What kind of kidney injury does Tafasitamab 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.

Is kidney injury from Tafasitamab reversible?

Reversible. Typical onset: Infusion reactions early (first cycle); tumor lysis early in responders..

How should kidney function be monitored during Tafasitamab therapy?

Vital signs during infusions (reactions); TLS labs in responders (uric acid, phosphate, potassium, creatinine); CBC per schedule (cytopenias); Renal function periodically (also to guide lenalidomide dosing).

How can kidney injury from Tafasitamab be prevented?

Infusion premedication and slow first infusions to limit reactions Tumor-lysis risk assessment with hydration +/- allopurinol or rasburicase

Who is at higher risk of kidney injury from Tafasitamab?

High tumor burden (tumor-lysis risk); Pre-existing CKD and concurrent nephrotoxins; Inadequate infusion premedication; Volume depletion.

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Printable monograph

Anti-CD19 antibody

Tafasitamab

Monjuvi · TAF

Anti-CD19 antibody · approved 2020 · 6 citations · FAERS AKI reporting ROR 2.01 (95% CI 1.16–3.47, 13 AKI reports)

Recent· through 2024

Deeply sourced8/9 · 7 signals

Met: 6 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 14y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2024
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.

Fc-engineered anti-CD19 antibody for DLBCL whose renal-relevant risks are infusion reactions and treatment-related tumor lysis rather than a direct nephropathy.

MildFc-engineered antibody era

Relapsed/refractory diffuse large B-cell lymphoma not eligible for autologous stem-cell transplant (with lenalidomide)

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Infusion-related reactions occur early (largely first cycle) and cytopenias are common; tumor lysis is an uncommon, treatment-related concern in responding lymphoma. Direct nephrotoxicity is not a recognized signal and AKI is secondary.Source: Salles et al., Lancet Oncol 2020 (L-MIND)

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Tumor lysis early in responders (first cycle).

Distilled from: “Infusion reactions early (first cycle); tumor lysis early in responders.”

§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).

§03

Kidney injury

Mechanism of kidney injury

Tafasitamab has no characteristic direct renal lesion. Its renal relevance is indirect: (1) infusion-related reactions (fever, hypotension) can transiently impair renal perfusion; (2) brisk cytoreduction in responding lymphoma can cause tumor lysis with urate/phosphate intratubular crystal nephropathy and ATN; (3) the lenalidomide partner contributes its own toxicities. The CD19 target is B-cell-restricted, so the antibody itself is not directly nephrotoxic.

Clinical presentation

Infusion reactions (chills, flushing, hypotension) chiefly during the first infusions; in responders, TLS labs (hyperuricemia, hyperphosphatemia, hyperkalemia, hypocalcemia) and AKI early in treatment. Otherwise a prerenal picture with intercurrent illness.

Management

Manage infusion reactions by slowing/holding the infusion and giving supportive care/premedication; restore perfusion for any transient prerenal AKI. Treat tumor lysis with hydration, urate-lowering therapy, electrolyte correction and dialysis if refractory. Renal effects are generally reversible.Lesion-level management framework

Risk factors

High tumor burden (tumor-lysis risk)
Pre-existing CKD and concurrent nephrotoxins
Inadequate infusion premedication
Volume depletion

Prevention

Infusion premedication and slow first infusions to limit reactions
Tumor-lysis risk assessment with hydration +/- allopurinol or rasburicase

Anticancer mechanism· how it treats cancer

Humanized, Fc-engineered (enhanced ADCC/ADCP) monoclonal antibody targeting CD19 on B cells. Combined with lenalidomide it enhances antibody-dependent cellular cytotoxicity and phagocytosis against diffuse large B-cell lymphoma.

Note · The renal link is indirect — infusion reactions and treatment-related tumor lysis rather than a direct lesion. Note that the lenalidomide combination partner (not tafasitamab) carries the renal dose-adjustment requirement.

§04

Clinical depth

Renal dose adjustment

No dose adjustment for renal impairment for the antibody (not renally cleared); the lenalidomide partner does require CrCl-based dose adjustment. Manage tafasitamab interruptions for infusion reactions/cytopenias.

Dialyzability & ESKD dosing

A monoclonal antibody; not dialyzable. ESKD dosing of the antibody is not specifically established; lenalidomide needs renal dose adjustment.

Differential diagnosis

Separate infusion-reaction transient prerenal AKI from tumor-lysis crystalline nephropathy (early, in responders) and from lenalidomide-related effects. The antibody itself is not directly nephrotoxic.

Monitoring

Vital signs during infusions (reactions)
TLS labs in responders (uric acid, phosphate, potassium, creatinine)
CBC per schedule (cytopenias)
Renal function periodically (also to guide lenalidomide dosing)

Key trials & series

L-MIND (Salles, Lancet Oncol 2020) — registrational tafasitamab + lenalidomide trial

Clinical pearls

Tafasitamab's renal risks are infusion reactions and tumor lysis, not a direct antibody nephrotoxicity.
Remember to renally dose-adjust the lenalidomide partner even though the antibody needs none.
Risk-stratify responders for tumor lysis and pre-treat with hydration +/- rasburicase.
First-cycle infusion reactions are the main acute event — premedicate and slow the infusion.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Tubular Lumen

The urine flow path

Injury signatures

Prerenal / Hemodynamic AKI Electrolyte Disturbance

§05

References

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

Evidence accrual

6 references · 2010–2024 · 2 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.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 898 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· 1 signal

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

Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
Electrolyte DisturbanceNo 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 12.1795% CI 6.07–24.42· 8 reports

FAERS outcomes & reporting trend· 14.5% of reports w/ death · 15.9% w/ hospitalization

14.5%

Reported with a death outcome

130 of 898 reports

15.9%

Reported with hospitalization

143 of 898 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 7 systems · 898 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 2.0195% CI 1.16–3.47· 13 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Immune / infection

Covid-1930Infection22Pneumonia22Sepsis18Cytokine Release Syndrome15

Blood & lymphatic

Neutropenia39Cytopenia26Pancytopenia15

General / constitutional

Pyrexia28Fatigue24Asthenia23

Gastrointestinal

Diarrhoea28Nausea15

Nervous system

Polyneuropathy29

Skin

Rash19

Vascular

Hypotension15

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 Tafasitamab 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

Mogamulizumab

Poteligeo · Anti-CCR4 antibody

Profile

Tumor lysis and rare AKI; cutaneous T-cell lymphoma.

PRELYTE

Mild#1 · 100% phenotype match

Tazemetostat

Tazverik · EZH2 inhibitor

Profile

Tumor lysis; generally low direct renal toxicity.

PRELYTE

Mild#2 · 89% phenotype match

Midostaurin

Rydapt · FLT3 / multikinase inhibitor

Profile

Tumor lysis, edema and QT in AML/mastocytosis.

PRELYTE

Mild#3 · 89% phenotype match

Zanidatamab

Ziihera · HER2 bispecific antibody

Profile

2024 biliary-tract HER2 bispecific; renal data emerging.

PRELYTE

Mild#4 · 88% phenotype match

Zenocutuzumab

Bizengri · HER2×HER3 bispecific antibody

Profile

2024 NRG1-fusion bispecific; mostly grade 1-2 AEs — at most diarrhea-related prerenal risk, no CRS/TLS mechanism.

PRELYTE

Mild#5 · 88% phenotype match

Daratumumab

Darzalex · Anti-CD38 antibody

Profile

Tumor lysis; usable in renal impairment.

PRELYTE

Mild#6 · 86% phenotype match

Compare Tafasitamab 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 Monoclonal antibodies (other)

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.