Cisplatin
Platinol · Platinum agent
Proximal tubular ATN + magnesium wasting; the archetype.
ATNLYTEPRE
SevereOpen →
Onconephrology · 817 verified citations
How cancer drugs
break the kidney
An interactive, citation-grounded atlas of anti-cancer drug nephrotoxicity — connecting 240+ agents by the toxic ties they share, from cisplatin to the 2026 frontier and MGRS.
0+
Drugs catalogued
0
Verified citations
0
Toxic signatures
0
Frontier signals
The signature feature
Open full network A web of toxic ties
Every agent is wired to each kidney injury it can cause. Drugs that share a toxic signature cluster around the same hub — revealing, at a glance, which chemically unrelated drugs fail the kidney in the same way.
240 agents · 505 toxic ties · tap a node
The toxic-ties network
Each agent is wired to every kidney injury it can cause. Drugs sharing a signature cluster around the same hub. Tap a node to inspect it.
Filter by signature
Why it matters
The kidney is collateral damage in cancer care
Onconephrology sits at the intersection of two epidemics. The numbers are stark — and every one is cited.
27%
of cancer patients develop AKI within 5 years
5-year cumulative incidence of acute kidney injury after a cancer diagnosis (1-year: 17.5%).
Christiansen et al., Eur J Intern Med 2011 · PMID 2176775953%
carry hidden kidney impairment at diagnosis
Reduced eGFR in solid-tumor patients despite a normal serum creatinine in 93% of them (IRMA study).
Launay-Vacher et al., Cancer 2007 · PMID 176349494.7×
higher odds of death with in-hospital AKI
Cancer inpatients who develop AKI face nearly fivefold mortality, +100% length of stay.
Salahudeen et al., CJASN 2013 · PMID 23243268~1 in 3
cisplatin courses cause acute kidney injury
The archetypal nephrotoxin injures the proximal tubule in roughly 20–35% of treated patients.
Tang et al., Nat Rev Nephrol 2022 · PMID 36229672Onconephrology. Onconephrology is the nephrology subspecialty at the bidirectional intersection of cancer and the kidney — the nephrotoxicity of anticancer therapy, AKI and CKD in cancer patients, electrolyte disorders, tumor lysis syndrome, paraneoplastic glomerular disease and drug dosing in renal impairment. The field coalesced around 2010–2014, with the ASN onconephrology forum established in 2011.
The vocabulary
The many ways a drug strikes — or fakes — the kidney
Filter the entire atlas by these signatures — the patterns of injury that recur across unrelated drug classes, plus pseudo-AKI, the creatinine-secretion artifact that mimics injury without harming the kidney.
ATNAINTMAGLOLYTFANXTAHTNPRESIACYSPSERCYCIN
Acute Tubular Necrosis
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.
Acute Interstitial Nephritis
Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors.
Thrombotic Microangiopathy
Endothelial injury with microvascular thrombi, hemolysis and thrombocytopenia — gemcitabine, mitomycin C, anti-VEGF.
Glomerular Injury / Proteinuria
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.
Electrolyte Wasting
Renal loss of magnesium, potassium or calcium — cisplatin and the anti-EGFR antibodies.
Fanconi Syndrome
Global failure of proximal tubule reabsorption — glucosuria, phosphaturia and acidosis, classically from ifosfamide.
Crystal / Obstructive Nephropathy
Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals.
Hypertension
On-target loss of endothelial nitric oxide from VEGF-pathway blockade — so consistent it marks drug activity.
Prerenal / Hemodynamic AKI
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
SIADH / Hyponatremia
Inappropriate water retention at the collecting duct — high-dose cyclophosphamide.
Hemorrhagic Cystitis
Acrolein injury to the bladder urothelium — an outflow toxicity of the oxazaphosphorines, prevented by mesna.
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.
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.
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.
Explore it
Eight ways into the data
The atlas is built to be interrogated, not just read — trace connections, browse by lesion, compare agents head-to-head, probe an organ, check renal dosing, or drop to the clinical detail.
Toxic-Ties Network
Every agent wired to each kidney injury it can cause — drugs sharing a signature cluster together.
The Injury Atlas
Browse by the lesion, not the drug — every agent grouped under the 14 kidney-injury signatures.
Renal Dosing & Dialyzability
A bedside reference: CrCl dose thresholds and whether each agent is removed by dialysis.
Compare Agents
Put two or three drugs side by side: signature lesion, severity, incidence and nephron site.
Organ Toxicity Oracle
Type a drug, pick an organ system, and surface the kidney and beyond-the-kidney signal.
Toxicity Landscape
All 200+ agents plotted by approval year and graded severity, colored by signature injury.
Kidney-Sparing Agents
The anti-cancer drugs that largely leave the kidney alone — with the caveats that still matter.
Clinical Companion
Electrolyte disorders, dialysis dosing, transplant onconephrology and pediatric specifics.
Interactive anatomy
Trace each drug to the exact segment it attacks
Different drugs injure different parts of the nephron. Walk the filtration unit from glomerulus to collecting duct and light up the agents that strike each segment.
Glomerulus
Filtration barrier (podocytes + endothelium)
Vasculature / Endothelium
Glomerular & peritubular capillaries
Proximal Tubule
Bulk reabsorption + drug uptake (OCT2, OATs)
Distal Tubule / Collecting Duct
Fine-tuning of Na, K, Mg, acid & water
Interstitium
Supporting tissue around the tubules
Tubular Lumen
The urine flow path
Deep profiles
All 240+ Start with the classics
All 240 agents carry full, citation-grounded profiles — mechanism, incidence, prevention, management, dose adjustment and clinical pearls.
Profile
Gemcitabine
Gemzar · Nucleoside analog
Dose-cumulative thrombotic microangiopathy.
TMAHTNGLOM
SevereOpen →
Checkpoint inhibitors (pembrolizumab · nivolumab · ipilimumab)
Immune checkpoint inhibitor
Acute interstitial nephritis with long latency.
AIN
ModerateOpen →
Bevacizumab
Avastin · Anti-VEGF antibody
Proteinuria, hypertension, glomerular TMA.
GLOMHTNTMA
ModerateOpen →
Ifosfamide
Ifex · Oxazaphosphorine alkylator
Chloroacetaldehyde → Fanconi syndrome.
FANCATNLYTE
SevereOpen →
Cetuximab & Panitumumab
Erbitux · Vectibix · Anti-EGFR antibody
TRPM6 magnesium wasting.
LYTE
MildOpen →
The frontier
Where the clinic is ahead of the literature
Real-world signals from a working international onconephrology group — adagrasib glomerular injury, enfortumab-vedotin AKI, amivantamab interstitial nephritis — plus graded theoretical toxicities for the newest and trial-stage agents.
0
Emerging signals
0
Theoretical, graded
0
2024–2026 agents
AdagrasibGLOM
Beyond the known 'creatinine bump' from blocked tubular secretion, clinicians report genuine AKI with glomerular-range albuminuria — reversible on withdrawal, recurrent on rechallenge — with near-normal light microscopy.
Enfortumab vedotinATN
The same Nectin-4 ADC has produced the full spectrum of AKI across centers — prerenal (diarrhea-driven), acute interstitial nephritis, and acute tubular necrosis.
AmivantamabAIN
A newly recognized acute interstitial nephritis pattern in lung-cancer patients, reported by multiple centers concurrently.
Part II
When the antibody itself is the toxin: MGRS
Monoclonal Gammopathy of Renal Significance — a small clone, a nephrotoxic immunoglobulin, and a kidney in the crossfire. Nine lesions, the full workup, and clone-directed therapy, current to the 2025 consensus.
Amyloid
organized
Cryo-GN
organized
ITG
organized
FGN
organized
MIDD
non
PGNMID
non
C3G-MG
non
LCPT
tubular
CSH
tubular
Stay current
The frontier digest
New drugs are added continuously — auto-discovered from PubMed and reviewed before they appear. Get the emerging-toxicity digest when the atlas grows.
Built with deep research across PubMed, an international onconephrology clinician group, and current nephrology digests. Not medical advice.