What kind of kidney injury does Gemtuzumab 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 Gemtuzumab ozogamicin therapy?

LFTs (especially bilirubin) and daily weight for VOD, before and after transplant; Tumor lysis labs during induction; Serum creatinine and volume status, particularly in evolving VOD.

How can kidney injury from Gemtuzumab ozogamicin be prevented?

Tumor lysis prophylaxis (hydration, allopurinol/rasburicase) VOD risk mitigation (fractionated lower dosing, avoid in significant hepatic dysfunction, monitor LFTs and weight)

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

High leukemic burden; Prior or subsequent hematopoietic stem-cell transplant; Hepatic dysfunction; Fractionated high cumulative exposure; Volume depletion; Pre-existing CKD.

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Printable monograph

Antibody-drug conjugate (CD33/calicheamicin)

Gemtuzumab ozogamicin

Mylotarg · GO

Antibody-drug conjugate (CD33/calicheamicin) · approved 2017 · 4 citations · FAERS AKI reporting ROR 1.87 (95% CI 1.41–2.48, 49 AKI reports)

Aging evidence· through 2020

Thinly sourced3/9 · 3 signals

Not met: 4 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 4y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Not met: Current through 2020
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 CD33/calicheamicin conjugate for AML — renal risk runs through tumor lysis and veno-occlusive disease.

ModerateAntibody-drug conjugate

Acute myeloid leukemia

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Direct nephrotoxicity is not a prominent signal. AKI is chiefly secondary to tumor lysis syndrome and to hepatic sinusoidal obstruction syndrome/veno-occlusive disease (VOD), the latter a recognized, sometimes fatal complication that produces hepatorenal-type AKI. Renal-specific incidence is not quantified.Source: Cortes et al., J Hematol Oncol 2020

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Early — tumor lysis with induction (VOD, non-renal, follows within weeks).

Distilled from: “Early — tumor lysis with induction; VOD typically within weeks, notably around hematopoietic stem-cell 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 leukemic-cell lysis causes tumor lysis with crystal nephropathy and electrolyte shifts; calicheamicin-mediated injury to hepatic sinusoidal endothelium produces VOD/SOS with fluid overload, portal hypertension, ascites and hepatorenal-pattern AKI (a functional renal failure of advanced liver injury). Direct tubular toxicity from calicheamicin is not a notable clinical signal.

Clinical presentation

Tumor-lysis labs (hyperuricemia, hyperphosphatemia, hyperkalemia, hypocalcemia) with AKI early in therapy; with VOD, weight gain, painful hepatomegaly, ascites, hyperbilirubinemia and a rising creatinine with low urine sodium (hepatorenal physiology).

Management

Tumor-lysis management (hydration, urate-lowering therapy, electrolyte correction); 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
Prior or subsequent hematopoietic stem-cell transplant
Hepatic dysfunction
Fractionated high cumulative exposure
Volume depletion
Pre-existing CKD

Prevention

Tumor lysis prophylaxis (hydration, allopurinol/rasburicase)
VOD risk mitigation (fractionated lower dosing, avoid in significant hepatic dysfunction, monitor LFTs and weight)

Anticancer mechanism· how it treats cancer

Antibody-drug conjugate targeting CD33 and delivering the DNA-damaging enediyne calicheamicin via a hydrolyzable linker. Approved for CD33-positive acute myeloid leukemia.

Note · Renal injury is mediated by tumor lysis and VOD rather than direct tubular toxicity; VOD carries the highest-stakes renal risk.

§04

Clinical depth

Renal dose adjustment

No specific renal dose adjustment; dose decisions are driven by hepatic function and VOD risk, not renal clearance. Calicheamicin is hepatically handled.

Dialyzability & ESKD dosing

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

Differential diagnosis

Distinguish tumor lysis AKI (early, electrolyte signature) from VOD-associated hepatorenal AKI (jaundice, weight gain, ascites, low urine sodium) and from sepsis/nephrotoxin ATN in the neutropenic host. VOD carries the highest-stakes renal trajectory.

Monitoring

LFTs (especially bilirubin) and daily weight for VOD, before and after transplant
Tumor lysis labs during induction
Serum creatinine and volume status, particularly in evolving VOD

Key trials & series

ALFA-0701 (registrational fractionated dosing)
Cortes J Hematol Oncol 2020 (adverse-event/VOD management review)

Clinical pearls

VOD is the dangerous renal pathway: weight gain + bilirubin + hepatomegaly + rising creatinine peri-transplant should trigger early defibrotide consideration.
Fractionated dosing was adopted partly to reduce VOD risk versus the original single high dose.
The kidney here is a bystander of liver and tumor - direct calicheamicin tubular toxicity is not the issue.

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

Class-level context for the major non-renal toxicities of the Antibody-drug conjugate (CD33/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 · 2016–2020 · 2 since 2018

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 (Dec 2025) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING: HEPATOTOXICITY Hepatotoxicity, including severe or fatal hepatic veno-occlusive disease (VOD), also known as sinusoidal obstruction syndrome (SOS), has been reported in association with the use of MYLOTARG as a single agent, and as part of a combination chemotherapy regimen. Monitor frequently for signs and symptoms of VOD after treatment with MYLOTARG. ( 5.1 and 6.1 ) WARNING: HEPATOTOXICITY See full prescribing information for complete boxed warning. Hepatotoxicity, including severe or fatal hepatic veno-occlusive disease (VOD), also known as sinusoidal obstruction syndrome (SOS), has been reported in association with the use of MYLOTARG. ( 5.1 , 6.1 )

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 3,635 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 3.3 — on the terms that name the lesion (ROR 4.17)
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 6.3795% CI 3.95–10.25· 17 reports

Electrolyte Disturbance

ROR 3.3095% CI 2.72–4.00· 107 reports

Hemorrhagic Cystitis

ROR 3.1095% CI 2.24–4.29· 37 reports

SIADH / Hyponatremia

ROR 1.8795% CI 1.27–2.75· 26 reports

FAERS outcomes & reporting trend· 31% of reports w/ death · 48% w/ hospitalization

31%

Reported with a death outcome

1,126 of 3,635 reports

48%

Reported with hospitalization

1,745 of 3,635 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 6 systems · 3,635 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 1.8795% CI 1.41–2.48· 49 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Blood & lymphatic

Febrile Neutropenia697Thrombocytopenia239Platelet Count Decreased235Neutropenia190White Blood Cell Count Decreased184

Hepatobiliary

Venoocclusive Liver Disease259Aspartate Aminotransferase Increased184Alanine Aminotransferase Increased163Blood Bilirubin Increased138

Immune / infection

Sepsis299Pneumonia196Infusion Related Reaction130Septic Shock107

General / constitutional

Pyrexia325Chills158Weight Increased112

Vascular

Hypotension142

Gastrointestinal

Nausea110

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 Gemtuzumab 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

Inotuzumab ozogamicin

Besponsa · Antibody-drug conjugate (CD22/calicheamicin)

Profile

Tumor lysis and VOD in ALL.

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 Gemtuzumab 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.