Pharmacology and Drug-Related Kidney Disease
Core concepts
Know nephrotoxic patterns: hemodynamic (NSAIDs, ACE inhibitors/ARBs, calcineurin inhibitors, SGLT2 inhibitors early), acute tubular injury (aminoglycosides, amphotericin, cisplatin, contrast), AIN (PPIs, NSAIDs, beta-lactams, checkpoint inhibitors), crystal nephropathy (acyclovir, indinavir, methotrexate, uric acid), TMA (calcineurin inhibitors, quinine, VEGF inhibitors), and osmotic nephrosis (IVIG, mannitol).
Dosing: adjust renally cleared drugs (aminoglycosides, vancomycin, gabapentin, metformin-avoid in severe CKD). Lithium causes nephrogenic diabetes insipidus and chronic interstitial disease. Tenofovir causes proximal tubulopathy (Fanconi). Contrast: use iso-osmolar/low-osmolar, minimize volume, hold nephrotoxins.
Traps
ACE inhibitor creatinine rise is expected-do not stop reflexively unless large or hyperkalemic. NSAIDs cause AKI especially with volume depletion, CKD, or RAS blockade. Check drug levels for vancomycin and aminoglycosides. Metformin should be held in AKI and severe CKD due to lactic acidosis risk.
Rule of thumb
Any new AKI: review every medication, contrast exposure, and herbal supplement before assuming intrinsic disease.
Worked example
A patient on lithium develops polyuria and hypernatremia: nephrogenic diabetes insipidus; manage with hydration and amiloride, and consider alternative mood stabilizer.