A teenager with salicylate poisoning is being managed with intravenous sodium bicarbonate infusion along with fluid resuscitation. The pharmacokinetic rationale for urinary alkalinization is:

• A Alkaline urine converts salicylic acid into its ionized form, reducing passive reabsorption in the distal tubule ✓
• B Bicarbonate competitively displaces salicylate from renal tubular organic acid transporters
• C Bicarbonate increases glomerular filtration of protein-bound salicylate
• D Alkaline urine promotes active secretion of salicylate by OAT transporters

Explanation

Salicylic acid is a weak acid. Raising urinary pH above its pKa shifts the equilibrium toward the ionized salicylate form, which cannot diffuse back across the lipid tubular membrane. This ion trapping increases net urinary excretion. Option B is wrong because bicarbonate does not compete at organic anion transporters, and enhanced secretion is achieved by other means such as acetazolamide use in specific settings, not by alkalinization itself.

Reference: Goodman and Gilman's The Pharmacological Basis of Therapeutics, 14th ed.

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