Is Kayexalate Effective for Hyperkalemia, and Is It Safe?

Summary and Comment |
June 9, 2010

Is Kayexalate Effective for Hyperkalemia, and Is It Safe?

  1. F. Bruder Stapleton, MD

Recent evidence fuels growing concerns about use of sodium polystyrene sulfonate with sorbitol.

  1. F. Bruder Stapleton, MD

Sodium polystyrene sulfonate (SPS; e.g., Kayexalate) has been used as an oral or rectal therapy for hyperkalemia since 1958 — before the FDA required drug manufacturers to prove efficacy and safety in 1962. SPS is an ion exchange resin that is thought to exchange sodium with potassium in the colon. Because constipation is a common complication, SPS is often mixed with sorbitol. In a clinical commentary, the authors reviewed the literature on SPS and sorbitol from the past 50 years and found no evidence of clinically significant lowering of serum potassium in patients with hyperkalemia. The strongest evidence for SPS efficacy is a drop in serum potassium of at least 0.4 mEq/L in 23 of 30 hyperkalemic patients (Circulation 1952; 5:747). A recent report described colonic necrosis in patients treated with SPS mixed with sorbitol (South Med J 2009; 102:493). In September 2009, the FDA issued a warning about concomitant use of SPS with sorbitol, although this combination is currently still available.


As a nephrologist who has used sodium polystyrene sulfonate for decades, I found this review startling. Although I was aware that the beneficial effect of SPS was, at best, slow and gradual, I was unaware about the risk for intestinal injury when SPS is combined with sorbitol. Fortunately, more rapid and effective measures are available to lower serum potassium in patients with hyperkalemia. These therapies include intravenous dextrose plus insulin, inhaled β-2 agonists, and sodium bicarbonate. On the basis of this commentary and literature review, I discourage prescribing SPS with sorbitol as a first-line therapy for hyperkalemia.


Reader Comments (5)

Jeff L Harris

Apart from dialysis, sodium/potassium exchange resins are the only reasonably effective means of removing excess potassium from the body in the setting of renal failure. I suppose the induction of a diarrhea can lead to GI potassium losses, but there is no way of controlling the losses or the other electrolytes that may also be lost.

Shifting potassium intracellularly may be effective in loweing serum potassium, but is only a temporary effect as the excess potassium will eventually shift back into the extracellular space. Whether 15 minutes, or several hours, I as a clinician will have to figure out a way to rid the excess potassium load.

It is interesting to observe nephrologists render negative opinions regarding the use of Kayexelate-sorbitol as the only other effective means of removing excessive potassium is dialysis. Dialysis itself is not a benign procedure and fraught with risks, especially for short term therapy, that might actually be worse than a single or even perhaps a few doses of Kayexelate.

Even more than a randomized DCT testing Kayexelate, I would like to see a head to head trial of Kayexelate versus dialysis in the short term management of hyperkalemia due to potassium excess, monitoring outcome events both in the short and long term.

Perhaps the majority of Kayexelate use can be avoided. Insulin and glucose can be administered regularly waiting for renal function to recover. Dialysis would be necessary in any case for those, whose renal recovery is delayed or fails to occur. However, in the short term, hyperkalemia is a very dangerous condition. Lowering the serum potassium is imperative. But, and this is a big but, there are no controlled trials assessing outcomes for any of the other potassium lowering modalities either.

Competing interests: None declared

Clyde H Sharpley

You tell any Doctor that has been using something they think works, that it actually doesn't work, there will be disagreement. Fact is most of the use of SPS is worthless; it is just something we do automatically. It only has a little benefit after potassium has been lowered by other means. You don't give SPS as an emergency solution, but to prevent elevations later. K can be controlled by other means which do last more than 15min. SPS also exchanges one meq of K+ for 1 meq of Na+.

Competing interests: None declared

Paul L Hacker

I agree with the other commentators - this review is less than helpful. The absence of evidence is not the same as the absence of efficacy. Hopefully an RCT can be mustered to provide better guidance.

Competing interests: None declared

Cynthia D. Owens

I agree. The other modalities available to treat hyperkalemia has variable peak effects and duration effects, which at best last for only 20 -30 miins. Thus multiple modalities are needed to treat this process. It would be beneficial to be informed of the number needed to treat to see this adverse effect.

Competing interests: None declared

Erik Deede

My understanding is that the other treatments you mentioned for lowering serum potassium (insulin/dextrose, inhaled beta-2 agonist, and sodium bicarbonate) just temporarily shift potassium into the cells. Won't the serum potassium just rebound to the same level once those wear off? Don't you need something that actually removes potassium from the body? Do you know how common this colonic necrosis is? This seems similar to the droperidol black-box warning from a few years ago- a few case reports of a complication despite millions and millions of uses render a treatment option medicolegally risky.

Competing interests: None declared

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