What should the nurse anticipate after administering sodium polystyrene sulfonate to a patient with hyperkalemia?

A. Improved kidney function: Sodium polystyrene sulfonate is a cation-exchange resin that works within the gastrointestinal tract and does not have a direct therapeutic effect on the nephrons. While lowering potassium can prevent cardiac complications of renal failure, the drug itself does not reverse underlying kidney pathology. It is a symptomatic treatment for electrolyte imbalance. B. Decreased serum potassium levels: This medication works by exchanging sodium ions for potassium ions across the intestinal mucosa, which are then excreted in the feces. The primary therapeutic goal is the significant reduction of potentially cardiotoxic extracellular potassium levels. It is a standard intervention for managing non-emergent hyperkalemia. C. Increased bowel motility: While the drug can sometimes be administered with a laxative to prevent impaction, its primary pharmacological mechanism is ion exchange, not peristaltic stimulation. In some cases, it can actually cause constipation if not managed correctly. Increased motility is a side effect or secondary effect rather than the primary anticipated outcome. D. Elevated serum sodium levels: Because the resin releases sodium in exchange for potassium, a modest increase in serum sodium can occur as a side effect. However, this is a secondary consequence that the nurse monitors for safety rather than a goal they anticipate as a therapeutic success. The focus remains on the reduction of potassium.