What kind of kidney injury does Obinutuzumab cause?

Crystal / Obstructive Nephropathy — Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals. Other reported patterns: Acute Tubular Necrosis, Prerenal / Hemodynamic AKI, Electrolyte Disturbance.

Is kidney injury from Obinutuzumab reversible?

Partially reversible. Typical onset: Acute — within hours to days of the first (split) dose..

How should kidney function be monitored during Obinutuzumab therapy?

TLS panel before and after the first (split) infusion and through the first cycle; Volume status and urine output during the first infusions; Infusion-reaction monitoring (highest risk at first infusion).

How can kidney injury from Obinutuzumab be prevented?

Split first-dose administration (day 1: 100 mg, day 2: 900 mg) Aggressive TLS prophylaxis (hydration plus rasburicase or allopurinol) Pre-medication for infusion reactions

Who is at higher risk of kidney injury from Obinutuzumab?

High circulating lymphocyte count / bulky CLL; Elevated LDH; Pre-existing CKD (CLL11 enrolled CrCl 30–69); Volume depletion.

Back to explorer

Printable monograph

Anti-CD20 antibody

Obinutuzumab

Gazyva · Obinu

Anti-CD20 antibody · approved 2013 · 8 citations · FAERS AKI reporting ROR 1.50 (95% CI 1.30–1.74, 178 AKI reports)

Up to date· through 2025

Deeply sourced8/9 · 7 signals

Met: 8 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 17y)
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.

A glycoengineered type II anti-CD20 antibody with the highest tumor-lysis risk among CD20 agents in CLL.

ModerateAnti-CD20 antibody (type II)

CLL/SLLFollicular lymphoma

§01

Signature kidney injury

Signature lesion

Crystal / Obstructive Nephropathy

Carries a high tumor-lysis risk in CLL — among the highest of the anti-CD20 agents — particularly with the first (split) infusion in high-burden disease (the CLL11 trial enrolled patients with CrCl 30–69 mL/min and saw higher infusion reactions/TLS). Direct nephrotoxicity is case-level.Source: Goede et al., NEJM 2014 (CLL11)

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Within hours to days of the first (split) dose.

Distilled from: “Acute — within hours to days of the first (split) dose.”

§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.

Crystal / Obstructive Nephropathy#1 · Signature10%PMID 26758269 (opens PubMed in a new tab)
TLS reported in ~10% of obinutuzumab-treated non-Hodgkin lymphoma patients in a systematic review of novel-/targeted-agent trials — higher than most anti-CD20 antibodies, reflecting rapid cytoreduction.
Acute Tubular NecrosisSecondaryqualitative — no citable incidence
Direct death of tubular epithelial cells — the dose-limiting lesion of the platinums and zoledronate.
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).
Prerenal / Hemodynamic AKIRarequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityModerate

ReversibilityPartially reversible

Evidence8 citations

Nephron map

Vasculature / Endothelium

Proximal Tubule

Distal Tubule / Collecting Duct

Tubular LumenThe urine flow path

Crystal / Obstructive Nephropathy

Intratubular precipitation of drug or metabolite — high-dose methotrexate and tumor lysis crystals.

§03

Kidney injury

Deep diveTumor lysis syndromeEffective therapy can kill a large, fast-dividing cancer so abruptly that the cells spill their contents into the blood — potassium, phosphate, and a flood of purines that becomes uric acid — and the two crystals that result, urate and calcium-phosphate, clog and poison the tubules: a metabolic emergency that is largely preventable with hydration, rasburicase, and, for venetoclax, a deliberately slow dose ramp-up.

Mechanism of kidney injury

More potent, rapid B-cell killing (enhanced direct death plus ADCC) releases uric acid and phosphate faster than rituximab; intratubular uric acid and calcium-phosphate crystals cause obstruction (crystal nephropathy) with urate-driven vasoconstriction and ischemic ATN — tumor-lysis AKI. In-vitro, CD20 antibodies kill within 12–24 h, explaining first-infusion TLS.

Clinical presentation

Tumor-lysis labs (hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia) and rising creatinine, especially around the first infusion; pronounced infusion-related reactions (concentrated at the first infusion); occasional thrombocytopenia.

Management

IV hydration, rasburicase, electrolyte correction; hold therapy and provide renal replacement therapy if severe (lower threshold given ongoing lysis).Lesion-level management framework

Risk factors

High circulating lymphocyte count / bulky CLL
Elevated LDH
Pre-existing CKD (CLL11 enrolled CrCl 30–69)
Volume depletion

Prevention

Split first-dose administration (day 1: 100 mg, day 2: 900 mg)
Aggressive TLS prophylaxis (hydration plus rasburicase or allopurinol)
Pre-medication for infusion reactions

Anticancer mechanism· how it treats cancer

Glycoengineered (afucosylated) type II humanized anti-CD20 IgG1 monoclonal antibody. Type II binding produces greater direct (non-apoptotic) cell death and, through afucosylation, markedly enhanced antibody-dependent cellular cytotoxicity (ADCC) versus rituximab, used in CLL and follicular lymphoma.

Note · TLS prophylaxis is mandatory in high-risk CLL; renal injury is tumor-lysis-mediated rather than a direct antibody effect. Its greater potency over rituximab also means a higher TLS/infusion-reaction burden.

§04

Clinical depth

Renal dose adjustment

No renal dose adjustment; antibody clearance is target-mediated/reticuloendothelial, not renal. CLL11 specifically included patients with CrCl 30–69 mL/min, supporting use in moderate renal impairment with appropriate TLS precautions.

Dialyzability & ESKD dosing

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

Differential diagnosis

Tumor-lysis crystal nephropathy (early, first-infusion, urate/phosphate profile) vs infusion-reaction hypotension causing prerenal AKI vs CLL-intrinsic kidney disease. The split-dose first-infusion timing of TLS is characteristic.

Monitoring

TLS panel before and after the first (split) infusion and through the first cycle
Volume status and urine output during the first infusions
Infusion-reaction monitoring (highest risk at first infusion)

Key trials & series

Goede et al., NEJM 2014 — CLL11 registrational trial (obinutuzumab-chlorambucil superior to rituximab-chlorambucil; enrolled renally impaired patients; higher infusion/TLS risk)

Clinical pearls

Obinutuzumab has the highest TLS risk of the anti-CD20 agents — the split first dose and rasburicase prophylaxis are essential.
CLL11 deliberately enrolled patients with CrCl 30–69, so it is usable in moderate CKD with full TLS precautions.
Greater potency than rituximab means more infusion reactions and faster tumor lysis — front-load monitoring at the first infusion.

§05

References

7 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

7 references · 2008–2025 · 4 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 · Limited[66/m-with chronic lymphocytic leukemia and acute renal failure under treatment with obinutuzumab and venetoclax : Preparation for the medical specialist examination: part 54].Kutsch N et al. · Internist (Berl) 2021 · PMID 34160636Case of a 66-year-old man with chronic lymphocytic leukemia who developed acute kidney injury during obinutuzumab plus venetoclax therapy, consistent with tumor lysis/crystal-related nephropathy (MeSH-indexed Acute Kidney Injury).

FDA label — boxed warning & renal dosing· boxed warning

Quoted verbatim from this agent's current FDA label (Dec 2025) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING: HEPATITIS B VIRUS REACTIVATION and PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY Hepatitis B Virus (HBV) reactivation, in some cases resulting in fulminant hepatitis, hepatic failure, and death, can occur in patients receiving CD20-directed cytolytic antibodies, including GAZYVA. Screen all patients for HBV infection before treatment initiation. Monitor HBV-positive patients during and after treatment with GAZYVA. Discontinue GAZYVA and concomitant medications in the event of HBV reactivation [see Warnings and Precautions (5.1) ] . Progressive Multifocal Leukoencephalopathy (PML) including fatal PML, can occur in patients receiving GAZYVA [see Warnings and Precautions (5.2) ] . WARNING: HEPATITIS B VIRUS REACTIVATION and PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY See full prescribing information for complete boxed warning. Hepatitis B Virus (HBV) reactivation, in some cases resulting in fulminant hepatitis, hepatic failure, and death. ( 5.1 ) Progressive Multifocal Leukoencephalopathy (PML) resulting in death. ( 5.2 )

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 16,355 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· 2 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 1.73 — on the terms that name the lesion (ROR 2.78)
Crystal / Obstructive NephropathyNo 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 Tubular NecrosisNot measurable in reporting — Reporters cannot reliably name this lesion, so its absence from FAERS is expected and is not evidence against the documented injury.
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Electrolyte Disturbance

ROR 1.7395% CI 1.53–1.96· 256 reports

Hemorrhagic Cystitis

ROR 1.3795% CI 1.09–1.72· 74 reports

FAERS outcomes & reporting trend· 13.2% of reports w/ death · 37.4% w/ hospitalization

13.2%

Reported with a death outcome

2,164 of 16,355 reports

37.4%

Reported with hospitalization

6,111 of 16,355 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 7 systems · 16,355 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 1.5095% CI 1.30–1.74· 178 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Blood & lymphatic

Neutropenia1,355Febrile Neutropenia1,042Thrombocytopenia927Anaemia722Myelosuppression520

Immune / infection

Covid-191,091Infusion Related Reaction854Pneumonia790Infection608Cytokine Release Syndrome506

General / constitutional

Pyrexia994Chills499Fatigue422

Gastrointestinal

Nausea526Diarrhoea500

Vascular

Haemorrhage385Hypotension362

Cardiac

Atrial Fibrillation598

Respiratory

Dyspnoea513

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 Obinutuzumab 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

Rituximab

Rituxan · Anti-CD20 antibody

Profile

Tumor lysis with bulky disease; treats some GN.

XTALATNPRE

Moderate#1 · 100% phenotype match

Odronextamab

Ordspono · Bispecific (CD20×CD3)

Profile

CD20×CD3 bispecific; tumor-lysis urate crystal nephropathy with CRS.

XTALPRELYTE

Moderate#2 · 86% phenotype match

Pivekimab sunirine

Decnupaz · CD123 antibody-drug conjugate

Profile

2026 CD123 ADC for BPDCN; renal risk indirect — TLS in the CD123+ disease plus the CD123-class capillary-leak concern; its own dose-limiting toxicity was reversible VOD.

PREXTALLYTE

Moderate#3 · 86% phenotype match

Venetoclax

Venclexta · BCL-2 inhibitor

Profile

Major tumor lysis syndrome risk on ramp-up.

XTALATNPRE

Severe#4 · 84% phenotype match

Lisocabtagene maraleucel

Breyanzi · CD19 CAR-T cell therapy

Profile

CRS-driven prerenal AKI and tumor-lysis crystal nephropathy in the first weeks; low severe-CRS rate softens the renal burden.

PREATNXTAL

Moderate#5 · 80% phenotype match

Idecabtagene vicleucel

Abecma · BCMA CAR-T cell therapy

Profile

CRS-driven AKI and tumor lysis in myeloma.

PREATNLYTE

Moderate#6 · 78% phenotype match

Compare Obinutuzumab 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 Obinutuzumab’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 Obinutuzumab; 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 85 clinical records among all 131 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.