What kind of kidney injury does Loncastuximab tesirine 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.

How should kidney function be monitored during Loncastuximab tesirine therapy?

Weight, edema and effusion assessment each cycle; Serum creatinine, albumin and electrolytes; TLS labs in responders (uric acid, phosphate, potassium); Liver tests and CBC per schedule.

How can kidney injury from Loncastuximab tesirine be prevented?

Premedicate (dexamethasone) per label to reduce fluid accumulation Avoid brisk diuresis — third-spacing leaves the intravascular space depleted despite edema Tumor-lysis risk assessment with hydration +/- urate-lowering therapy Dose delay/reduction for significant edema/effusions

Who is at higher risk of kidney injury from Loncastuximab tesirine?

Pre-existing cardiac/renal dysfunction or hypoalbuminemia; Higher cumulative ADC exposure; High tumor burden (tumor-lysis risk); Concurrent nephrotoxins.

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Printable monograph

Antibody-drug conjugate (CD19/PBD)

Loncastuximab tesirine

Zynlonta · LON

Antibody-drug conjugate (CD19/PBD) · approved 2021 · 5 citations

Recent· through 2024

Fairly sourced4/9 · 4 signals

Not met: 5 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 4y)
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.

CD19-directed pyrrolobenzodiazepine ADC whose capillary-leak-type edema, effusions and fluid overload are the renal-relevant signals in DLBCL.

ModeratePyrrolobenzodiazepine ADC era

Relapsed/refractory large B-cell lymphoma (DLBCL not otherwise specified, high-grade B-cell lymphoma) after >=2 systemic therapies

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Edema and effusions (pleural, pericardial, peritoneal) are characteristic PBD-payload toxicities and were common in LOTIS-2; the resulting fluid shifts and AKI are not separately quantified. Tumor lysis is an additional consideration in responding lymphoma.Source: Caimi et al., Lancet Oncol 2021 (LOTIS-2)

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Prerenal changes track fluid shifts as edema/effusions accumulate over cycles.

Distilled from: “Edema/effusions accumulate over cycles; prerenal changes track the fluid shifts.”

§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

The PBD payload causes endothelial/vascular injury producing a capillary-leak-type syndrome with peripheral edema, serosal effusions and fluid extravasation. Intravascular volume depletion from third-spacing drives prerenal azotemia, while fluid overload can complicate management; severe capillary leak can cause hemodynamic AKI. The CD19 target is restricted to B cells, so the renal injury is payload-mediated and hemodynamic rather than a direct antibody-target nephrotoxicity. Tumor lysis can add crystalline injury in responders.

Clinical presentation

Progressive peripheral edema, weight gain, dyspnea from pleural/pericardial effusions and ascites; a prerenal creatinine rise from intravascular depletion despite total-body fluid excess. TLS labs may appear in responders.

Management

Manage edema/effusions with judicious diuresis (avoiding worsening prerenal physiology), drainage of symptomatic effusions, and dose modification/delay. Restore effective circulating volume for prerenal AKI. Treat tumor lysis with hydration, urate-lowering therapy and electrolyte correction. Renal effects generally improve as fluid shifts resolve.Lesion-level management framework

Risk factors

Pre-existing cardiac/renal dysfunction or hypoalbuminemia
Higher cumulative ADC exposure
High tumor burden (tumor-lysis risk)
Concurrent nephrotoxins

Prevention

Premedicate (dexamethasone) per label to reduce fluid accumulation
Avoid brisk diuresis — third-spacing leaves the intravascular space depleted despite edema
Tumor-lysis risk assessment with hydration +/- urate-lowering therapy
Dose delay/reduction for significant edema/effusions

Anticancer mechanism· how it treats cancer

Antibody-drug conjugate of an anti-CD19 antibody linked to a pyrrolobenzodiazepine (PBD) dimer payload. After CD19 binding and internalization, the released PBD cross-links DNA, causing death of malignant B cells in diffuse large B-cell lymphoma.

Note · The renal link is indirect — payload-driven capillary-leak edema/effusions cause fluid shifts and prerenal AKI rather than a direct target nephrotoxicity; tumor lysis adds risk in responders.

§04

Clinical depth

Renal dose adjustment

No dose adjustment for mild-moderate renal impairment; severe impairment/ESKD not well studied. As an ADC, clearance is not primarily renal.

Dialyzability & ESKD dosing

A large antibody-drug conjugate; not dialyzable. ESKD dosing is not established.

Differential diagnosis

Distinguish capillary-leak/effusion-related prerenal AKI (intravascular depletion despite edema) from cardiac failure, nephrotic-range proteinuria, and tumor-lysis nephropathy. Assess effective circulating volume before diuresing.

Monitoring

Weight, edema and effusion assessment each cycle
Serum creatinine, albumin and electrolytes
TLS labs in responders (uric acid, phosphate, potassium)
Liver tests and CBC per schedule

Key trials & series

LOTIS-2 (Caimi, Lancet Oncol 2021) — registrational single-arm trial characterizing edema/effusion toxicity

Clinical pearls

PBD-payload capillary leak causes total-body fluid excess with intravascular depletion — diurese cautiously.
Edema and serosal effusions are the signature ADC toxicities to track each cycle.
Premedication (dexamethasone) mitigates fluid accumulation.
As an ADC it is not dialyzable; clearance is not renal.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Injury signatures

Prerenal / Hemodynamic AKI Electrolyte Disturbance

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

Class-level context for the major non-renal toxicities of the Antibody-drug conjugate (CD19/PBD) 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

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

Evidence accrual

5 references · 2020–2024 · 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 393 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.

Acute Interstitial Nephritis

ROR 5.7295% CI 1.43–22.96· 2 reports

FAERS outcomes & reporting trend· 34.4% of reports w/ death · 26.5% w/ hospitalization

34.4%

Reported with a death outcome

135 of 393 reports

26.5%

Reported with hospitalization

104 of 393 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 393 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 1.4195% CI 0.53–3.76· 4 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Blood & lymphatic

Neutropenia17Anaemia15Thrombocytopenia15Platelet Count Decreased9Cytopenia7

Skin

Rash32Photosensitivity Reaction18

General / constitutional

Fatigue21Oedema14Oedema Peripheral11

Immune / infection

Pneumonia14Covid-1913Infection9Sepsis8

Respiratory

Pleural Effusion24Dyspnoea8

Hepatobiliary

Gamma-Glutamyltransferase Increased9Hepatic Enzyme Increased6

Cardiac

Pericardial Effusion9

Gastrointestinal

Diarrhoea8

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 Loncastuximab tesirine 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

Capivasertib

Truqap · AKT inhibitor

Profile

2023 breast-cancer AKT inhibitor; AKI with diarrhea/hyperglycemia.

PRELYTE

Moderate#1 · 89% phenotype match

Afamitresgene autoleucel (Afami-cel)

Tecelra · MAGE-A4 TCR-T cell therapy

Profile

First TCR-T cell therapy for a solid tumor; CRS-associated hemodynamic AKI.

PRELYTE

Moderate#2 · 89% phenotype match

Ziftomenib

Komzifti · Menin inhibitor

Profile

2025 NPM1-mutated AML menin inhibitor; differentiation syndrome and tumor lysis.

PRELYTE

Moderate#3 · 89% phenotype match

Catumaxomab

Removab · Trifunctional bispecific (EpCAM×CD3)

Profile

Intraperitoneal; cytokine-release- and ascites/paracentesis-driven prerenal AKI; withdrawn (EU) 2017.

PRELYTE

Moderate#4 · 88% phenotype match

Avapritinib

Ayvakit · KIT / PDGFRA inhibitor

Profile

Edema, intracranial bleeding and cognitive effects.

PRELYTE

Mild#5 · 83% phenotype match

Quizartinib

Vanflyta · FLT3 inhibitor

Profile

2023 AML FLT3 inhibitor; tumor lysis and QT.

PRELYTE

Mild#6 · 83% phenotype match

Compare Loncastuximab tesirine 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.