What kind of kidney injury does Daratumumab 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 Daratumumab therapy?

Serum free light chains / paraprotein and renal function (track renal response); TLS labs in high-burden disease at initiation; Infusion-reaction monitoring (first infusion highest risk); Note daratumumab interference with indirect antiglobulin (Coombs) crossmatch — inform the blood bank.

How can kidney injury from Daratumumab be prevented?

TLS risk assessment with hydration and urate-lowering therapy in high-burden disease Continue/optimize myeloma therapy to protect and recover renal function Infusion-reaction premedication

Who is at higher risk of kidney injury from Daratumumab?

High tumor burden; Baseline cast nephropathy / high free light-chain burden; Volume depletion.

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Printable monograph

Anti-CD38 antibody

Daratumumab

Darzalex · Dara

Anti-CD38 antibody · approved 2015 · 9 citations

Up to date· through 2025

Fairly sourced4/9 · 4 signals

Met: 9 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 5y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Met: Current through 2025
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.

An anti-CD38 antibody that improves outcomes even in renal impairment — tumor lysis is its main kidney caveat.

MildAnti-CD38 antibody

Multiple myeloma (newly diagnosed and relapsed/refractory)AL amyloidosis

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Direct nephrotoxicity is uncommon; tumor lysis can occur with high tumor burden. Crucially, daratumumab-based regimens IMPROVE outcomes (PFS, and OS in relapsed disease) in myeloma patients with renal insufficiency, including dialysis-dependent patients, and can drive renal recovery.Source: Jiang et al., Hematology 2024 (meta-analysis: PFS/OS benefit in renal insufficiency)

Onset & rechallenge

Time to injuryVariable / unpredictable

Any tumor lysis is early, while renal benefit accrues gradually across treatment as paraprotein/free light chains fall.

Distilled from: “Tumor lysis (if any) early; renal benefit accrues over treatment as paraprotein/free light chains fall.”

§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

Rapid plasma-cell killing in high-burden disease can release uric acid/phosphate, causing tumor-lysis AKI; otherwise renal effects are hemodynamic (e.g., infusion-reaction-related). By rapidly controlling myeloma and lowering the nephrotoxic free light-chain load, daratumumab reduces cast-nephropathy/light-chain–mediated kidney injury — so its net renal effect in myeloma is frequently favorable.

Clinical presentation

Usually stable or improving renal function as myeloma responds (renal recovery, including dialysis independence in some cases); occasionally tumor-lysis labs with bulky disease. Infusion reactions are common (especially first infusion) but not directly nephrotoxic.

Management

Standard TLS management if it occurs; no renal dose adjustment required — usable across renal-function strata, including dialysis. The therapeutic goal is rapid disease control to recover renal function.Lesion-level management framework

Risk factors

High tumor burden
Baseline cast nephropathy / high free light-chain burden
Volume depletion

Prevention

TLS risk assessment with hydration and urate-lowering therapy in high-burden disease
Continue/optimize myeloma therapy to protect and recover renal function
Infusion-reaction premedication

Anticancer mechanism· how it treats cancer

Anti-CD38 IgG1κ monoclonal antibody killing myeloma plasma cells via complement-dependent cytotoxicity, ADCC, antibody-dependent phagocytosis, direct apoptosis and immunomodulation (depleting CD38+ regulatory cells); a backbone of newly diagnosed and relapsed/refractory multiple myeloma and AL amyloidosis regimens.

Note · Net effect on the kidney is often favorable in myeloma (renal response/recovery); tumor lysis is the principal direct renal risk. Daratumumab also interferes with serologic crossmatch (binds CD38 on red cells), a transfusion-medicine pitfall relevant to renal-impaired/transfused patients.

§04

Clinical depth

Renal dose adjustment

No renal dose adjustment; antibody clearance is target-mediated/reticuloendothelial, not renal. Standard IV or subcutaneous dosing is used regardless of CrCl, including in dialysis-dependent patients per trial and case data.

Dialyzability & ESKD dosing

Not dialyzed — a large IgG1 antibody not removed by HD/PD; full standard dosing in ESKD. Renal recovery off dialysis has been reported with daratumumab-based therapy.

Differential diagnosis

Distinguish a creatinine change from the underlying myeloma kidney disease (cast nephropathy, light-chain effects, hypercalcemia) and tumor lysis from a true drug effect (rare). Improving renal function usually reflects disease response, not toxicity.

Monitoring

Serum free light chains / paraprotein and renal function (track renal response)
TLS labs in high-burden disease at initiation
Infusion-reaction monitoring (first infusion highest risk)
Note daratumumab interference with indirect antiglobulin (Coombs) crossmatch — inform the blood bank

Key trials & series

Jiang et al., Hematology 2024 — meta-analysis (10 RCTs, 5003 patients): PFS/OS benefit in renal-impaired myeloma
Leypoldt et al. (GMMG-DANTE), Cancers 2023 — daratumumab-bortezomib-dexamethasone in severe renal impairment (GFR <30/dialysis); 67% renal response
Palladini et al. (ANDROMEDA), Blood 2020 — daratumumab-CyBorD in AL amyloidosis with organ (incl. renal) response

Clinical pearls

Daratumumab is renal-friendly: it improves outcomes and can recover renal function (even off dialysis) by clearing nephrotoxic light chains — no dose adjustment for CrCl.
Tumor lysis in high-burden disease is the main direct renal caveat — prophylax at initiation.
Daratumumab binds CD38 on red cells and confounds the antibody crossmatch — always alert the blood bank before transfusion.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Injury signatures

Prerenal / Hemodynamic AKI Electrolyte Disturbance

§05

References

8 primary references — trials, cohorts, mechanism, and reviews. Single-patient case reports are listed separately below, graded by strength. Citation metadata via PubMed / NLM.

Evidence accrual

8 references · 2020–2025 · 6 since 2023

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.

Case reports — ranked by strength· 1

Single-patient and small-series reports, graded by evidentiary strength — A Strong (biopsy-proven plus a series and/or positive rechallenge), B Moderate, and C Limited (a single clinically-diagnosed case). Strongest first. Grades are inferred automatically from each report's abstract and journal — a heuristic ranking aid, not a formal quality appraisal.

CaseC · LimitedTumor Lysis Syndrome Associated with Monoclonal Antibodies in Patients with Multiple Myeloma: A Pharmacovigilance Study Based on the FAERS Database.Xia S et al. · Clin Pharmacol Ther 2023 · PMID 37086211FAERS pharmacovigilance analysis showing daratumumab carries the strongest disproportionate tumor lysis syndrome signal among multiple myeloma monoclonal antibodies, with associated hyperkalemia, hypocalcemia and urate elevation driving acute kidney injury.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 2,880 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· 3.9% of reports w/ death · 14.7% w/ hospitalization

3.9%

Reported with a death outcome

111 of 2,880 reports

14.7%

Reported with hospitalization

423 of 2,880 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 2,880 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 0.4395% CI 0.22–0.82· 9 AKI reports ·AKI is reported less often than for other drugs (CI entirely below 1) — no disproportionate signal.

General / constitutional

Fatigue218Pyrexia73Chills67Pain60Asthenia59

Gastrointestinal

Diarrhoea136Nausea113Constipation57Vomiting47

Nervous system

Neuropathy Peripheral99Dizziness74Headache56

Blood & lymphatic

Neutropenia83White Blood Cell Count Decreased66Platelet Count Decreased58

Skin

Rash151Pruritus55

Immune / infection

Pneumonia71Covid-1961Infusion Related Reaction60

Respiratory

Dyspnoea100

Vascular

Hypotension44

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 Daratumumab 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

Isatuximab

Sarclisa · Anti-CD38 antibody

Profile

Tumor lysis in myeloma.

PRELYTE

Mild#1 · 100% phenotype match

Zanidatamab

Ziihera · HER2 bispecific antibody

Profile

2024 biliary-tract HER2 bispecific; renal data emerging.

PRELYTE

Mild#2 · 97% 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#3 · 97% phenotype match

Avapritinib

Ayvakit · KIT / PDGFRA inhibitor

Profile

Edema, intracranial bleeding and cognitive effects.

PRELYTE

Mild#4 · 86% phenotype match

Quizartinib

Vanflyta · FLT3 inhibitor

Profile

2023 AML FLT3 inhibitor; tumor lysis and QT.

PRELYTE

Mild#5 · 86% phenotype match

Mogamulizumab

Poteligeo · Anti-CCR4 antibody

Profile

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

PRELYTE

Mild#6 · 86% phenotype match

Compare Daratumumab 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.

Who studies this

The leading contributors to Daratumumab’s clinical kidney literature on PubMed, ranked by a blend of publication volume and citation impact — filtered toward clinical work via the PubMed Humans heading and clinical publication types (trials, cohorts, case reports, guidelines, reviews). Names link to that author’s work on Daratumumab; the PMIDs beside each name are up to three of their most recent papers on it, not the full count.

Ranked by a 50/50 blend of publication volume and a position-weighted, capped Relative Citation Ratio (NIH iCite) on this agent’s renal literature; the citation count shown is the raw total, not the ranking score — counted over the 113 clinical records among all 138 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.