are same possibilities I came up with:
• A higher intake of acidic food may cause potassium levels to rise. Potassium is alkaline, phosphorous is not. Phosphorous is also excreted via the urine. Thus, in the absence of normal kidney function, the body may intentionally raise potassium in the blood to buffer the rise in phosphorous.
• I would question how well controlled these studies were. How did they ensure that the participants really ate only as much potassium as they claimed? Did they lock them in a hospital and deliver them their food ready-to-eat? Or did they just have them keep a food journal? Those with supposedly low potassium intake may have forgot to write down the 10 potato chips they had at a party or the vinegar they put on their salad.
• Did these studies account (or eliminate) potassium chloride? The 1915 Smillie study, which initially correlated potassium intake with sickness in patients with kidney failure, was conducted using inorganic potassium salt (potassium chloride) not natural potassium-rich foods. This chemical additive may not be usable by the cells and would thus accumulate rapidly in the blood unless urinated. It’s often added to processed foods (especially meat) and could easily have gone unaccounted for in these studies.
• Urine is not the only way to eliminate potassium. In 1967 Hayes et al. discovered that potassium in the stools of HD patients (avg. 37%) was three times higher than those with normal kidney function (avg. 12%). They reported that as much as 80% of dietary potassium (up to 3,000 mg per day) ends up in the stools of those with insufficient kidney function. So while people may eat more potassium, they may also eliminate more via the colon. This seems likely, since potassium-rich foods (like vegetables, whole grains and beans) are fiber-rich and would promote larger and more frequent bowel movements.
• Sweating is another way the body eliminates potassium. Exercise, hot baths and showers, saunas and warmer climates may have all eschewed results.
• Many of these studies may simply not have tried hard enough. For example, the BalanceWise Study cites its high-potassium group as only consuming 3,000mg per day. A pound (half-kilo) of yams alone has more than that according to CalorieKing. 3,000mg doesn’t even meet the World Health Organization’s recommended daily intake of 3,510mg. Nicole was eating up to 9,000mg a day.
In the end, Nicole was sweating potassium every day in the sauna, having more than enough bowel movements (between enemas and diarrhea) to clear potassium through her colon, she ate no acidic meat or dairy, she didn’t eat anything containing potassium salt… yet she went into near-fatal hyperkalemia. Our n=1 study sure suggests that dietary potassium from natural plant foods is sufficient in itself to kill a dialysis patient (if taken in beyond a hard-to-determine limit).
I think the mistake the New York University review article has made is assuming that because other factors (or lack thereof) raise potassium levels, that dietary potassium does not play a significant role. In our experience, it does. Yes, other factors such as consuming potassium salt appear to be even more dangerous. Yet just because yams and legumes are less dangerous doesn’t make them safe for someone with little kidney function.
Half-way to our destination the paramedic radioed the ER in London. The triage nurse said they had a bed already for Nicole in ER with the dialysis machines being set up.
“Wow!” said the paramedic. “That’s the best triage nurse ever.”
We soon completed the second fastest trip to London I’ve ever experienced. (The fastest was with this crazy Timbit-popping taxi driver who swore he could make the trip in under 30 minutes.) We pulled in behind three other ambulances. The paramedics threw open the doors and got Nicole’s stretcher out just in time… for us to spend about a half-hour waiting in the ER corridor for that bed that apparently the “best triage nurse” had already for Nicole over an hour ago.
When they finally did bring Nicole to the spot reserved for her there was neither bed nor dialysis machines. The bed took another ten minutes. The dialysis machine probably another 40.
Next post, I’ll tell you how we spent to next seven hours in a big city emergency room. And I’ll let you know what changes we made to Nicole’s diet to normalize her potassium levels.
In the trenches with T1D & ESRD,
–John C. A. Manley
P.S. Did you know that five countries have far more kidney failure patients than any other nation in the world? Check out this earlier post to find out which ones: Top 5 Countries For Failed Kidneys
