Mechanism of action: Trimethoprim balliculeVisual mnemonic: Trimethoprim mascot “Trim & prim” Bananas in bunches → ↑ serum potassium
What it isDihydrofolate reductase inhibitor, usually paired with sulfamethoxazole; urinary infection.
Why this oneThe sequential folate blockade with sulfamethoxazole is synergistic.
What limits itRaises creatinine by blocking tubular secretion without changing GFR, and causes hyperkalemia by blocking the epithelial sodium channel.
Molecular structure: Trimethoprim
Trimethoprim prescription history
Animated chart of estimated U.S. prescriptions per year, Antibacterials (systemic) (1938–2026). Trimethoprim enters in 1980 (estimated).
FDA-approved for
UTIs (~1980)
Principal riskHyperkalemia; raises creatinine without lowering GFR
Sulfonamide
Sulfonamide partner (not a sulfonamide)
A diaminopyrimidine, not a sulfonamide — but after a reaction to TMP-SMX it should still be avoided: nobody knows which component reacted, and trimethoprim itself causes hypersensitivity reactions including anaphylaxis.
Renal CrCl 15-30: 50 mg q12h; CrCl <15: not recommended
Hepatic No dose guidance; give with caution in hepatic impairment
Instructions
Complete the full 10-day course even if feeling better
Available strengths
tab 100 mg
Contraindications
Documented megaloblastic anemia due to folate deficiency
Cautions
Hematologic toxicity: may interfere with hematopoiesis (esp. large doses/prolonged use); sore throat, fever, pallor, or purpura may herald serious blood disorder — obtain CBC and discontinue if a formed element significantly reduced
Give with caution in possible folate deficiency (folates may be co-administered without loss of antibacterial effect)