What kind of kidney injury does Rituximab 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 Rituximab reversible?

Partially reversible. Typical onset: Acute — typically within hours to a few days of the first infusion..

How should kidney function be monitored during Rituximab therapy?

TLS panel (uric acid, potassium, phosphate, calcium, creatinine) before and during the first cycle in at-risk patients; Volume status and urine output; Infusion-reaction monitoring (premedicate; not nephrotoxic but can cause hemodynamic instability).

How can kidney injury from Rituximab be prevented?

Risk-stratified TLS prophylaxis (hydration, allopurinol or rasburicase) Fractionated/step-up first-dose administration in high-burden disease Rasburicase for high-risk patients (rapidly lowers uric acid and improves GFR)

Who is at higher risk of kidney injury from Rituximab?

Bulky disease / high tumor burden (e.g., Burkitt, high-grade B-NHL); Elevated baseline LDH (≥2× ULN); Pre-existing CKD; Volume depletion; High circulating tumor cell count.

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Printable monograph

Anti-CD20 antibody

Rituximab

Rituxan · Ritux

Anti-CD20 antibody · approved 1997 · 8 citations · FAERS AKI reporting ROR 1.77 (95% CI 1.70–1.83, 2,786 AKI reports)

Recent· through 2024

Deeply sourced8/9 · 7 signals

Met: 8 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 16y)
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.

The anti-CD20 workhorse — its rapid kill of bulky B-cell disease can ignite tumor lysis and crystal nephropathy.

ModerateAnti-CD20 antibody

B-cell non-Hodgkin lymphomaCLL/SLLAutoimmune/glomerular disease (e.g., membranous nephropathy, ANCA vasculitis)

§01

Signature kidney injury

Signature lesion

Crystal / Obstructive Nephropathy

Clinical tumor lysis with the first cycle is uncommon with modern prophylaxis (~1% clinical TLS in a real-world fractionated-rituximab aggressive-B-NHL series), but risk rises sharply with bulky disease, high LDH and Burkitt histology.Source: Mohamad et al., Cancer Rep 2024 (~1% clinical TLS)

Onset & rechallenge

Time to injuryAcute (~1–7 days)

Acute AKI within hours to a few days of the first infusion.

Distilled from: “Acute — typically within hours to a few days of the first infusion.”

§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 · Signature1%PMID 39410860 (opens PubMed in a new tab)
Clinical TLS in ~1% and laboratory TLS in ~6% of aggressive B-NHL patients in real-world practice with prophylaxis; TLS risk concentrated in Burkitt / high-LDH disease, not intrinsic anti-CD20 nephrotoxicity.
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

Mechanism of kidney injury

Rapid, complement- and ADCC-mediated lysis of bulky/high-burden B-cell malignancy releases potassium, phosphate and nucleic acids; uric acid (from nucleic-acid catabolism) and calcium-phosphate crystallize within distal tubules causing intratubular obstruction (crystal nephropathy), with urate-mediated afferent vasoconstriction and ischemic ATN — tumor-lysis AKI. In-vitro work shows CD20 antibodies can kill target cells within 12–24 h, accounting for the early TLS window.

Clinical presentation

Hyperuricemia, hyperkalemia, hyperphosphatemia, hypocalcemia and rising creatinine, usually within the first cycle of treatment of bulky disease. Infusion-related reactions (cytokine release) are common but not directly nephrotoxic.

Management

IV hydration, rasburicase for hyperuricemia, correct hyperkalemia/hyperphosphatemia/hypocalcemia; renal replacement therapy for severe/refractory cases (lower threshold given ongoing lysis).Lesion-level management framework

Risk factors

Bulky disease / high tumor burden (e.g., Burkitt, high-grade B-NHL)
Elevated baseline LDH (≥2× ULN)
Pre-existing CKD
Volume depletion
High circulating tumor cell count

Prevention

Risk-stratified TLS prophylaxis (hydration, allopurinol or rasburicase)
Fractionated/step-up first-dose administration in high-burden disease
Rasburicase for high-risk patients (rapidly lowers uric acid and improves GFR)

Anticancer mechanism· how it treats cancer

Chimeric anti-CD20 IgG1 monoclonal antibody depleting B cells through complement-dependent cytotoxicity (CDC), antibody-dependent cellular cytotoxicity (ADCC)/phagocytosis, and direct signaling-induced cell death; backbone of B-cell non-Hodgkin lymphoma and CLL regimens and a therapeutic in several glomerular/autoimmune diseases.

Note · Rituximab itself is not directly tubulotoxic; the renal risk is tumor-lysis-mediated. Paradoxically, rituximab is also used therapeutically to TREAT glomerular diseases (e.g., membranous nephropathy, ANCA vasculitis) — a notable double identity in onconephrology.

§04

Clinical depth

Renal dose adjustment

No renal dose adjustment; as a monoclonal antibody it is cleared by reticuloendothelial/target-mediated mechanisms, not the kidney, and is dosed by BSA/flat dose regardless of CrCl. Renal function changes are driven by the tumor-lysis risk it provokes, not by drug accumulation.

Dialyzability & ESKD dosing

Not dialyzed — a ~145 kDa IgG1 antibody is not removed by hemodialysis or peritoneal dialysis. No supplemental dosing around dialysis; usable in ESKD at standard doses. Dialysis is used to treat TLS metabolic complications.

Differential diagnosis

Tumor-lysis crystal nephropathy (urate/phosphate profile, early post-infusion) vs lymphomatous renal infiltration vs obstruction from bulky retroperitoneal nodes vs prerenal azotemia. When rituximab is given FOR glomerular disease, a creatinine change reflects the underlying nephropathy, not drug toxicity.

Monitoring

TLS panel (uric acid, potassium, phosphate, calcium, creatinine) before and during the first cycle in at-risk patients
Volume status and urine output
Infusion-reaction monitoring (premedicate; not nephrotoxic but can cause hemodynamic instability)

Key trials & series

Coiffier et al., JCO 2008 — foundational pediatric/adult TLS management guideline anchoring B-NHL risk stratification
Galardy et al., Br J Haematol 2013 — Children's Oncology Group: rasburicase prevents renal failure and improves GFR in advanced B-NHL TLS
Mohamad et al., Cancer Rep 2024 — real-world fractionated rituximab with ~1% clinical TLS

Clinical pearls

Rituximab's nephrotoxicity is tumor-lysis-mediated — highest with bulky, high-LDH, Burkitt-type disease; prophylax accordingly.
Fractionated first dosing and rasburicase blunt the TLS/AKI risk; clinical TLS is now ~1% in real-world aggressive B-NHL.
Remember its dual role: rituximab also TREATS membranous nephropathy and ANCA vasculitis.

§05

References

6 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

6 references · 2008–2024 · 3 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.

Case reports — ranked by strength· 2

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 · LimitedRefractory hyperkalaemic cardiac arrest - What to do first: Treat the reversible cause or initiate E-CPR?.Klingkowski U et al. · Resuscitation 2019 · PMID 31330202Pediatric Burkitt lymphoma case in which rituximab precipitated tumor lysis syndrome with severe hyperkalaemia and need for renal dialysis, reflecting crystal-obstructive nephropathy from massive cell lysis.CaseC · LimitedSuccessful Intensive Care Treatment of Severe Lactic Acidosis and Tumor Lysis Syndrome Related to Intravascular Lymphoma.Mase H et al. · J Nippon Med Sch 2020 · PMID 31308316Intravascular large B-cell lymphoma patient developed tumor lysis syndrome after rituximab-containing chemotherapy, with acute renal failure requiring renal replacement therapy (urate/phosphate crystal-obstructive nephropathy mechanism).

FDA label — boxed warning & renal dosing· boxed warning

Quoted verbatim from this agent's current FDA label (Aug 2026) — not paraphrased or interpreted. Full label on DailyMed .

Boxed warning

WARNING: FATAL INFUSION-RELATED REACTIONS, SEVERE MUCOCUTANEOUS REACTIONS, HEPATITIS B VIRUS REACTIVATION and PROGRESSIVE MULTIFOCAL LEUKOENCEPHALOPATHY Infusion-Related Reactions Administration of rituximab products can result in serious, including fatal, infusion-related reactions. Deaths within 24 hours of rituximab infusion have occurred. Approximately 80% of fatal infusion-related reactions occurred in association with the first infusion. Monitor patients closely. Discontinue RUXIENCE infusion for severe reactions and provide medical treatment for Grade 3 or 4 infusion-related reactions [see Warnings and Precautions (5.1) , Adverse Reactions (6.1) ] . Severe Mucocutaneous Reactions Severe, including fatal, mucocutaneous reactions can occur in patients receiving rituximab products [see Warnings and Precautions (5.2) ] . Hepatitis B Virus (HBV) Reactivation HBV reactivation can occur in patients treated with rituximab products, in some cases resulting in fulminant hepatitis, hepatic failure, and death. Screen all patients for HBV infection before treatment initiation, and monitor patients during and after treatment with RUXIENCE. Discontinue RUXIENCE and concomitant medications in the event of HBV reactivation [see Warnings and Precautions (5.3) ] . Progressive Multifocal Leukoencephalopathy (PML) Progressive Multifocal Leukoencephalopathy (PML), including fatal PML, can…

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 220,215 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· 8 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

Crystal / Obstructive Nephropathycorroborated · ROR 1.8
Electrolyte Disturbancecorroborated · ROR 1.73 — on the terms that name the lesion (ROR 1.24)
Acute Tubular Necrosiscorroborated · ROR 1.45
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 4.6195% CI 4.28–4.97· 720 reports

Glomerular Injury / Proteinuria

ROR 4.2695% CI 4.03–4.51· 1,254 reports

Hypertension

ROR 3.4995% CI 3.43–3.55· 13,198 reports

Hemorrhagic Cystitis

ROR 2.3595% CI 2.24–2.47· 1,681 reports

Crystal / Obstructive Nephropathy

ROR 1.8095% CI 1.69–1.92· 1,043 reports

Electrolyte Disturbance

ROR 1.7395% CI 1.67–1.79· 3,420 reports

Acute Tubular Necrosis

ROR 1.4595% CI 1.23–1.71· 149 reports

SIADH / Hyponatremia

ROR 1.0995% CI 1.02–1.16· 918 reports

FAERS outcomes & reporting trend· 17.2% of reports w/ death · 31.9% w/ hospitalization

17.2%

Reported with a death outcome

37,930 of 220,215 reports

31.9%

Reported with hospitalization

70,159 of 220,215 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 7 systems · 220,215 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 1.7795% CI 1.70–1.83· 2,786 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

Pneumonia13,272Infusion Related Reaction13,016Infection11,196Drug Hypersensitivity9,907Hypersensitivity9,389

General / constitutional

Pain18,157Fatigue17,788Pyrexia12,070

Musculoskeletal

Rheumatoid Arthritis20,317Arthralgia13,626Joint Swelling11,993

Skin

Rash13,783Alopecia10,915Systemic Lupus Erythematosus9,802

Gastrointestinal

Nausea12,156Abdominal Discomfort10,472Diarrhoea9,937

Respiratory

Dyspnoea10,855

Nervous system

Headache10,407

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 Rituximab 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

Obinutuzumab

Gazyva · Anti-CD20 antibody

Profile

High tumor-lysis risk in CLL.

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 Rituximab 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 Rituximab’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 Rituximab; 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 243 clinical records among the 300 most-relevant of 2,770 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.