Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

Renal loss of magnesium, potassium or calcium — cisplatin and the anti-EGFR antibodies.

Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.

Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.

On-target loss of endothelial nitric oxide from VEGF-pathway blockade — so consistent it marks drug activity.

Endothelial injury with microvascular thrombi, hemolysis and thrombocytopenia — gemcitabine, mitomycin C, anti-VEGF.

The great mimic — a rise in creatinine from blocked tubular secretion (OCT2/MATE), NOT true injury. The GFR is intact; confirm with cystatin C before stopping effective therapy.

Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors.

Inappropriate water retention at the collecting duct — high-dose cyclophosphamide.

Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals.

Global failure of proximal tubule reabsorption — glucosuria, phosphaturia and acidosis, classically from ifosfamide.

Slow, cumulative tubulointerstitial scarring — fibrosis, tubular atrophy and glomerulosclerosis with no discrete acute phase. The nitrosourea (carmustine/lomustine) lesion and delayed radioligand (radiation) nephropathy; often irreversible and detected only as a creeping creatinine months to years later.

Acrolein injury to the bladder urothelium — an outflow toxicity of the oxazaphosphorines, prevented by mesna.

Drug-induced complex renal cysts — the distinctive ALK-inhibitor lesion, classically crizotinib. Usually asymptomatic, dose/duration-related, and they tend to regress when the drug is stopped.