What kind of kidney injury does Isatuximab 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 Isatuximab reversible?

Reversible. Typical onset: Tumor lysis (if any) early; renal benefit over the treatment course..

How should kidney function be monitored during Isatuximab therapy?

Serum free light chains / paraprotein and renal function (track renal response); TLS labs at initiation in high-burden disease; Infusion-reaction monitoring (first infusion highest risk); Note CD38-antibody interference with the antiglobulin crossmatch — inform the blood bank.

How can kidney injury from Isatuximab be prevented?

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

Who is at higher risk of kidney injury from Isatuximab?

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

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Printable monograph

Anti-CD38 antibody

Isatuximab

Sarclisa · Isa

Anti-CD38 antibody · approved 2020 · 7 citations · FAERS AKI reporting ROR 3.79 (95% CI 3.22–4.45, 151 AKI reports)

Up to date· through 2025

Fairly sourced6/9 · 6 signals

Met: 7 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 6y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2025
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 effective even with reduced GFR; tumor lysis on rapid myeloma response is the renal caveat.

MildAnti-CD38 antibody

Relapsed/refractory multiple myeloma

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Direct nephrotoxicity is uncommon; tumor lysis can occur with high tumor burden. In the ICARIA-MM and IKEMA renal-impairment subgroups, isatuximab regimens remained effective and produced renal responses; real-world data show inferior PFS with eGFR <60 but persistent benefit.Source: Dimopoulos et al., Leukemia 2020 (ICARIA-MM renal subgroup)

Onset & rechallenge

Time to injuryVariable / unpredictable

Any tumor lysis is early, with renal benefit accruing over the treatment course.

Distilled from: “Tumor lysis (if any) early; renal benefit over the treatment course.”

§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 lysis can precipitate tumor-lysis AKI in high-burden disease; otherwise renal effects are hemodynamic/infusion-related. As with daratumumab, controlling myeloma reduces nephrotoxic free light-chain load and cast nephropathy, supporting and often improving renal function in renal-impaired patients.

Clinical presentation

Generally stable renal function with myeloma response (renal response in a meaningful fraction of renally impaired patients); possible tumor-lysis labs in bulky disease; infusion reactions occur but are not nephrotoxic.

Management

Standard TLS management if it occurs; usable in renal impairment without specific renal dose adjustment. Aim for rapid disease control to support renal recovery.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
Maintain effective myeloma therapy to protect/recover renal function
Infusion-reaction premedication

Anticancer mechanism· how it treats cancer

Anti-CD38 IgG1 monoclonal antibody binding a distinct CD38 epitope from daratumumab; it induces plasma-cell death via ADCC, CDC, antibody-dependent phagocytosis and notably strong direct, CD38-enzyme-inhibiting pro-apoptotic effects, used with pomalidomide/dexamethasone (ICARIA) or carfilzomib/dexamethasone (IKEMA) in relapsed/refractory multiple myeloma.

Note · As with daratumumab, the net renal effect in myeloma is often favorable; tumor lysis is the principal direct renal risk. Isatuximab likewise interferes with CD38-based serologic testing — alert the blood bank.

§04

Clinical depth

Renal dose adjustment

No renal dose adjustment; antibody clearance is target-mediated/reticuloendothelial, not renal. Standard weight-based dosing (10 mg/kg) is used across renal-function strata; ICARIA-MM and IKEMA included patients with renal impairment.

Dialyzability & ESKD dosing

Not dialyzed — a large IgG1 antibody not removed by HD/PD; standard dosing in ESKD. Dialysis treats TLS complications, not drug levels.

Differential diagnosis

Distinguish a creatinine change from underlying myeloma kidney disease (cast nephropathy, light-chain effects, hypercalcemia) and from tumor lysis rather than a direct drug effect. Improving renal function usually reflects disease response.

Monitoring

Serum free light chains / paraprotein and renal function (track renal response)
TLS labs at initiation in high-burden disease
Infusion-reaction monitoring (first infusion highest risk)
Note CD38-antibody interference with the antiglobulin crossmatch — inform the blood bank

Key trials & series

Dimopoulos et al., Leukemia 2020 — ICARIA-MM renal-impairment subgroup (renal response, retained efficacy)
Capra et al., Haematologica 2022 — IKEMA renal-impairment subgroup analysis
Attal et al., Lancet 2019 — ICARIA-MM registrational parent trial

Clinical pearls

Isatuximab retains efficacy and yields renal responses in renal-impaired myeloma (ICARIA/IKEMA subgroups) — no CrCl dose adjustment.
Tumor lysis in high-burden disease is the main direct renal risk — prophylax at initiation.
Like daratumumab, isatuximab confounds the antibody crossmatch via red-cell CD38 — notify transfusion services.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Injury signatures

Prerenal / Hemodynamic AKI Electrolyte Disturbance

§05

References

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

Evidence accrual

7 references · 2019–2025 · 2 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.

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 5,605 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· 3 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 2.5 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Thrombotic Microangiopathy

ROR 22.7295% CI 18.48–27.93· 92 reports

Electrolyte Disturbance

ROR 2.5095% CI 2.10–2.98· 126 reports

Hypertension

ROR 1.6295% CI 1.39–1.89· 165 reports

FAERS outcomes & reporting trend· 13.2% of reports w/ death · 51.3% w/ hospitalization

13.2%

Reported with a death outcome

742 of 5,605 reports

51.3%

Reported with hospitalization

2,875 of 5,605 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 5,605 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 3.7995% CI 3.22–4.45· 151 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Renal & urinary

Acute Kidney Injury151

Blood & lymphatic

Neutropenia524Thrombocytopenia323Anaemia280Febrile Neutropenia150Platelet Count Decreased126

Immune / infection

Pneumonia382Covid-19299Infusion Related Reaction256Infection142Sepsis119

General / constitutional

Pyrexia283Fatigue144Asthenia102

Gastrointestinal

Diarrhoea244Nausea171Vomiting104

Respiratory

Dyspnoea204Cough121Pulmonary Embolism114

Vascular

Hypertension115

Cardiac

Cardiac Failure90

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 Isatuximab 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

Daratumumab

Darzalex · Anti-CD38 antibody

Profile

Tumor lysis; usable in renal impairment.

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 Isatuximab 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 Isatuximab’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 Isatuximab; 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 10 clinical records among all 12 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.