Browse by the lesion, not the drug
The kidney has a finite vocabulary of injury. Every nephrotoxin in the atlas resolves to one of 14 signatures — pick a lesion to see which agents cause it, where they act in the nephron, and how the damage behaves.
Prerenal / Hemodynamic AKI
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Electrolyte Disturbance
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).
Acute Tubular Necrosis
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.
Glomerular Injury / Proteinuria
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.
Crystal / Obstructive Nephropathy
Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals.
Thrombotic Microangiopathy
Endothelial injury with microvascular thrombi, hemolysis and thrombocytopenia — gemcitabine, mitomycin C, anti-VEGF.
Hypertension
Raised blood pressure — archetypally on-target loss of endothelial nitric oxide from VEGF-pathway blockade, studied as a pharmacodynamic marker of drug exposure. Other agents raise it too: vascular effects of BCR-ABL, BTK and RET inhibitors and of copanlisib; abiraterone's mineralocorticoid excess; androgen suppression or blockade.
Pseudo-AKI
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.
Acute Interstitial Nephritis
Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors.
SIADH / Hyponatremia
Inappropriate water retention at the collecting duct — high-dose cyclophosphamide.
Hemorrhagic Cystitis
Bleeding inflammation of the bladder urothelium — classically acrolein injury from the oxazaphosphorines (prevented by mesna), but also reported as immune-related, intravesical-chemical, or radiation-recall injury.
Chronic Interstitial Nephropathy
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.
Fanconi Syndrome
Global failure of proximal tubule reabsorption — glucosuria, phosphaturia and acidosis, classically from ifosfamide.
Renal Cysts
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.
Counts reflect the 290 agents with citation-grounded profiles. A drug appears once under its signature lesion and again wherever it causes an associatedinjury — many nephrotoxins injure the kidney in more than one way.
By mechanism
The cards above sort by phenotype — the lesion you see. This lens sorts by mechanism — the biology behind the damage. Drugs that injure the kidney through the same pathway group here, regardless of drug class.
Direct tubular injury
The drug or its metabolite concentrates in and kills tubular epithelium, or impairs 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 drug-induced hypertension, archetypally from VEGF-pathway blockade.
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 injure the kidney through other mechanisms — see each drug’s full profile.