What kind of kidney injury does Oxaliplatin cause?

Thrombotic Microangiopathy — Endothelial injury with microvascular thrombi, hemolysis and thrombocytopenia — gemcitabine, mitomycin C, anti-VEGF. Other reported patterns: Acute Tubular Necrosis.

Is kidney injury from Oxaliplatin reversible?

Reversible. Typical onset: Acute if immune-mediated (often on re-challenge)..

How should kidney function be monitored during Oxaliplatin therapy?

Check serum creatinine/eGFR before each cycle; oxaliplatin AKI is uncommon, so a rise should prompt a search for an alternative cause (volume depletion, obstruction, contrast, concurrent nephrotoxins).; On re-exposure or near infusion, monitor CBC and hemoglobin for an abrupt drop plus haptoglobin, LDH, and direct antiglobulin (Coombs) test if immune hemolysis is suspected.; If hemolysis/thrombocytopenia appears, send a peripheral smear for schistocytes to detect drug-induced TMA and stop oxaliplatin immediately.; Document and watch for infusion-reaction symptoms (back pain, hemoglobinuria, hypotension), which can herald acute immune hemolysis with pigment-related AKI.; Track urine output and consider urinalysis for hemoglobinuria during/after infusion in patients with prior reactions..

How can kidney injury from Oxaliplatin be prevented?

No re-challenge after a documented immune hemolytic or TMA event — reactions recur faster and more severely

Who is at higher risk of kidney injury from Oxaliplatin?

Repeated exposure (immune reactions); Pre-existing CKD.

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Printable monograph

Platinum agent

Oxaliplatin

Eloxatin · Oxali

Platinum agent · approved 2002 · 10 citations · FAERS AKI reporting ROR 2.34 (95% CI 2.21–2.47, 1,234 AKI reports)

Up to date· through 2026

Fairly sourced5/9 · 4 signals

Met: 10 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 21y)
Not met: Beyond single case reports
Not met: Peer-reviewed sources
Not met: Landmark reference
Met: Current through 2026
Met: Real-world FAERS signal

Describes how this page is sourced, not how dangerous the drug is. Thinly sourced means fewer of the sourcing signals are met — not that the agent is kidney-safe. A rule-based summary, not a formal certainty appraisal.

The renal-sparing platinum — neuropathy is its hallmark, not nephrotoxicity.

MildThird-generation platinum

ColorectalGastricPancreatic

§01

Signature kidney injury

Signature lesion

Thrombotic Microangiopathy

Lowest nephrotoxic potential of the platinums; AKI is rare and case-level, in some cases immune-mediated.Source: Gupta et al., Adv Chronic Kidney Dis 2021

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Acute when immune-mediated, characteristically on re-challenge rather than first exposure.

Distilled from: “Acute if immune-mediated (often on re-challenge).”

RechallengeContraindicated on rechallenge

Re-exposure after a documented immune hemolytic or TMA event is avoided — reactions recur faster and more severely.

Long-term outlook & thresholds

Renal recoveryUsually reversible

AKI is usually reversible: the characteristic immune-hemolysis-driven injury on re-exposure has recovered renal function with drug cessation plus supportive care (transfusion, and in reported cases plasma exchange, corticosteroids and transient hemodialysis). Rarely, a biopsy-proven acute tubular necrosis has progressed to dialysis-dependent end-stage renal failure.PMID 36978021 (opens PubMed in a new tab)

Dialysis / RRT.: A single-dose biopsy-proven ATN case required dialysis and progressed to end-stage renal failure; immune-hemolytic cases have needed transient hemodialysis during the acute event before recovering.

Early-detection biomarkers

Urinary KIM-1 and NGAL — Subclinical proximal tubular injury (ATN). PRECLINICAL, and cisplatin rather than oxaliplatin: in a rat model given a single cisplatin dose, urinary KIM-1 rose by 24 h and NGAL and NAG by day 2, all ahead of the serum-creatinine rise that appeared on day 3 — establishing a temporal hierarchy the authors explicitly say now needs clinical study. There is no oxaliplatin arm and no human data, so this is a mechanistic rationale for watching tubular markers, not a validated oxaliplatin monitoring test.PMID 23360846 (opens PubMed in a new tab)
Direct antiglobulin (Coombs) test with haptoglobin, LDH and peripheral-smear schistocytes — Immune-mediated intravascular hemolysis / drug-induced TMA — oxaliplatin's signature severe renal event. Oxaliplatin's severe AKI is antibody-driven acute hemolysis, typically after multiple prior cycles; a positive DAT with low haptoglobin, high LDH and schistocytes on smear pins the hemolytic/TMA mechanism and mandates immediate, permanent discontinuation.PMID 22450906 (opens PubMed in a new tab)

Long-term outcome and threshold data distilled from the agent's cited literature — educational, not a substitute for the primary sources.

Recovery across agents

§02

Renal toxicities, ranked

This agent's kidney lesions ordered by prominence — the #1 signature lesion first, then secondary and rare patterns. Cited incidence is shown where a citable figure exists; otherwise the tier stands qualitatively.

Thrombotic Microangiopathy#1 · Signatureno population incidence denominator
Rare, characteristic complication (drug-induced TMA/HUS with microangiopathic hemolytic anemia, thrombocytopenia, acute renal failure); reported in case reports, no population incidence denominator PMID 35303936 (opens PubMed in a new tab)
Acute Tubular NecrosisSecondaryno population incidence denominator
Case-level only; ATN listed among recognized oxaliplatin nephrotoxicity forms (also tubular vacuolization, RTA, interstitial nephritis); no population incidence figure PMID 24615628 (opens PubMed in a new tab)

§03

Kidney injury

Deep diveCisplatin acute tubular necrosis & hypomagnesemiaThe 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.

Mechanism of kidney injury

Lower proximal tubular accumulation than cisplatin. Rare immune-mediated reactions (drug-dependent antibodies) can cause acute hemolysis with pigment/TMA AKI, classically on re-exposure.

Clinical presentation

Usually no significant renal change; peripheral neuropathy dominates. Rare acute hemolysis with hemoglobinuria and AKI.

Management

Stop drug, supportive care, transfusion if hemolysis.Lesion-level management framework

Risk factors

Repeated exposure (immune reactions)
Pre-existing CKD

Prevention

No re-challenge after a documented immune hemolytic or TMA event — reactions recur faster and more severely

Anticancer mechanism· how it treats cancer

DACH-platinum forming DNA cross-links; the backbone of FOLFOX colorectal regimens.

Note · Often the platinum of choice in established CKD.

§04

Clinical depth

Renal dose adjustment

No dose reduction is required for mild-to-moderate impairment; the FDA label permits the standard 85 mg/m2 starting dose down to CrCl ~30 mL/min, with reduction to 65 mg/m2 advised for severe impairment (CrCl <30 mL/min). Unlike cisplatin, oxaliplatin is not directly tubulotoxic, so renal dosing is driven by accumulation of the renally-cleared platinum moiety rather than by nephrotoxicity risk. Hold or reduce for an acute rise in creatinine and reassess before re-exposure.

Dialyzability & ESKD dosing

Ultrafilterable (protein-unbound) platinum is dialyzable, but the large fraction irreversibly bound to plasma proteins and erythrocytes is not, so hemodialysis removes only a minor portion of total platinum; data are limited to case reports. Scheduling chemotherapy a few hours before an HD session has been used pragmatically in dialysis-dependent patients, but no validated protocol exists.

Differential diagnosis

Oxaliplatin AKI is most often an immune-mediated phenomenon presenting on later cycles (acute hemolysis/oxaliplatin-induced TMA causing pigment nephropathy or hemolytic-uremic-like injury), distinguishing it from cisplatin's dose-dependent direct ATN and from gemcitabine TMA by its abrupt, antibody-driven onset tied to re-exposure. A positive DAT, intravascular hemolysis, and temporal link to infusion point to oxaliplatin rather than contrast nephropathy, pre-renal azotemia, or 5-FU/leucovorin co-medication.

Monitoring

Check serum creatinine/eGFR before each cycle; oxaliplatin AKI is uncommon, so a rise should prompt a search for an alternative cause (volume depletion, obstruction, contrast, concurrent nephrotoxins).
On re-exposure or near infusion, monitor CBC and hemoglobin for an abrupt drop plus haptoglobin, LDH, and direct antiglobulin (Coombs) test if immune hemolysis is suspected.
If hemolysis/thrombocytopenia appears, send a peripheral smear for schistocytes to detect drug-induced TMA and stop oxaliplatin immediately.
Document and watch for infusion-reaction symptoms (back pain, hemoglobinuria, hypotension), which can herald acute immune hemolysis with pigment-related AKI.
Track urine output and consider urinalysis for hemoglobinuria during/after infusion in patients with prior reactions.

Key trials & series

MOSAIC (Andre et al., NEJM 2004) - registrational adjuvant FOLFOX trial that established oxaliplatin's standard 85 mg/m2 regimen; notable for the absence of meaningful nephrotoxicity versus cisplatin-era platinums.
NCI Organ Dysfunction Working Group PK study (Takimoto et al., J Clin Oncol 2003) - showed unbound oxaliplatin platinum clearance falls with declining renal function yet was tolerated without added toxicity across CrCl strata, supporting limited dose adjustment in mild-moderate impairment.

Clinical pearls

Oxaliplatin is markedly less nephrotoxic than cisplatin - it does not require forced saline diuresis and rarely causes classic dose-dependent ATN, so a significant creatinine rise should raise suspicion for an immune or hemolytic mechanism.
The signature severe renal event is immune-mediated: drug-dependent antibodies trigger acute intravascular hemolysis and occasionally TMA, typically after multiple prior exposures rather than on first dose.
Pigment (hemoglobin) nephropathy from acute hemolysis, not direct tubular toxicity, is a key route to AKI with oxaliplatin.
Rechallenge after a documented immune hemolytic or TMA event is contraindicated - reactions recur faster and more severely.
Because platinum binds plasma proteins and red cells, total platinum persists for months; this complicates interpretation of levels and limits the utility of dialysis for clearance.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Proximal Tubule

Bulk reabsorption + drug uptake (OCT2, OATs)

Injury signatures

Thrombotic Microangiopathy Acute Tubular Necrosis

Beyond the kidney — non-renal toxicities· 3 organ systems

Class-level context for the major non-renal toxicities of the Platinum agent class.

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

Peripheral neuropathy (esp. oxaliplatin) and ototoxicity (cisplatin)

Hematologic

Cytopenias, thrombosis, TMA

Myelosuppression — thrombocytopenia prominent with carboplatin

Gastrointestinal

Diarrhea, colitis, mucositis, perforation

Severe nausea and vomiting

§05

References

5 primary references — trials, cohorts, mechanism, and reviews. Single-patient case reports are listed separately below, graded by strength. Citation metadata via PubMed / NLM.

Evidence accrual

5 references · 2014–2026 · 1 since 2024

Primary (non–case-report) references per year — a proxy for how actively the agent's renal literature is accruing. Recent years are highlighted. Reflects curation depth, not a systematic bibliometric count.

Case reports — ranked by strength· 5

Single-patient and small-series reports, graded by evidentiary strength — A Strong (biopsy-proven plus a series and/or positive rechallenge), B Moderate, and C Limited (a single clinically-diagnosed case). Strongest first. Grades are inferred automatically from each report's abstract and journal — a heuristic ranking aid, not a formal quality appraisal.

CaseB · ModerateA case of biopsy-proven oxaliplatin-induced acute tubulointerstitial nephritis with thrombocytopenia and anemia.Yamada S et al. · CEN Case Rep 2019 · PMID 30827015Biopsy-proven, dialysis-dependent oxaliplatin-induced acute tubulointerstitial nephritis, a tubular form of AKI overlapping the ATN signature.CaseB · ModerateOxaliplatin induced acute tubular necrosis.Jain A et al. · Indian J Cancer 2015 · PMID 26905139Case report of biopsy-context acute tubular necrosis attributed to oxaliplatin, matching the drug's signature kidney injury.CaseC · LimitedOxaliplatin-induced thrombotic microangiopathy: a case report.Saad R et al. · J Med Case Rep 2022 · PMID 3530393673-year-old with metastatic colon cancer re-exposed to oxaliplatin developed fulminant TMA hours after infusion: microangiopathic hemolytic anemia, thrombocytopenia, severe AKI suggestive of HUS; recovered with plasma exchange, steroids, and hemodialysis. Dose-dependent mechanism suggested.CaseC · LimitedRenal toxicity of oxaliplatin.Labaye J et al. · Nephrol Dial Transplant 2005 · PMID 15827046Case of oxaliplatin-induced acute kidney injury with acute tubular necrosis in a patient treated for ovarian adenocarcinoma.CaseC · LimitedOxaliplatin-Induced Thrombotic Microangiopathy in a Patient with Stage IV Gallbladder Carcinoma: Primary Association or Multiple Hits?Fuentes-Lacouture MC et al. · Case Rep Oncol 2020 · PMID 33173484Gallbladder carcinoma patient developed TMA with microthrombi, platelet consumption, and systemic damage in temporal and sole relation to oxaliplatin, illustrating chemotherapy-induced TMA from a poorly understood agent.

Conference abstracts & journal reports· 1 non-PubMed

Non-PubMed sources — conference abstracts (e.g. ASN Kidney Week, badged Abstract) and case reports from non-indexed field journals (e.g. Journal of Onco-Nephrology, badged Journal). Included for completeness; weigh below peer-reviewed PubMed citations.

AbstractOxaliplatin-Induced HypomagnesemiaKhanin Y, Sachdeva M, Uppal NN · ASN Kidney Week 2020 2020 · Abstract PUB216Profound renal magnesium wasting from oxaliplatin (serum Mg 0.8 mg/dL with a fractional excretion confirming renal loss) precipitated atrial fibrillation — extending the platinum-class distal-tubular magnesium leak, classically attributed to cisplatin, to oxaliplatin.

FDA label — boxed warning & renal dosing· boxed warning · renal impairment

Quoted verbatim from this agent's current FDA label (Aug 2026) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING: HYPERSENSITIVITY REACTIONS, INCLUDING ANAPHYLAXIS Serious and fatal hypersensitivity adverse reactions, including anaphylaxis, can occur with oxaliplatin within minutes of administration and during any cycle. Oxaliplatin is contraindicated in patients with hypersensitivity reactions to oxaliplatin and other platinum-based drugs [see Contraindications (4) ] . Immediately and permanently discontinue oxaliplatin for hypersensitivity reactions and administer appropriate treatment for management of the hypersensitivity reaction [see Warnings and Precautions (5.1) ]. WARNING: HYPERSENSITIVITY REACTIONS, INCLUDING ANAPHYLAXIS See full prescribing information for complete boxed warning. Serious and fatal hypersensitivity adverse reactions, including anaphylaxis, can occur with oxaliplatin within minutes of administration and during any cycle. Oxaliplatin is contraindicated in patients with hypersensitivity reactions to oxaliplatin and other platinum-based drugs. Immediately and permanently discontinue oxaliplatin for hypersensitivity reactions and administer appropriate treatment. ( 4 , 5.1 )

Renal impairment — from the label

The AUC of unbound platinum in plasma ultrafiltrate was increased in patients with renal impairment [see Clinical Pharmacology (12.3) ] . No dose reduction is recommended for patients with mild (creatinine clearance 50 to 79 mL/min) or moderate (creatinine clearance 30 to 49 mL/min) renal impairment, calculated by Cockcroft-Gault equation. Reduce the dose of oxaliplatin in patients with severe renal impairment (creatinine clearance less than 30 mL/min) [see Dosage and Administration (2.3) ].

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 73,752 of them for this agent. Nobody counts the patients who were fine, so none of these numbers is an incidence, a risk, or a rate: they describe what gets reported, shaped by a drug's fame, its indication, and who was watching. How these numbers work.

Reporting odds ratio (ROR) — is kidney injury named in this agent's reports more often than in every other drug's? Above 1 means yes, disproportionately.
Renal phenotypes — the same question asked separately for each kind of kidney injury, so the ratios differ from the overall one and from each other.
Outcomes — a share of this agent's own reports, not of patients: how many were filed as involving a death or a hospitalization. Not a case-fatality rate.

FAERS reported renal phenotypes· 9 signals

Only significant signals appear (95% CI lower bound above 1) — a phenotype missing here was tested and did not reach significance, except Prerenal / Hemodynamic AKI, Pseudo-AKI, Renal Cysts, Chronic Interstitial Nephropathy — outside the clinician-reviewed MedDRA term map, never queried — and ATN and AIN, queried but biopsy-bound: real cases are filed as generic “acute kidney injury”, so their absence is not a negative. As of 2026-10-01.

What reporting says about this profile's documented lesions

Thrombotic Microangiopathycorroborated · ROR 5.29
Acute Tubular Necrosiscorroborated · ROR 1.89

Glomerular Injury / Proteinuria

ROR 5.7195% CI 5.25–6.20· 571 reports

Thrombotic Microangiopathy

ROR 5.2995% CI 4.71–5.96· 283 reports

Electrolyte Disturbance

ROR 3.3195% CI 3.17–3.46· 2,162 reports

SIADH / Hyponatremia

ROR 2.0595% CI 1.89–2.23· 577 reports

Acute Tubular Necrosis

ROR 1.8995% CI 1.48–2.41· 65 reports

Acute Interstitial Nephritis

ROR 1.6095% CI 1.32–1.94· 105 reports

Hypertension

ROR 1.5395% CI 1.47–1.60· 2,052 reports

Fanconi Syndrome

ROR 1.5095% CI 1.03–2.19· 27 reports

Hemorrhagic Cystitis

ROR 1.3695% CI 1.22–1.51· 330 reports

FAERS outcomes & reporting trend· 14.5% of reports w/ death · 39.4% w/ hospitalization

14.5%

Reported with a death outcome

10,723 of 73,752 reports

39.4%

Reported with hospitalization

29,030 of 73,752 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 73,752 reports

Bars rank systems by summed reaction-term mentions (a report counts once per term it names) — an ordinal “more vs less reported” cue, not a tally of distinct reports. Renal & urinary first. As of 2026-10-01.

Disproportionality (acute kidney injury):ROR 2.3495% CI 2.21–2.47· 1,234 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Gastrointestinal

Diarrhoea6,871Nausea5,479Vomiting4,415Abdominal Pain2,032

Blood & lymphatic

Neutropenia4,207Thrombocytopenia3,525Anaemia2,425Febrile Neutropenia1,820Myelosuppression1,731

General / constitutional

Pyrexia2,870Fatigue2,822Asthenia2,360Malaise1,388

Nervous system

Neuropathy Peripheral4,317Paraesthesia1,608Neurotoxicity1,474

Skin

Rash1,607Erythema1,417Palmar-Plantar Erythrodysaesthesia Syndrome1,395

Metabolic & electrolyte

Decreased Appetite2,145Dehydration1,459

Respiratory

Dyspnoea3,084

Vascular

Hypertension1,447

Guidelines & consensus· 15

Each recommendation below is this atlas's faithful summary of the source, not a quotation from it — follow the PubMed link for the wording the society published. Summaries may be superseded; consult the current full text and individualize to the patient.

ADQIConventional cytotoxic chemotherapy-associated nephrotoxicity: consensus report of the 34th Acute Disease Quality Initiative (ADQI) WorkgroupKidney Int 2026 · PMID 41881107Cisplatin is identified as a leading cytotoxic nephrotoxin; the workgroup details preventive measures (adequate isotonic hydration, correction of volume depletion, avoidance of concurrent nephrotoxins, attention to electrolyte/magnesium wasting) and management of cisplatin-associated AKI, with a research agenda for knowledge gaps.Expert ConsensusThe Prevention of Cisplatin-Induced Nephrotoxicity: A General Consensus Statement of a Group of Oncologist-Hematologists, Adult and Pediatric Nephrologists, Radiation Oncologists, Clinical Pathologists, Clinical Pharmacologists, and Renal Physiologists on Cisplatin Therapy in Cancer PatientsInt J Prev Med 2022 · PMID 35392316Consensus on modifiable factors for cisplatin nephrotoxicity prevention, addressing hydration methods, magnesium supplementation, dextrose, avoidance of NSAIDs and renin-angiotensin system inhibitors and contrast agents around cisplatin, GFR assessment, antioxidants, and patient factors (age, sex, female hormones).

General onco-nephrology references

ADQIThe nephrotoxic effects of anti-cancer therapies: consensus report of the 34th Acute Disease Quality Initiative workgroupNat Rev Nephrol 2026 · PMID 41361704Provides expert-based statements (modified Delphi) on preventing and managing cisplatin/platinum-associated AKI, including isotonic IV hydration, attention to volume status and concomitant nephrotoxins, and incorporates evidence that IV magnesium supplementation may reduce cisplatin-associated AKI; emphasizes risk stratification and standardized AKI definitions.SIRMSIRM-SIN-AIOM: appropriateness criteria for evaluation and prevention of renal damage in the patient undergoing contrast medium examinations-consensus statements from Italian College of Radiology (SIRM), Italian College of Nephrology (SIN) and Italian Association of Medical Oncology (AIOM)Radiol Med 2022 · PMID 35303246Recommends eGFR-based renal risk assessment and pre/post-contrast isotonic saline or sodium bicarbonate hydration; advises maintaining a 5-7 day interval between iodinated contrast administration and cisplatin in cancer patients to reduce additive nephrotoxicity.KDIGOKDIGO Controversies Conference on onco-nephrology: understanding kidney impairment and solid-organ malignancies, and managing kidney cancerKidney Int 2020 · PMID 33126977Identifies platinum compounds (especially cisplatin) as leading cytotoxic causes of acute tubular injury, AKI, and electrolyte/magnesium wasting; calls for interdisciplinary onco-nephrology care, accurate GFR estimation, and individualized drug dosing in patients with reduced kidney function.KDIGOKDIGO Controversies Conference on onco-nephrology: kidney disease in hematological malignancies and the burden of cancer after kidney transplantationKidney Int 2020 · PMID 33276867Addresses chemotherapy-associated AKI/CKD in hematologic cancer, GFR estimation and chemotherapy dosing in patients with reduced kidney function, and management priorities and research gaps for onco-nephrology care.ADDIKDIntegrating International Consensus Guidelines for Anticancer Drug Dosing in Kidney Dysfunction (ADDIKD) into everyday practiceEClinicalMedicine 2025 · PMID 40290844Provides GRADE-based, drug-specific dose-adjustment recommendations for anticancer agents in kidney dysfunction (illustrated for methotrexate, cisplatin, carboplatin and nivolumab); the recommendations build on Part 1's standardised CKD-EPI eGFR assessment rather than Cockcroft-Gault creatinine clearance.ADDIKDAligning kidney function assessment in patients with cancer to global practices in internal medicineEClinicalMedicine 2025 · PMID 40290845Three consensus recommendations: assess kidney function by GFR (measured GFR or CKD-EPI eGFR), classify it using KDIGO categories, and use this uniform approach to dose anticancer drugs — moving cancer medicine away from Cockcroft-Gault estimated creatinine clearance.ADDIKDA methodology for determining dosing recommendations for anticancer drugs in patients with reduced kidney functionEClinicalMedicine 2025 · PMID 40290846Establishes that, where RCT evidence is lacking, anticancer drug dosing recommendations in kidney dysfunction should be derived by critically appraising observational literature via GRADE combined with structured international multidisciplinary consensus voting.KDIGODiagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1)Crit Care 2013 · PMID 23394211Defines/stages AKI by serum creatinine and urine output; emphasizes avoiding nephrotoxins, maintaining euvolemia/perfusion, dose-adjusting drugs to kidney function, and monitoring high-risk patients — the framework applied to nephrotoxic anti-cancer agents.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: known knowns and known unknownsKidney Int 2024 · PMID 38519239Evaluate and risk-stratify CKD, manage to delay progression and its complications, and practise explicit medication management and drug stewardship — the framework the atlas's G1–G5 eGFR banding and every renal dose-adjustment recommendation sit inside. Because the guideline excludes dialysis and transplant recipients by its own statement of scope, its recommendations do not carry to those settings, where this atlas's dialyzability and post-transplant guidance rests on other sources.KDIGOExecutive summary of the KDIGO 2021 Guideline for the Management of Glomerular DiseasesKidney Int 2021 · PMID 34556300Provides the staging/treatment framework for drug-associated glomerular lesions (e.g., bisphosphonate- and interferon-related collapsing FSGS, VEGF-inhibitor podocytopathy/proteinuria), including immunosuppression and supportive RAAS-blockade strategies.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of ANCA-Associated VasculitisKidney Int 2024 · PMID 38388147Updates immunosuppressive induction (rituximab/cyclophosphamide), incorporates avacopan and lower-dose or glucocorticoid-sparing regimens — the management framework for drug- and checkpoint-inhibitor-associated ANCA/pauci-immune glomerulonephritis.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of Lupus NephritisKidney Int 2024 · PMID 38182299Updates first-line lupus nephritis therapy to combination immunosuppression with the addition of belimumab or a calcineurin inhibitor (voclosporin) — informs management of immune-complex/lupus-like glomerulonephritis encountered with immunotherapy.KDIGOExecutive summary of the KDIGO 2025 Clinical Practice Guideline for the Management of Immunoglobulin A Nephropathy (IgAN) and Immunoglobulin A Vasculitis (IgAV)Kidney Int 2025 · PMID 40975525Encourages liberal kidney biopsy and stricter proteinuria control (<0.5 g/d, ideally <0.3 g/d) with RAAS blockers, SGLT2 inhibitors, and targeted-release budesonide — the framework for IgA-dominant glomerular lesions, including those triggered by immune-modulating cancer therapy.

Where Oxaliplatin sits in nephrotoxicity space — each dot is an anti-cancer agent, positioned so neighbors share a kidney-injury phenotype. Its 6 closest are filled and lead to a numbered marker, matching the numbered cards below.

Position is a 2-D projection (MDS) of each agent's injury signature, nephron target, severity, and class, so two dots can sit close on the page while differing on an axis the projection flattened — the numbered ranking is computed from the full metric, not from the distance you see. Open the full map.

Phenotype-similar agents· the numbered markers on the map above

mTOR inhibitors (everolimus · temsirolimus)

mTOR inhibitor

Profile

Podocyte injury → proteinuria and FSGS.

GLOMATNTMA

Mild#1 · 58% phenotype match

Binimetinib

Mektovi · MEK inhibitor

Profile

Creatinine rise; rhabdomyolysis reports.

ATNPRE

Mild#2 · 57% phenotype match

Olaparib

Lynparza · PARP inhibitor

Profile

Benign creatinine rise via OCT2/MATE inhibition.

PSEUDOTMA

Mild#3 · 57% phenotype match

Sotorasib

Lumakras · KRAS G12C inhibitor

Profile

Newer agent; renal data emerging.

PREATN

Mild#4 · 57% phenotype match

Pegaspargase

Oncaspar · Enzyme (asparaginase)

Profile

Rare AKI; pancreatitis- and thrombosis-mediated.

PREATN

Mild#5 · 56% phenotype match

Afatinib

Gilotrif · EGFR TKI

Profile

Diarrhea-driven prerenal AKI.

PREATNLYTE

Mild#6 · 53% phenotype match

Compare Oxaliplatin with its nearest agents

Nearest agents by kidney-injury phenotype (shared injuries, nephron target, severity, class) — a similarity approximation, not a claim of shared drug identity or mechanism.

Kidney risk across Platinum agents

Same-class agents ordered by their documented kidney-injury profile — atlas severity, an acute-kidney-injury FAERS signal, and how many injury types each is documented to cause. Agents nearer the top carry the lighter documented renal profile.

1Oxaliplatin· this agentTMA — Thrombotic MicroangiopathyFAERS AKIMild
2CarboplatinATN — Acute Tubular NecrosisFAERS AKIMild
3NedaplatinATN — Acute Tubular NecrosisModerate
4CisplatinATN — Acute Tubular NecrosisFAERS AKISevere

A comparison of documented kidney-injury data within one drug class — not a substitution recommendation. Efficacy, indication, and non-renal toxicity differ between these agents and are out of scope here. Educational only, not medical advice.

Who studies this

The leading contributors to Oxaliplatin’s clinical kidney literature on PubMed, ranked by a blend of publication volume and citation impact — filtered toward clinical work via the PubMed Humans heading and clinical publication types (trials, cohorts, case reports, guidelines, reviews). Names link to that author’s work on Oxaliplatin; the PMIDs beside each name are up to three of their most recent papers on it, not the full count.

Ranked by a 50/50 blend of publication volume and a position-weighted, capped Relative Citation Ratio (NIH iCite) on this agent’s renal literature; the citation count shown is the raw total, not the ranking score — counted over the 190 clinical records among all 278 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.