Cisplatin
Platinol · Platinum agent
Proximal tubular ATN + magnesium wasting; the archetype.
ATNLYTEPRE
Severe
The Atlas of Anti-Cancer Drug Nephrotoxicity
How anticancer drugs injure the kidney.
A citation-grounded onconephrology reference that connects 291 agents — chemotherapy, targeted therapy, immunotherapy — by the toxic ties they share, from cisplatin to the 2026 frontier and MGRS.
291 agents · 14 signatures · 1,629 citations · updated August 2026
Every claim tied to a primary source.
Look up an agent
Search all 291 agents, 14 injury signatures, and every profile citation. Opens the command palette —⌘Kanywhere on the site.
Search the atlasWork up a case
Start from the patient: enter the regimen and the kidney picture, and rank which agent most plausibly explains it — with the evidence behind each call.
Open the culprit consoleExplore the data
The data behind the atlas: phenotype similarity, nephron anatomy, how the evidence base grew, and FAERS reporting signals.
Open Insights§ 00Start here
Choose a path through the atlas
Short, ordered journeys matched to why you came.
At the BedsideFrom an unexplained creatinine bump to a named culprit and a concrete plan.Learn the FieldBuild onco-nephrology from vocabulary to pattern to a worked syndrome, then test it.Follow the EvidenceSurvey the field from altitude, then trace every claim to its source and the people behind it.The Classic NephrotoxinsThe nephrotoxins every onco-nephrologist must know, each a different lesion.Dose It RightScreen the protocol for kidney risk, then set and compute the right dose.Vet a Brand-New AgentBuild a kidney-risk read on an agent with almost no published profile.
§ 01The toxic ties
Agents that injure the kidney the same way
Every agent is wired to each injury it can cause. Chemically unrelated drugs that share a signature pull toward the same hub — drag a node, or open the full network.
The vocabulary · filter the atlas by injury signature
Acute Tubular NecrosisAcute Interstitial NephritisThrombotic MicroangiopathyGlomerular Injury / ProteinuriaElectrolyte DisturbanceFanconi SyndromeCrystal / Obstructive NephropathyHypertensionPrerenal / Hemodynamic AKISIADH / HyponatremiaHemorrhagic CystitisPseudo-AKIRenal CystsChronic Interstitial Nephropathy
§ 02Why it matters
Kidney injury is a common complication of cancer therapy
Onconephrology sits where two epidemics meet. Every figure below links to its primary source.
| Incidence | Clinical finding | Source |
|---|---|---|
| 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 21767759 |
| 53% | carry hidden kidney impairment at diagnosis Abnormal renal function by aMDRD in solid-tumor patients, yet only 7.2% of the cohort had an elevated serum creatinine (IRMA study). | Launay-Vacher et al., Cancer 2007 · PMID 17634949 |
| 4.7× | 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 36229672 |
Onconephrology. 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. Read the field primer
§ 03Deep profiles
Start with the foundational agents
All 291 agents carry full, citation-grounded profiles — mechanism, incidence, prevention, management, dose adjustment, clinical pearls, and a real-world FAERS signal where the data exists.
§ 04Deep dives
The syndromes, told in full
Anti-angiogenics & the glomerular endothelium
VEGF-inhibitor TMA
Starve a tumor of its blood supply and you also cut the survival signal podocytes whisper to the glomerular endothelium next door — the capillary tuft answers with thrombi, protein spilling into the urine, and a blood pressure that will not come down.
7 landmark studies
Platinum & the proximal tubuleCisplatin ATN & hypomagnesemia
The drug that cures testicular cancer poisons its own portal of entry — pumped into the kidney's S3 tubule by OCT2, cisplatin necroses the proximal tubule and, downstream, silences the distal magnesium channel, leaving patients wasting magnesium long after the last dose.
7 landmark studies
Anti-EGFR antibodies & the distal tubuleEGFR-inhibitor hypomagnesemia
By occupying the EGF receptor that keeps the TRPM6 channel trafficked to the apical membrane of the distal tubule, cetuximab and panitumumab convert the kidney into a magnesium sieve — an on-target, designed-in toxicity that deepens the longer the drug keeps working.
7 landmark studies
Oxazaphosphorine alkylators & the proximal tubuleIfosfamide Fanconi
Mesna guards the bladder, but nothing guards the proximal tubule — ifosfamide's chloroacetaldehyde metabolite is made inside the tubular cell itself, draining its energy and its reabsorptive machinery until phosphate, glucose, bicarbonate, and amino acids leak into the urine.
4 landmark studies
Antifolates & the slow erosion of the tubulePemetrexed tubulopathy
Pemetrexed leaves the body through the kidney, so the tubule sees the drug at every cycle — and the injury accumulates quietly, cycle by cycle, into a tubulointerstitial scar that often does not heal once the drug is finally stopped.
4 landmark studies
Immunotherapy & the loss of renal toleranceICI nephritis
Release the brakes on the immune system to fight the cancer and, weeks to months later, the same unleashed T cells can turn on the kidney's interstitium — a delayed, often steroid-responsive nephritis that hides behind a bland urine and a slowly rising creatinine.
6 landmark studies
An antifolate, an acidic tubule, and enzymatic rescueHD-MTX nephropathy
High-dose methotrexate is cleared by the kidney, so when it and its poorly-soluble metabolite crystallize in the acidic tubular lumen the kidney injures itself — and because that same kidney is what clears the drug, injury feeds a spiral of rising levels that leucovorin cannot break but an enzyme can.
4 landmark studies
When the cumulative dose poisons the endotheliumCytotoxic TMA
Two old cytotoxics — mitomycin and gemcitabine — injure the microvascular endothelium directly and in proportion to the cumulative dose, so months into therapy the small vessels clot, red cells shear, platelets fall, and the kidney fails: a dose-dependent thrombotic microangiopathy that is not TTP, does not respond to plasma exchange, and is answered first by stopping the drug.
4 landmark studies
When the tumor dies faster than the kidney can clear itTumor lysis
Effective therapy can kill a large, fast-dividing cancer so abruptly that the cells spill their contents into the blood — potassium, phosphate, and a flood of purines that becomes uric acid — and the two crystals that result, urate and calcium-phosphate, clog and poison the tubules: a metabolic emergency that is largely preventable with hydration, rasburicase, and, for venetoclax, a deliberately slow dose ramp-up.
4 landmark studies
A targeted drug that hits the wrong target — in the kidneyBRAF/MEK tubular
Vemurafenib was built to block a mutated melanoma kinase, but in the kidney its damage is off-target: it injures the proximal tubule and can produce a Fanconi picture, usually early and usually mild — and, paradoxically, pairing it with a MEK inhibitor makes it gentler on the kidney, not harsher.
4 landmark studies
One drug class, two very different kidney lesionsBisphosphonate injury
The intravenous bisphosphonates that protect bone in myeloma and metastatic cancer split the nephron between them — pamidronate poisons the podocyte and produces a collapsing FSGS with nephrotic-range proteinuria, while zoledronate poisons the proximal tubule and produces a toxic ATN — and both are dose- and infusion-rate-dependent, so the same monitoring that catches them also prevents them.
4 landmark studies
The kidney caught in the cytokine stormCAR-T AKI
CAR-T cells cure by inflammation, and the same cytokine-release syndrome that fevers and drops the blood pressure starves the kidney of perfusion — so the acute kidney injury after CAR-T is mostly pre-renal and mostly reversible, yet the patients who develop it are the sicker ones, and they do worse.
4 landmark studies
Carfilzomib, the endothelium & the complement thresholdProteasome-inhibitor TMA
Weeks into carfilzomib — often with an infection as the second hit — the microvascular endothelium tips into thrombotic microangiopathy: schistocytes and falling platelets, an acute kidney injury the drug set in motion, and an ADAMTS13 that comes back normal because this was never TTP.
6 landmark studies
Blocked tubular secretion, not injuryPseudo-AKI
Creatinine does not only filter — a fifth of it is pushed into the urine by tubular transporters, and a drug that blocks those transporters raises the number without touching the glomerulus, producing a rise that looks like acute kidney injury on every axis except the one that matters.
5 landmark studies
Retained water, not lost saltDrug-induced SIADH
Hyponatremia is the commonest electrolyte disorder in oncology and its commonest explanation is the cancer itself — which is exactly why a drug that impairs free-water excretion can go on being given for months while the sodium is treated as a feature of the disease.
6 landmark studies
§ 05Beyond the core atlas
Three more ways in — anatomy, the frontier, and MGRS
The interactive nephron
Trace each drug to the segment it injures, glomerulus to collecting duct.
6 segments
The frontier
Emerging real-world signals and graded theoretical toxicities for the newest agents.
14 signals · 10 graded
MGRS — Part II
When the antibody itself is nephrotoxic: nine lesions, workup, clone-directed therapy.
9 lesions
Updates to the atlas
New agents are discovered from the PubMed literature and reviewed before they appear, with an optional email notice whenever the atlas is updated.
Built on deep research across PubMed and current nephrology literature. Educational reference — not medical advice.