Evaluation of Sodium Polystyrene Sulfonate Dosing Strategies in the Inpatient Management of Hyperkalemia

Sodium polystyrene sulfonate (SPS), an ion-exchange resin designed to bind potassium in the colon, was approved in 1958 as a treatment for hyperkalemia by the US Food and Drug Administration, 4 years before drug manufacturers were required to prove the effectiveness and safety of their drugs. In September 2009, citing reports of colonic necrosis, the Food and Drug Administration issued a warning advising against concomitant administration of sorbitol, an osmotic cathartic used to prevent SPS-induced fecal impaction and to speed delivery of resin to the colon, with the powdered resin; however, a premixed suspension of SPS in sorbitol, the only preparation stocked by many hospital pharmacies, is prescribed routinely for treatment of hyperkalemia. We can find no convincing evidence that SPS increases fecal potassium losses in experimental animals or humans and no evidence that adding sorbitol to the resin increases its effectiveness as a treatment for hyperkalemia. There is growing concern, however, that suspensions of SPS in sorbitol can be harmful. It would be wise to exhaust other alternatives for managing hyperkalemia before turning to these largely unproven and potentially harmful therapies.

The aim of this systematic review was to study the benefits and risks of beta-adrenergic antagonists (beta-blockers) in patients with chronic kidney disease (CKD). There is an excess burden of cardiovascular disease and death in people with CKD. Despite their potential benefits, the effects of beta-blockers in this population are uncertain. CENTRAL (Cochrane Central Register of Controlled Trials), Medline (Medical Literature Analysis and Retrieval System Online), and Embase (Excerpta Medical Database) were searched for randomized controlled trials with at least 3 months of follow-up in patients with CKD stages 3 to 5 that reported mortality outcomes. Summary estimates of effect were obtained using a random effects model. Eight trials met criteria for review: 6 placebo-controlled trials involving 5,972 participants with chronic systolic heart failure and 2 angiotensin-converting enzyme inhibitor-comparator trials involving 977 participants not known to have heart failure. In CKD patients with heart failure, compared with placebo, beta-blocker treatment reduced the risk of all-cause (risk ratio [RR]: 0.72, 95% confidence interval [CI]: 0.64 to 0.80) and cardiovascular mortality (RR: 0.66, 95% CI: 0.49 to 0.89), but increased the risk of bradycardia (RR: 4.92, 95% CI: 3.20 to 7.55) and hypotension (RR: 5.08, 95% CI: 3.48 to 7.41). Quantitative meta-analysis was not performed for the non-heart failure studies due to substantial clinical diversity or lack of informative data. Treatment with beta-blockers improved all-cause mortality in patients with CKD and chronic systolic heart failure. There is insufficient evidence to conclude whether people with CKD who are not known to have heart failure derive benefit from beta-blockers. Copyright © 2011 American College of Cardiology Foundation. Published by Elsevier Inc. All rights reserved.

Significant hyperkalaemia occurred in 406 out of 29 063 patients admitted to a major Scottish teaching hospital in one year (1.4%). Mortality was higher in these patients than in control patients and was strongly correlated with the severity of the hyperkalaemia. Overall seven deaths were directly due to hyperkalaemia (out of 58 deaths among patients with hyperkalaemia). Factors contributing to a poor prognosis were severity and speed of onset of hyperkalaemia and the presence of appreciable renal impairment. Patients with hyperkalaemia were older and more likely to be male; this trend was present in all diagnostic subcategories. Genitourinary disease, gastrointestinal disease, and cancer were significantly more common among the patients with hyperkalaemia than the controls. Hyperkalaemia due to drug treatment was invariably mild and non-fatal, whereas genitourinary disease was often associated with moderate to severe hyperkalaemia, which in two cases proved fatal. Use of electrocardiographic monitoring was rare, and although the treatment of hyperkalaemia was effective, it was often used when not required. Hyperkalaemia is a potential hazard in diabetic ketoacidosis, and use of potassium supplements should be carefully monitored during correction of the acidosis.