Group by how it injures
The injury atlas sorts by phenotype — the lesion you see. This lens sorts by mechanism — the way the damage happens. Drugs that strike the kidney through the same biology gather here, regardless of their drug class.
Direct tubular injury
The drug (or its metabolite) concentrates in and kills tubular epithelium, or wrecks proximal reabsorption.
Tubular transport / electrolyte
Disrupted segment-specific handling of magnesium, potassium and other electrolytes — true wasting, not a lab artifact.
Transporter creatinine artifact
Blocked tubular secretion of creatinine (OCT2/MATE) raises serum creatinine without a real fall in GFR — pseudo-AKI.
Immune-mediated inflammation
Loss of tolerance drives interstitial nephritis (and chronic interstitial scarring) — the checkpoint-inhibitor lesion.
Endothelial / microvascular
Injury to the microvascular lining: thrombotic microangiopathy and VEGF-pathway hypertension.
Glomerular / podocyte
Damage to the filtration barrier — podocyte injury, FSGS and proteinuria.
Crystal & obstructive
Intratubular precipitation of drug, metabolite or tumor-lysis urate obstructing flow.
Hemodynamic & systemic
Renal hypoperfusion from cytokine release, capillary leak or volume loss, and inappropriate water retention.
Lower tract & cystic
Beyond the nephron: acrolein hemorrhagic cystitis and the distinctive ALK-inhibitor renal cysts.
Agents are grouped by the mechanism behind their signature lesion. Many also cause injuries through other mechanisms — see each drug’s full profile.