The treatment of hyperkaliemia is usually not difficult. If it is extreme (greater than 6.5 mEq per liter), urgent treatment is indicated. Therapy may include intravenous glucose and insulin, intravenous calcium salts, or albuterol inhalation. If these measures are inadequate, it may be nec essary to initiate dialysis. In less urgent cases, sodium polystyrene sulfonate, an exchange resin taken in the sodium form that is not absorbed in the intestine, but takes up potassium in exchange for sodium and is excreted in the stool, can be taken by mouth. This drug is expensive and difficult to take. (It tastes like sand.) It is usually dispensed in sorbitol suspension so as to reduce its constipating effects. However, in some patients the sorbitol leads to diarrhea or to more serious intestinal problems. Other laxatives may be safer and may in fact lower potassium somewhat when given alone (that is, without the SPS). SPS without sorbitol is also available (Kionex). In mild cases, reduction of dietary potassium also may help, though in my opinion that idea is a nonstarter. I never use this last option because small doses of SPS are so effective and these patients already struggle with a multitude of dietary restrictions. If there is associated acidosis and the hyperkaliemia is mild, sodium bicarbonate (see Chapter 10) can address both problems.
Twenty percent of my patients on the very-low-protein diet supplemented by essential amino acids have required SPS continuously, mostly because they were receiving ACE inhibitors; another 20 percent on ACE inhibitors did not develop hyperkaliemia. Some patients not on ACE inhibitors nevertheless require SPS. The very-low-protein diet supplemented by essential amino acids may impair potassium excretion because of the decreased amounts of sulfate and phosphate requiring excretion. A fall in the intake of sulfate and phosphate may make hyper-kaliemia more likely.
The flavored form of amino acids (see Appendix 1) may tend to bind potassium in the gut, acting like SPS.
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