What kind of kidney injury does Ifosfamide cause?

Fanconi Syndrome — Global failure of proximal tubule reabsorption — glucosuria, phosphaturia and acidosis, classically from ifosfamide. Other reported patterns: Acute Tubular Necrosis, Electrolyte Disturbance, Hemorrhagic Cystitis.

How should kidney function be monitored during Ifosfamide therapy?

Baseline and serial serum creatinine/eGFR plus electrolytes including phosphate, potassium, magnesium, and bicarbonate before each cycle to detect proximal tubulopathy.; Screen for Fanconi syndrome: urine glucose in the absence of hyperglycemia (glucosuria), low-molecular-weight proteinuria, aminoaciduria, hypophosphatemia, and a normal-anion-gap (type 2) renal tubular acidosis.; Track serum phosphate and tubular reabsorption of phosphate, and watch for hypophosphatemic rickets/osteomalacia and growth failure in children, who are most vulnerable.; Monitor cumulative ifosfamide dose; risk of persistent tubulopathy and GFR decline rises steeply above ~60-100 g/m2 and with prior or concurrent cisplatin.; Urinalysis for hematuria each cycle to detect hemorrhagic cystitis despite mesna and adequate hydration..

How can kidney injury from Ifosfamide be prevented?

Mesna (protects bladder, NOT tubules) Dose limitation

Who is at higher risk of kidney injury from Ifosfamide?

Young age (<5 yr); High cumulative dose; Prior / concurrent cisplatin; Reduced renal mass.

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Printable monograph

Oxazaphosphorine alkylator

Ifosfamide

Ifex · Ifos

Oxazaphosphorine alkylator · approved 1988 · 15 citations · FAERS AKI reporting ROR 2.98 (95% CI 2.71–3.27, 459 AKI reports)

Up to date· through 2026

Deeply sourced9/9 · 8 signals

Met: 15 citations
Met: 12+ references
Met: Accrued over 10+ years (span: 35y)
Met: Beyond single case reports
Met: High-impact journal
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 Fanconi-maker — its metabolite poisons proximal tubule mitochondria.

SevereOxazaphosphorine alkylator

SarcomaGerm-cellPediatric solid tumors

§01

Signature kidney injury

Signature lesion

Fanconi Syndrome

Representative incidence5%

Subclinical tubular dysfunction is common while overt Fanconi is not, and the gap is the point. In 183 children investigated prospectively at least 5 years out — none of whom received any platinum, so the toxicity is attributable — the tubular threshold for phosphate was reduced in 24% and glycosuria detected in 37%, yet glycosuria exceeded 0.5 g/24 h in only 5%, bicarbonate and calcium were normal in every patient, and 89.5% had normal tubular function overall at a median 10 years. GFR was abnormal in 21.5%. Ifosfamide dose and time since therapy both predicted tubulopathy. Rates elsewhere span 0% to 84% depending on the definition and cohort used, so a single figure is only meaningful with its threshold attached.Source: Oberlin et al., J Clin Oncol 2009 (PMID 19826134); Cochrane review, Kooijmans et al. 2019 (PMID 30855726)

Onset & rechallenge

Time to injuryVariable / unpredictable

Acute tubulopathy during therapy, but chronic Fanconi/CKD can surface months to years later.

Distilled from: “Acute tubulopathy during therapy; chronic Fanconi/CKD can emerge months–years later.”

Long-term outlook & thresholds

Renal recoveryOften permanent

Proximal tubulopathy is frequently irreversible: subclinical tubular dysfunction tends to persist or progress rather than recover after the drug is stopped, and a normal creatinine on the last cycle does not exclude later injury.PMID 29606257 (opens PubMed in a new tab)

CKD trajectory.: Chronic Fanconi syndrome and CKD can be immediate or delayed, surfacing months to years after therapy, so long-term glomerular and tubular follow-up is warranted.
Dialysis / RRT.: In the cited adult cohort the injury was often severe, with progression to stage 5 CKD requiring dialysis in a subset of patients.

Cumulative-dose threshold

≥60 g/m² cumulative ifosfamide

In a critical review of the pediatric risk-factor literature, cumulative dose ≥60 g/m² was the most consistent independent predictor of both the development and the severity of nephrotoxicity; age <5 years was associated primarily with the more severe, chronic forms of proximal tubulopathy. Concurrent platinum probably POTENTIATES ifosfamide renal damage rather than acting as a major independent risk factor — incidence and severity of proximal tubulopathy were comparable in children who did and did not also receive cisplatin.PMID 9606250 (opens PubMed in a new tab)

Early-detection biomarkers

Urinary β2-microglobulin (± retinol-binding protein) — Proximal tubular injury — low-molecular-weight tubular proteinuria. Rises before routine renal-function tests change and can predict ifosfamide tubulopathy even when creatinine, phosphate and urinalysis are normal; the elevation often persists after the drug is stopped.PMID 9261752 (opens PubMed in a new tab)
Serum phosphate with tubular reabsorption of phosphate (TmP/GFR) — Proximal tubular phosphate wasting — the Fanconi phenotype. Hypophosphatemia with inappropriately high fractional phosphate excretion (low tubular reabsorption) is an early, sensitive sign of dose-dependent proximal tubulopathy and can appear while creatinine is still normal.PMID 8270973 (opens PubMed in a new tab)
Serum cystatin C (with creatinine-based eGFR) — Glomerular filtration — long-term GFR surveillance. Harmonized survivorship guidance recommends estimating GFR from serum creatinine, preferably combined with serum cystatin C, for glomerular-dysfunction surveillance every 2-5 years in ifosfamide-treated survivors.PMID 40393013 (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

Host risk modifiers

Germline / pharmacogenomic variants that shift an individual's risk of this agent's kidney injury. Research-grade — not routine clinical testing.

GSTP1Ile105Val (rs1695; codon 105 A>G)
Carriers of the GSTP1 codon-105 A->G (Ile105Val) variant show higher urinary excretion of toxic ifosfamide metabolites and lower creatinine clearance (median 81.1 vs 105.0 mL/min/1.73m2, p=0.03), marking increased risk of ifosfamide proximal tubular / renal toxicity. PMID 16282887 (opens PubMed in a new tab)

§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.

Fanconi Syndrome#1 · Signature4%PMID 8625085 (opens PubMed in a new tab)
~4% incidence of overt Fanconi-like syndrome after high-dose ifosfamide; acute subclinical proximal tubular dysfunction seen in essentially all treated patients (prospective pediatric/young-adult cohort).
Electrolyte DisturbanceSecondaryno population incidence denominator
Renal wasting of phosphate, potassium, magnesium and calcium is a near-universal subclinical accompaniment of the proximal tubulopathy; a minority develop chronic tubular electrolyte loss requiring oral supplementation. PMID 8625085 (opens PubMed in a new tab)
Hemorrhagic CystitisSecondary3%PMID 27380806 (opens PubMed in a new tab)
Hemorrhagic cystitis in ~3% of ifosfamide cycles (14/425) with routine mesna + hydration prophylaxis; markedly higher and dose-limiting without uroprotection.
Acute Tubular NecrosisRarequalitative — no citable incidence
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

5%incidence

SeveritySevere

ReversibilityOften irreversible

Evidence15 citations

Nephron map

Proximal TubuleBulk reabsorption + drug uptake (OCT2, OATs)

Distal Tubule / Collecting Duct

Bladder / Urothelium

Fanconi Syndrome

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

§03

Kidney injury

Deep diveIfosfamide Fanconi syndromeMesna 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.Appears in 1 documented synergy combination

Mechanism of kidney injury

The toxic metabolite chloroacetaldehyde damages proximal tubular mitochondria, collapsing reabsorption and producing Fanconi syndrome (glucosuria, aminoaciduria, phosphaturia, bicarbonaturia). Acrolein separately injures the bladder urothelium.

Clinical presentation

Hypophosphatemia (rickets/osteomalacia in children), proximal renal tubular acidosis, glucosuria with normal blood glucose, hypokalemia, low-molecular-weight proteinuria; hematuria from cystitis.

Management

Electrolyte, phosphate and bicarbonate repletion; vitamin D for rickets; stop drug if severe.Lesion-level management framework

Risk factors

Young age (<5 yr)
High cumulative dose
Prior / concurrent cisplatin
Reduced renal mass

Prevention

Mesna (protects bladder, NOT tubules)
Dose limitation

Anticancer mechanism· how it treats cancer

Oxazaphosphorine prodrug activated by hepatic CYP450 into a DNA-alkylating mustard. Sarcomas, germ-cell and pediatric tumors.

§04

Clinical depth

Renal dose adjustment

No specific renal dose-adjustment thresholds are given in the FDA label, but ifosfamide is used cautiously in pre-existing renal impairment and dose should be individualized; some clinicians reduce or avoid it when CrCl falls below ~30-50 mL/min given accumulation of neurotoxic and nephrotoxic metabolites (chloroacetaldehyde). A reduced renal reserve, prior cisplatin, young age (<5 yr), and high cumulative dose (>60-100 g/m2) all raise tubulopathy risk and warrant a more conservative dose. Mesna does NOT prevent tubular nephrotoxicity (only hemorrhagic cystitis), so it is not protective against the Fanconi signature.

Dialyzability & ESKD dosing

Limited data on dialytic removal in routine practice; ifosfamide and its metabolites are partly removed by hemodialysis given low molecular weight and modest protein binding, but it is rarely dosed against HD. Hemodialysis is used as salvage for life-threatening encephalopathy/overdose and to clear toxic metabolites rather than as scheduled supplemental dosing, so timing relative to HD is not standardized.

Differential diagnosis

The hallmark is proximal (type 2) renal tubular acidosis with full or partial Fanconi syndrome - glucosuria with normoglycemia, phosphate/bicarbonate/potassium wasting, and LMW proteinuria - which distinguishes it from cisplatin's classic distal magnesium wasting and acute tubular necrosis, and from cyclophosphamide, which causes hemorrhagic cystitis but essentially no Fanconi tubulopathy. Co-administered cisplatin, aminoglycosides, or tenofovir can produce overlapping proximal tubulopathy, so timing and drug sequence help attribution; hypophosphatemic rickets in a treated child strongly implicates ifosfamide.

Monitoring

Baseline and serial serum creatinine/eGFR plus electrolytes including phosphate, potassium, magnesium, and bicarbonate before each cycle to detect proximal tubulopathy.
Screen for Fanconi syndrome: urine glucose in the absence of hyperglycemia (glucosuria), low-molecular-weight proteinuria, aminoaciduria, hypophosphatemia, and a normal-anion-gap (type 2) renal tubular acidosis.
Track serum phosphate and tubular reabsorption of phosphate, and watch for hypophosphatemic rickets/osteomalacia and growth failure in children, who are most vulnerable.
Monitor cumulative ifosfamide dose; risk of persistent tubulopathy and GFR decline rises steeply above ~60-100 g/m2 and with prior or concurrent cisplatin.
Urinalysis for hematuria each cycle to detect hemorrhagic cystitis despite mesna and adequate hydration.

Key trials & series

Skinner et al. (UKCCSG long-term renal follow-up series) - documented persistent and frequently progressive subclinical tubular dysfunction and GFR decline years after ifosfamide, establishing the often-irreversible nature of the tubulopathy.
Loebstein & Koren (pediatric cohort analyses) - identified young age, high cumulative ifosfamide dose, and prior cisplatin/nephrectomy as key risk factors for ifosfamide-induced renal tubular toxicity.
Skinner et al. (Ifosfamide Nephrotoxicity Grading study) - validated a clinical grading scale (electrolyte wasting, tubular proteinuria, GFR) used to classify severity of ifosfamide tubulopathy.

Clinical pearls

The toxic metabolite chloroacetaldehyde, not the parent drug, drives proximal tubular injury - mesna scavenges acrolein in the bladder and does NOT protect the tubule.
Tubulopathy is often subclinical at the end of therapy and can present or progress years later, so a normal creatinine on the last cycle does not exclude future Fanconi syndrome or CKD.
Hypophosphatemia with inappropriately high urinary phosphate (low tubular reabsorption) is an early, sensitive marker - check phosphate even when creatinine is normal.
In children, ifosfamide Fanconi syndrome can cause hypophosphatemic rickets and growth retardation; aggressive phosphate and bicarbonate replacement is the mainstay since the lesion is frequently irreversible.
Glomerular (GFR) and tubular toxicities can occur independently - a patient may have falling GFR with preserved tubular function or florid Fanconi with near-normal GFR, so monitor both.

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

Class-level context for the major non-renal toxicities of the Oxazaphosphorine alkylator class.

Hematologic

Cytopenias, thrombosis, TMA

Myelosuppression; secondary malignancy risk

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

Ifosfamide encephalopathy (chloroacetaldehyde)

Cardiac

Cardiomyopathy, QT, ischemia, myocarditis

High-dose cyclophosphamide cardiotoxicity

§05

References

10 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

10 references · 1991–2026 · 2 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 · ModerateFanconi syndrome with karyomegalic interstitial nephritis after ifosfamide treatment for osteosarcoma: a case report.Kita Y et al. · CEN Case Rep 2025 · PMID 38955949An 18-year-old with osteosarcoma developed Fanconi syndrome and progressive renal dysfunction, with biopsy-proven karyomegalic interstitial nephritis after ifosfamide/cisplatin.CaseC · LimitedIfosfamide-induced nephrogenic diabetes insipidus and Fanconi syndrome in a patient with femur osteosarcoma.Concepción-Zavaleta M et al. · Caspian J Intern Med 2024 · PMID 3935943116-year-old with femur osteosarcoma developed delayed Fanconi syndrome (hypokalemia, hypophosphatemia, glycosuria, proteinuria) and nephrogenic diabetes insipidus over a year after high cumulative ifosfamide; managed with electrolyte repletion and potassium-sparing diuretics.CaseC · LimitedIfosfamide induced renal rickets.Lionel AP et al. · Indian J Pediatr 2014 · PMID 23912821A 4-year-old boy developed proximal renal tubulopathy with florid rickets a year after ifosfamide therapy for Ewing sarcoma.CaseC · LimitedManaging Ifosfamide-Induced Arginine Vasopressin Resistance: Diagnostic and Treatment Strategies.Williams AA et al. · Cureus 2025 · PMID 4029117342-year-old after 6th cycle of doxorubicin-ifosfamide developed AKI, polyuria from arginine vasopressin resistance (nephrogenic DI), plus proximal tubular injury with hypophosphatemia, metabolic acidosis, hypokalemia, glucosuria; managed with supratherapeutic desmopressin, copeptin used diagnostically.CaseC · LimitedThe Atypical Presentation of Ifosfamide-Induced Renal Tubular Acidosis.Vayzband V et al. · Cureus 2024 · PMID 39100050A patient on ifosfamide for metastatic osteosarcoma presented with acute symptomatic hypokalemia and suspected combined proximal/distal (type 3) renal tubular acidosis.

Conference abstracts & journal reports· 2 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.

AbstractIfosfamide-Induced Fanconi Syndrome Presenting with Severe Electrolyte Wasting: A Diagnostic ChallengeASN Kidney Week 2025 2025 · Abstract FR-PO0624Proximal tubular (Fanconi) dysfunction after etoposide/ifosfamide with normoglycemic glucosuria, hypokalemia, hypophosphatemia, and a normal-anion-gap metabolic acidosis despite preserved GFR — the classic ifosfamide tubulopathy, easily missed when creatinine is normal.AbstractAn Interesting Case of Proximal Renal Tubular Acidosis and Fanconi Syndrome due to Ifosfamide NephrotoxicityASN Kidney Week 2020 2020 · Abstract PUB222Proximal RTA and Fanconi syndrome (non-anion-gap acidosis, hypokalemia, hypophosphatemia, glycosuria, proteinuria) after a relatively low cumulative ifosfamide dose, managed supportively with electrolyte repletion — a reminder that the tubulopathy is not strictly dose-dependent.

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

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

Boxed warning

WARNING: MYELOSUPPRESSION, NEUROTOXICITY, and UROTOXICITY Myelosuppression can be severe and lead to fatal infections. Monitor blood counts prior to and at intervals after each treatment cycle. CNS toxicities can be severe and result in encephalopathy and death. Monitor for CNS toxicity and discontinue treatment for encephalopathy. Nephrotoxicity can be severe and result in renal failure. Hemorrhagic cystitis can be severe and can be reduced by the prophylactic use of mesna. [see Warnings and Precautions ( 5.1 - 5.3 )] WARNING: MYELOSUPPRESSION, NEUROTOXICITY, and UROTOXICITY See full prescribing information for complete boxed warning. • Myelosuppression can be severe and lead to fatal infections ( 5.1 ) • CNS toxicities can be severe and result in encephalopathy and death ( 5.2 ) • Nephrotoxicity can be severe and result in renal failure. Hemorrhagic cystitis can be severe. ( 5.3 )

Renal impairment — from the label

No formal studies were conducted in patients with renal impairment. Ifosfamide and its metabolites are known to be excreted by the kidneys and may accumulate in plasma with decreased renal function. Patients with renal impairment should be closely monitored for toxicity and dose reduction may be considered. Ifosfamide and its metabolites are dialyzable. 8.7 Use in Patients with

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 21,570 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· 8 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

Fanconi Syndromecorroborated · ROR 34.62 — on the terms that name the lesion (ROR 52.41)
Hemorrhagic Cystitiscorroborated · ROR 3.1 — on the terms that name the lesion (ROR 30.05)
Acute Tubular Necrosiscorroborated · ROR 2.78
Electrolyte Disturbancecorroborated · ROR 2.69 — on the terms that name the lesion (ROR 3.73)

Fanconi Syndrome

ROR 34.6295% CI 29.75–40.28· 175 reports

Acute Interstitial Nephritis

ROR 6.2995% CI 5.25–7.53· 120 reports

Thrombotic Microangiopathy

ROR 3.7295% CI 2.88–4.81· 59 reports

Hemorrhagic Cystitis

ROR 3.1095% CI 2.71–3.54· 219 reports

Acute Tubular Necrosis

ROR 2.7895% CI 1.92–4.02· 28 reports

Electrolyte Disturbance

ROR 2.6995% CI 2.47–2.94· 520 reports

Glomerular Injury / Proteinuria

ROR 2.5895% CI 2.06–3.23· 77 reports

SIADH / Hyponatremia

ROR 1.9895% CI 1.69–2.31· 163 reports

FAERS outcomes & reporting trend· 20.6% of reports w/ death · 30.9% w/ hospitalization

20.6%

Reported with a death outcome

4,442 of 21,570 reports

30.9%

Reported with hospitalization

6,658 of 21,570 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 6 systems · 21,570 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 2.9895% CI 2.71–3.27· 459 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Renal & urinary

Acute Kidney Injury459

Blood & lymphatic

Febrile Neutropenia2,756Neutropenia1,910Thrombocytopenia1,553Anaemia1,263Pancytopenia808

Gastrointestinal

Vomiting759Nausea750Mucosal Inflammation738Diarrhoea635

Immune / infection

Sepsis886Infection811Pneumonia466

General / constitutional

Pyrexia1,011

Nervous system

Encephalopathy632

Guidelines & consensus· 14

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.

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 Ifosfamide 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

Streptozocin

Zanosar · Nitrosourea alkylator

Profile

Classic proximal tubular toxin → Fanconi and dose-limiting AKI.

FANCATNLYTE

Severe#1 · 73% phenotype match

Cisplatin

Platinol · Platinum agent

Profile

Proximal tubular ATN + magnesium wasting; the archetype.

ATNLYTEPRE

Severe#2 · 62% phenotype match

Trastuzumab deruxtecan

Enhertu · Antibody-drug conjugate (HER2/DXd)

Profile

Emerging AKI/proteinuria reports — under-published.

ATNFANCLYTE

Moderate#3 · 56% phenotype match

Melphalan flufenamide (melflufen)

Pepaxto · Peptide-conjugated alkylator

Profile

Delivers melphalan intracellularly; BRIDGE supports a reduced 30 mg dose in moderate renal impairment.

ATNLYTE

Moderate#4 · 52% phenotype match

Plicamycin (mithramycin)

Mithracin · Antitumor antibiotic

Profile

Cumulative tubular ATN; hypocalcemia is an on-target antiresorptive effect.

ATNLYTE

Moderate#5 · 52% phenotype match

Trabectedin

Yondelis · Marine alkylating agent

Profile

Rhabdomyolysis → pigment nephropathy; hepatotoxicity.

ATNLYTE

Moderate#6 · 51% phenotype match

Compare Ifosfamide 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 Alkylating 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.

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 Ifosfamide’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 Ifosfamide; 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 131 clinical records among the 300 most-relevant of 566 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.