What kind of kidney injury does Inotuzumab ozogamicin cause?

Prerenal / Hemodynamic AKI — Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome. Other reported patterns: Electrolyte Disturbance, Crystal / Obstructive Nephropathy.

How should kidney function be monitored during Inotuzumab ozogamicin therapy?

LFTs (bilirubin) and daily weight for VOD, especially around transplant; Tumor lysis labs during initial therapy; Serum creatinine and volume status in evolving VOD.

How can kidney injury from Inotuzumab ozogamicin be prevented?

Tumor lysis prophylaxis (hydration, allopurinol/rasburicase) Limit cycles before transplant and avoid dual-alkylator conditioning to reduce VOD

Who is at higher risk of kidney injury from Inotuzumab ozogamicin?

High leukemic burden; Subsequent allogeneic stem-cell transplant; Dual-alkylator conditioning; Hepatic dysfunction; Volume depletion; Pre-existing CKD.

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Printable monograph

Antibody-drug conjugate (CD22/calicheamicin)

Inotuzumab ozogamicin

Besponsa · InO

Antibody-drug conjugate (CD22/calicheamicin) · approved 2017 · 4 citations · FAERS AKI reporting ROR 2.75 (95% CI 2.12–3.57, 58 AKI reports)

Recent· through 2023

Fairly sourced5/9 · 5 signals

Not met: 4 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 7y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2023
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.

A CD22/calicheamicin conjugate for ALL — tumor lysis and veno-occlusive disease drive its renal risk.

ModerateAntibody-drug conjugate

Acute lymphoblastic leukemia

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Direct nephrotoxicity is not a prominent signal. AKI is chiefly secondary to tumor lysis and to hepatic sinusoidal obstruction syndrome/veno-occlusive disease (VOD) — a notable, sometimes fatal complication, particularly around subsequent allogeneic stem-cell transplant. Renal-specific incidence is not quantified.Source: Kantarjian et al., N Engl J Med 2016 (INO-VATE)

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Early — tumor lysis during initial therapy (VOD, non-renal, is peri-transplant).

Distilled from: “Early — tumor lysis during initial therapy; VOD typically peri-transplant.”

§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.

Prerenal / Hemodynamic AKI#1 · Signaturequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.
Electrolyte DisturbanceSecondaryqualitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).
Crystal / Obstructive NephropathySecondaryqualitative — no citable incidence
Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityModerate

ReversibilityVariable

Evidence4 citations

Nephron map

Vasculature / Endothelium

Distal Tubule / Collecting Duct

Tubular Lumen

Prerenal / Hemodynamic AKI

Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

§03

Kidney injury

Mechanism of kidney injury

Indirect: rapid lysis of bulky ALL causes tumor lysis with crystal nephropathy and electrolyte shifts; calicheamicin injury to hepatic sinusoidal endothelium produces VOD with fluid overload and hepatorenal-pattern AKI, with markedly elevated VOD risk after allogeneic transplant (and with dual-alkylator conditioning). Direct tubular toxicity is not a notable clinical signal.

Clinical presentation

Tumor-lysis labs with AKI early in therapy; with VOD, weight gain, ascites, hyperbilirubinemia, hepatomegaly and rising creatinine with low urine sodium, especially in the peri-transplant period.

Management

Tumor-lysis management; for VOD, supportive care and defibrotide with careful fluid/renal management; supportive AKI care including dialysis if severe.Lesion-level management framework

Risk factors

High leukemic burden
Subsequent allogeneic stem-cell transplant
Dual-alkylator conditioning
Hepatic dysfunction
Volume depletion
Pre-existing CKD

Prevention

Tumor lysis prophylaxis (hydration, allopurinol/rasburicase)
Limit cycles before transplant and avoid dual-alkylator conditioning to reduce VOD

Anticancer mechanism· how it treats cancer

Antibody-drug conjugate targeting CD22 and delivering the DNA-damaging calicheamicin payload via a hydrolyzable linker. Approved for relapsed/refractory B-cell precursor acute lymphoblastic leukemia (ALL).

Note · Renal injury is mediated by tumor lysis and VOD rather than direct tubular toxicity; VOD risk is heightened around transplant.

§04

Clinical depth

Renal dose adjustment

No specific renal dose adjustment; decisions are driven by hepatic function/VOD risk rather than renal clearance. Calicheamicin is hepatically handled.

Dialyzability & ESKD dosing

Not appreciably dialyzed (large ADC; protein-bound calicheamicin). HD/CRRT in VOD supports AKI, not drug removal.

Differential diagnosis

Tumor lysis AKI (early, electrolyte signature) versus VOD hepatorenal AKI (jaundice, weight gain, ascites, low urine sodium) versus sepsis/nephrotoxin ATN. VOD risk is the defining peri-transplant concern.

Monitoring

LFTs (bilirubin) and daily weight for VOD, especially around transplant
Tumor lysis labs during initial therapy
Serum creatinine and volume status in evolving VOD

Key trials & series

INO-VATE (Kantarjian NEJM 2016, R/R ALL; VOD signal)
Jabbour Lancet Haematol 2023 (mini-hyper-CVD + inotuzumab; long-term VOD data)

Clinical pearls

Minimize inotuzumab cycles before allogeneic transplant and avoid dual-alkylator conditioning - both reduce the VOD that drives hepatorenal AKI.
Like gemtuzumab, the calicheamicin ADCs threaten the kidney via the liver (VOD) and the tumor (lysis), not the tubule.
Early defibrotide is the key intervention once VOD with renal involvement is recognized.

Beyond the kidney — non-renal toxicities· 4 organ systems

Class-level context for the major non-renal toxicities of the Antibody-drug conjugate (CD22/calicheamicin) class.

Hematologic

Cytopenias, thrombosis, TMA

Myelosuppression (payload-dependent)

Ophthalmic

Keratopathy, uveitis, retinopathy

Keratopathy (belantamab, mirvetuximab, tisotumab)

Pulmonary

Pneumonitis, ILD, effusions, hypertension

Interstitial lung disease (deruxtecan ADCs)

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

Peripheral neuropathy (MMAE payloads)

§05

References

4 primary references — trials, cohorts, mechanism, and reviews. Citation metadata via PubMed / NLM.

Evidence accrual

4 references · 2016–2023 · 1 since 2021

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.

FDA label — boxed warning & renal dosing· boxed warning

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

Boxed warning

WARNING: HEPATOTOXICITY, INCLUDING HEPATIC VENO-OCCLUSIVE DISEASE (VOD) (ALSO KNOWN AS SINUSOIDAL OBSTRUCTION SYNDROME) and INCREASED RISK OF POST-HEMATOPOIETIC STEM CELL TRANSPLANT (HSCT) NON-RELAPSE MORTALITY WARNING: HEPATOTOXICITY, INCLUDING HEPATIC VENO-OCCLUSIVE DISEASE (VOD) (ALSO KNOWN AS SINUSOIDAL OBSTRUCTION SYNDROME) and INCREASED RISK OF POST- HEMATOPOIETIC STEM CELL TRANSPLANT (HSCT) NON-RELAPSE MORTALITY See full prescribing information for complete boxed warning. • Hepatotoxicity, including fatal and life-threatening VOD occurred in patients who received BESPONSA. ( 5.1 ) • A higher post-HSCT non-relapse mortality rate occurred in patients receiving BESPONSA ( 5.2 ) HEPATOTOXICITY, INCLUDING VOD • Hepatotoxicity, including fatal and life-threatening VOD occurred in patients with relapsed or refractory acute lymphoblastic leukemia (ALL) who received BESPONSA. The risk of VOD was greater in patients who underwent HSCT after BESPONSA treatment; use of HSCT conditioning regimens containing 2 alkylating agents and last total bilirubin level ≥ upper limit of normal (ULN) before HSCT were significantly associated with an increased risk of VOD. • Other risk factors for VOD in patients treated with BESPONSA included ongoing or prior liver disease, prior HSCT, increased age, later salvage lines, and a greater number of BESPONSA treatment cycles. • Elevation of liver…

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 2,937 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· 4 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

Electrolyte Disturbancecorroborated · ROR 3.12 — on the terms that name the lesion (ROR 4.65)
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
Crystal / Obstructive NephropathyNo disproportionate reporting — This phenotype IS reportable and this agent has enough reports, yet the reporting is not disproportionate — the one genuinely informative negative of the four.

Thrombotic Microangiopathy

ROR 14.4695% CI 10.15–20.61· 31 reports

SIADH / Hyponatremia

ROR 5.0495% CI 3.87–6.57· 56 reports

Electrolyte Disturbance

ROR 3.1295% CI 2.51–3.89· 82 reports

Hemorrhagic Cystitis

ROR 2.6995% CI 1.83–3.96· 26 reports

FAERS outcomes & reporting trend· 33.9% of reports w/ death · 40.3% w/ hospitalization

33.9%

Reported with a death outcome

996 of 2,937 reports

40.3%

Reported with hospitalization

1,184 of 2,937 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 7 systems · 2,937 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 2.7595% CI 2.12–3.57· 58 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 Injury58

Blood & lymphatic

Febrile Neutropenia265Thrombocytopenia148Platelet Count Decreased121Neutropenia118Anaemia79

Hepatobiliary

Venoocclusive Liver Disease258Venoocclusive Disease132Blood Bilirubin Increased82Aspartate Aminotransferase Increased57

Immune / infection

Sepsis136Cytokine Release Syndrome133Pneumonia96Infection93

General / constitutional

Pyrexia192Multiple Organ Dysfunction Syndrome81Fatigue69

Gastrointestinal

Nausea74Diarrhoea66

Nervous system

Neurotoxicity55

Guidelines & consensus· 13

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.

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 Inotuzumab ozogamicin 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

Gemtuzumab ozogamicin

Mylotarg · Antibody-drug conjugate (CD33/calicheamicin)

Profile

Tumor lysis and veno-occlusive disease.

PRELYTEXTAL

Moderate#1 · 100% phenotype match

Brentuximab vedotin

Adcetris · Antibody-drug conjugate (CD30/MMAE)

Profile

Tumor lysis in lymphoma.

PRELYTEXTAL

Mild#2 · 95% phenotype match

Polatuzumab vedotin

Polivy · Antibody-drug conjugate (CD79b/MMAE)

Profile

Tumor lysis; emerging renal data.

PRELYTEXTAL

Mild#3 · 95% phenotype match

Epcoritamab

Epkinly · Bispecific (CD20×CD3)

Profile

CRS and tumor lysis — emerging.

PRELYTEXTAL

Moderate#4 · 89% phenotype match

Glofitamab

Columvi · Bispecific (CD20×CD3)

Profile

CRS and tumor lysis — emerging.

PRELYTEXTAL

Moderate#5 · 89% phenotype match

Mosunetuzumab

Lunsumio · Bispecific (CD20×CD3)

Profile

CRS and tumor lysis in lymphoma.

PRELYTEXTAL

Moderate#6 · 89% phenotype match

Compare Inotuzumab ozogamicin 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 Antibody-drug conjugates

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.