What kind of kidney injury does Mosunetuzumab 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 Mosunetuzumab therapy?

Serum creatinine and electrolytes (K, phosphate, uric acid, calcium) before and during cycle 1 step-up dosing; CRS vital signs and inflammatory markers (CRP, ferritin) during the priming phase; Tumor lysis labs every 6-12 h in high-burden disease during initial dosing.

How can kidney injury from Mosunetuzumab be prevented?

Step-up (priming) dosing in cycle 1 Early tocilizumab and corticosteroids at the first signs of CRS Tumor lysis prophylaxis (hydration, allopurinol or rasburicase) in high-risk patients Volume optimization before infusions

Who is at higher risk of kidney injury from Mosunetuzumab?

High tumor burden; Bulky/rapidly proliferative disease; Volume depletion; Pre-existing CKD; Concurrent nephrotoxins.

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Printable monograph

Bispecific (CD20×CD3)

Mosunetuzumab

Lunsumio · Mosun

Bispecific (CD20×CD3) · approved 2022 · 8 citations

Recent· through 2024

Fairly sourced5/9 · 5 signals

Met: 8 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 8y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2024
Not 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 CD20×CD3 bispecific whose kidney risk runs through cytokine release and tumor lysis, not the tubule.

ModerateT-cell-engaging bispecific

Follicular lymphomaB-cell non-Hodgkin lymphoma

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Representative incidence0.9%

No direct tubular nephrotoxic signal. AKI is a downstream/case-level consequence of cytokine release syndrome (CRS, ~44% any-grade, almost all grade 1-2 and concentrated in cycle 1) and tumor lysis syndrome; renal-specific incidence is not quantified. Reported rate: tumor lysis syndrome in 0.9% — 218 patients with relapsed/refractory non-Hodgkin lymphoma, including 90 with relapsed/refractory follicular lymphoma,… (Matasar 2024, PMID 38195322).Source: Matasar et al., Clin Lymphoma Myeloma Leuk 2024

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Early — cycle 1 step-up dosing with CRS (first days to ~2 weeks).

Distilled from: “Early — during cycle 1 step-up dosing, coincident with CRS (first days to ~2 weeks).”

§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.

0.9%incidence

SeverityModerate

ReversibilityReversible

Evidence8 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

Kidney injury is indirect. T-cell activation releases IL-6, IFN-gamma and TNF; the resulting fever, vasodilation, hypotension and capillary leak lower renal perfusion to produce hemodynamic/prerenal AKI. In parallel, rapid B-cell lysis can precipitate tumor lysis syndrome with hyperuricemia and hyperphosphatemia, driving intratubular urate/calcium-phosphate crystal deposition. Step-up (priming) dosing across cycle 1 is designed to blunt the CRS peak that mediates this risk.

Clinical presentation

Rising creatinine in the setting of CRS (fever, hypotension, hypoxia, often with elevated CRP/ferritin/IL-6); with tumor lysis, hyperkalemia, hyperphosphatemia, hyperuricemia and hypocalcemia. Hypophosphatemia was a common grade 3-4 laboratory abnormality in the pivotal trial. Urinalysis is typically bland.

Management

Treat CRS with supportive care, IL-6 blockade (tocilizumab) and corticosteroids per grade; restore renal perfusion with isotonic fluids; manage tumor-lysis electrolytes (rasburicase for hyperuricemia, phosphate binders); provide supportive AKI care including renal replacement therapy if refractory.Lesion-level management framework

Risk factors

High tumor burden
Bulky/rapidly proliferative disease
Volume depletion
Pre-existing CKD
Concurrent nephrotoxins

Prevention

Step-up (priming) dosing in cycle 1
Early tocilizumab and corticosteroids at the first signs of CRS
Tumor lysis prophylaxis (hydration, allopurinol or rasburicase) in high-risk patients
Volume optimization before infusions

Anticancer mechanism· how it treats cancer

CD20×CD3 T-cell-engaging bispecific antibody that crosslinks CD3 on host T cells to CD20 on malignant B cells, forming an immunologic synapse that drives granzyme/perforin-mediated B-cell lysis. Approved for relapsed/refractory follicular lymphoma after two or more prior lines.

§04

Clinical depth

Renal dose adjustment

No specific renal dose adjustment is defined; mild-to-moderate renal impairment is not expected to alter exposure of an IgG bispecific. No data in severe impairment/ESKD — dose on clinical grounds.

Dialyzability & ESKD dosing

Not dialyzable (~145 kDa IgG cleared by reticuloendothelial catabolism, not renal filtration). No supplemental dosing needed for HD/PD.

Differential diagnosis

Distinguish CRS-driven prerenal AKI (hypotension, fever, fluid-responsive, bland sediment) from tumor lysis AKI (urate/phosphate elevation, characteristic electrolytes) and from CAR-T/bispecific-associated collapsing glomerulopathy (nephrotic-range proteinuria — biopsy-described but rare). Drug-intrinsic tubular toxicity is not expected.

Monitoring

Serum creatinine and electrolytes (K, phosphate, uric acid, calcium) before and during cycle 1 step-up dosing
CRS vital signs and inflammatory markers (CRP, ferritin) during the priming phase
Tumor lysis labs every 6-12 h in high-burden disease during initial dosing

Key trials & series

GO29781 / Budde Lancet Oncol 2022 pivotal phase 2 (CRS 44%, mostly grade 1-2)

Clinical pearls

The renal story here is hemodynamic and metabolic, not tubular — fix the CRS and the electrolytes and the kidney usually follows.
Step-up dosing exists largely to flatten the cycle-1 CRS peak; most AKI clusters in that window.
Hypophosphatemia is a frequent lab abnormality and can be multifactorial (tumor lysis correction, refeeding) — interpret in context.

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

Class-level context for the major non-renal toxicities of the Bispecific (CD20×CD3) class.

Immune / Infusion

CRS, infusion reactions, irAEs, anaphylaxis

Cytokine release syndrome

Neurologic

Neuropathy, encephalopathy, ICANS, PRES

ICANS / neurotoxicity

Hematologic

Cytopenias, thrombosis, TMA

Cytopenias, hypogammaglobulinemia

§05

References

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

Evidence accrual

8 references · 2016–2024 · 5 since 2022

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 (Jun 2026) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING: CYTOKINE RELEASE SYNDROME Cytokine release syndrome (CRS), including serious or life-threatening reactions, can occur in patients receiving LUNSUMIO. Initiate treatment with the LUNSUMIO step-up dosing schedule to reduce the risk of CRS. Withhold LUNSUMIO until CRS resolves or permanently discontinue based on severity [see Dosage and Administration (2.1 and 2.4) and Warnings and Precautions (5.1) ] . WARNING: CYTOKINE RELEASE SYNDROME See full prescribing information for complete boxed warning. Cytokine release syndrome (CRS), including serious or life-threatening reactions, can occur in patients receiving LUNSUMIO. Initiate treatment with the LUNSUMIO step-up dosing schedule to reduce the risk of CRS. Withhold LUNSUMIO until CRS resolves or permanently discontinue based on severity. ( 2.1 , 2.4 , 5.1 )

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 916 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.
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 outcomes & reporting trend· 15.3% of reports w/ death · 45.3% w/ hospitalization

15.3%

Reported with a death outcome

140 of 916 reports

45.3%

Reported with hospitalization

415 of 916 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 4 systems · 916 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 1.0595% CI 0.50–2.21· 7 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Immune / infection

Cytokine Release Syndrome213Covid-1968Pneumonia47Covid-19 Pneumonia40Infection21

Blood & lymphatic

Neutropenia82Thrombocytopenia31Febrile Neutropenia19

General / constitutional

Pyrexia63Vasogenic Cerebral Oedema31Fatigue19

Skin

Rash34

Guidelines & consensus· 19

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.

ASCOManagement of Immune-Related Adverse Events in Patients Treated With Chimeric Antigen Receptor T-Cell Therapy: ASCO GuidelineJ Clin Oncol 2021 · PMID 34724386Grade toxicities by ASTCT criteria; manage CRS with supportive care escalating to tocilizumab with or without corticosteroids, and manage moderate-to-severe ICANS with corticosteroids and supportive care given potential for rapid decline.TLS Expert PanelGuidelines for the management of pediatric and adult tumor lysis syndrome: an evidence-based reviewJ Clin Oncol 2008 · PMID 18509186Prevention is the best management: hydration plus prophylactic rasburicase for high-risk patients, hydration plus allopurinol or rasburicase for intermediate-risk, and monitoring for low-risk; for established TLS add aggressive hydration and diuresis plus allopurinol or rasburicase for hyperuricemia. Urinary alkalinization is NOT recommended.TLS Consensus PanelRecommendations for the evaluation of risk and prophylaxis of tumour lysis syndrome (TLS) in adults and children with malignant diseases: an expert TLS panel consensusBr J Haematol 2010 · PMID 20331465Stratify each patient as low/intermediate/high TLS risk using tumor type, bulk/stage, proliferation rate, baseline laboratory TLS, and renal impairment/involvement, then match prophylaxis intensity (monitoring vs allopurinol vs rasburicase) to the assigned risk level.BCSHGuidelines for the management of tumour lysis syndrome in adults and children with haematological malignancies on behalf of the British Committee for Standards in HaematologyBr J Haematol 2015 · PMID 25876990Risk-adapted prophylaxis and management of TLS in haematological malignancy: hydration with allopurinol for lower-risk and rasburicase for high-risk patients, with monitoring of electrolytes and renal function to prevent and treat AKI.Cairo-BishopTumour lysis syndrome: new therapeutic strategies and classificationBr J Haematol 2004 · PMID 15384972Defines the Cairo-Bishop criteria distinguishing laboratory TLS (>=2 metabolic abnormalities: hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia within 3 days before to 7 days after therapy) from clinical TLS (laboratory TLS plus AKI, cardiac arrhythmia, or seizure), with a severity grading scheme adopted by subsequent guidelines.ASTCTASTCT Consensus Grading for Cytokine Release Syndrome and Neurologic Toxicity Associated with Immune Effector CellsBiol Blood Marrow Transplant 2019 · PMID 30592986Grade CRS by fever, hypotension and hypoxia (grades 1-4) and grade ICANS using the ICE/encephalopathy score plus level of consciousness, seizures, motor findings and raised intracranial pressure/edema; this is the standard severity framework that triggers tocilizumab and corticosteroid escalation in CAR-T and bispecific antibody toxicity (the Lee 2019 consensus).

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 Mosunetuzumab 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

Epcoritamab

Epkinly · Bispecific (CD20×CD3)

Profile

CRS and tumor lysis — emerging.

PRELYTEXTAL

Moderate#1 · 100% phenotype match

Glofitamab

Columvi · Bispecific (CD20×CD3)

Profile

CRS and tumor lysis — emerging.

PRELYTEXTAL

Moderate#2 · 100% phenotype match

Gemtuzumab ozogamicin

Mylotarg · Antibody-drug conjugate (CD33/calicheamicin)

Profile

Tumor lysis and veno-occlusive disease.

PRELYTEXTAL

Moderate#3 · 89% phenotype match

Inotuzumab ozogamicin

Besponsa · Antibody-drug conjugate (CD22/calicheamicin)

Profile

Tumor lysis and VOD in ALL.

PRELYTEXTAL

Moderate#4 · 89% phenotype match

Revumenib

Revuforj · Menin inhibitor

Profile

2024 leukemia agent; differentiation syndrome and tumor lysis.

PRELYTEXTAL

Moderate#5 · 86% phenotype match

Brentuximab vedotin

Adcetris · Antibody-drug conjugate (CD30/MMAE)

Profile

Tumor lysis in lymphoma.

PRELYTEXTAL

Mild#6 · 84% phenotype match

Compare Mosunetuzumab 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 Bispecifics / T-cell engagers

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.