What kind of kidney injury does Duvelisib cause?

Prerenal / Hemodynamic AKI — Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome. Other reported patterns: Acute Interstitial Nephritis.

How should kidney function be monitored during Duvelisib therapy?

Stool frequency and volume status; weight at each visit; LFTs every 2 weeks initially, then periodically; Serum creatinine/electrolytes during diarrheal episodes; CMV viral load and clinical infection surveillance.

How can kidney injury from Duvelisib be prevented?

Early reporting and prompt management of diarrhea; exclude infection (including CMV) Vigorous rehydration during diarrheal episodes Infection prophylaxis (PJP) per label Interrupt for grade 3+ diarrhea/colitis

Who is at higher risk of kidney injury from Duvelisib?

Pre-existing CKD, diuretic therapy or baseline volume depletion; Concurrent nephrotoxins; Older age and frailty; Delayed recognition of severe diarrhea.

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Printable monograph

PI3Kδ/γ inhibitor

Duvelisib

Copiktra · DUV

PI3Kδ/γ inhibitor · approved 2018 · 7 citations

Up to date· through 2025

Fairly sourced5/9 · 5 signals

Met: 7 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 7y)
Met: Beyond single case reports
Met: High-impact journal
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.

Dual PI3K-delta/gamma inhibitor with the same immune-colitis Achilles heel — diarrhea and volume loss are the path to prerenal AKI.

MildDual-isoform PI3K inhibitor

Relapsed/refractory chronic lymphocytic leukemia or small lymphocytic lymphoma (>=2 prior therapies)Relapsed/refractory follicular lymphoma (historically; indication later narrowed)

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

Diarrhea/colitis is common (any-grade ~50%, grade 3+ roughly 15-20% in DUO); the resulting volume-depletion prerenal AKI is not separately tabulated. Direct nephrotoxicity is uncommon.Source: Flinn et al., Blood 2018 (DUO); Flinn et al., J Clin Oncol 2019 (DYNAMO)

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Diarrhea/colitis often appears after several months, whereas rash and transaminitis can appear earlier.

Distilled from: “Diarrhea/colitis often after several months; rash and transaminitis can appear earlier.”

§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.
Acute Interstitial NephritisSecondaryqualitative — no citable incidence
Immune-mediated inflammation of the renal interstitium — the signature kidney injury of checkpoint inhibitors.

§03

Kidney injury

Mechanism of kidney injury

As with idelalisib, PI3K-delta/gamma inhibition impairs regulatory T-cell tolerance and produces immune-mediated colitis, hepatitis and pneumonitis. The PI3K-gamma component adds effects on myeloid/innate immunity. Renal injury is secondary — secretory diarrhea and reduced intake cause volume contraction and prerenal azotemia, with ischemic ATN possible if hypoperfusion is severe and prolonged; immune-mediated interstitial nephritis is plausible but not a defining feature.

Clinical presentation

Profuse, sometimes late-onset diarrhea or frank colitis, dehydration and orthostasis; creatinine rises with a prerenal urine profile (low FeNa, high urine osmolality). Transaminitis, rash and pneumonitis may coexist as part of the immune toxicity.

Management

Interrupt duvelisib for severe diarrhea/colitis, exclude infectious causes, rehydrate, and treat immune colitis with corticosteroids (budesonide or systemic steroids). Restore euvolemia to reverse prerenal AKI; consider AIN with steroid trial if creatinine fails to recover despite volume repletion. Permanently discontinue for life-threatening events.Lesion-level management framework

Risk factors

Pre-existing CKD, diuretic therapy or baseline volume depletion
Concurrent nephrotoxins
Older age and frailty
Delayed recognition of severe diarrhea

Prevention

Early reporting and prompt management of diarrhea; exclude infection (including CMV)
Vigorous rehydration during diarrheal episodes
Infection prophylaxis (PJP) per label
Interrupt for grade 3+ diarrhea/colitis

Anticancer mechanism· how it treats cancer

Oral dual inhibitor of the delta and gamma isoforms of PI3K. PI3K-delta drives malignant B-cell proliferation while PI3K-gamma modulates the supportive tumor microenvironment; combined inhibition is active in CLL/SLL and follicular lymphoma.

Note · Renal involvement is indirect, mediated by immune colitis/diarrhea and volume depletion. Quantified AKI rates are lacking; the signal is inferred from the dominant GI toxicity.

§04

Clinical depth

Renal dose adjustment

No renal dose adjustment specified (hepatic CYP3A4 metabolism); use caution in CKD. Dose modifications are driven by colitis, hepatotoxicity, infection and cytopenias.

Dialyzability & ESKD dosing

Highly protein-bound; not expected to be dialyzable. No ESKD dosing established.

Differential diagnosis

Separate prerenal AKI (volume-responsive, low FeNa) from infectious colitis (C. difficile, CMV) driving the losses and from immune AIN; concurrent hepatotoxicity can confound with hepatorenal physiology.

Monitoring

Stool frequency and volume status; weight at each visit
LFTs every 2 weeks initially, then periodically
Serum creatinine/electrolytes during diarrheal episodes
CMV viral load and clinical infection surveillance

Key trials & series

DUO (Flinn, Blood 2018) — registrational RCT vs ofatumumab defining the colitis/diarrhea signal
DYNAMO (Flinn, J Clin Oncol 2019) — indolent NHL safety dataset

Clinical pearls

Mechanistically and clinically a sibling of idelalisib — anticipate immune colitis and dehydration.
Late-onset severe diarrhea is the classic and most dangerous toxicity; rehydrate early.
Exclude CMV before attributing colitis to the drug and starting steroids.
PJP prophylaxis and CMV vigilance are part of standard care.

Where it strikes· nephron segments & injury signatures

Nephron segments

Vasculature / Endothelium

Glomerular & peritubular capillaries

Interstitium

Supporting tissue around the tubules

Injury signatures

Prerenal / Hemodynamic AKI Acute Interstitial Nephritis

§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 · 2018–2022 · 2 since 2020

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.

CaseB · ModerateCutaneous and Systemic Complications in Primary CD8+ Aggressive Epidermotropic Cytotoxic T-cell Lymphoma.Nikakis J et al. · Cureus 2025 · PMID 41607964Patient on duvelisib developed nephrotic-range proteinuria and acute kidney injury requiring dialysis, with renal-limited thrombotic microangiopathy on biopsy attributed in part to duvelisib exposure.

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: TREATMENT-RELATED MORTALITY AND SERIOUS TOXICITIES: INFECTIONS, DIARRHEA OR COLITIS, CUTANEOUS REACTIONS, AND PNEUMONITIS Treatment-related mortality occurred in 15% of COPIKTRA-treated patients [see Warnings and Precautions ( 5.1 )] . Fatal and/or serious infections occurred in 31% of COPIKTRA-treated patients. Monitor for signs and symptoms of infection. Withhold COPIKTRA if infection is suspected [see Warnings and Precautions ( 5.2 )]. Fatal and/or serious diarrhea or colitis occurred in 18% of COPIKTRA-treated patients. Monitor for the development of severe diarrhea or colitis. Withhold COPIKTRA [see Warnings and Precautions ( 5.3 )] . Fatal and/or serious cutaneous reactions occurred in 5% of COPIKTRA-treated patients. Withhold COPIKTRA [see Warnings and Precautions ( 5.4 )] . Fatal and/or serious pneumonitis occurred in 5% of COPIKTRA-treated patients. Monitor for pulmonary symptoms and interstitial infiltrates. Withhold COPIKTRA [see Warnings and Precautions ( 5.5 )]. WARNING: TREATMENT-RELATED MORTALITY AND SERIOUS TOXICITIES: INFECTIONS, DIARRHEA OR COLITIS, CUTANEOUS REACTIONS, and PNEUMONITIS See full prescribing information for complete boxed warning Treatment-related mortality occurred in 15% of COPIKTRA-treated patients. ( 5.1 ) Fatal and/or serious infections occurred in 31% of COPIKTRA-treated patients. Monitor for signs and symptoms of infection.…

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 765 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· 22.6% of reports w/ death · 32.9% w/ hospitalization

22.6%

Reported with a death outcome

173 of 765 reports

32.9%

Reported with hospitalization

252 of 765 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 765 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 1.6395% CI 0.84–3.14· 9 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Gastrointestinal

Diarrhoea107Nausea49Vomiting28Constipation24Colitis20

General / constitutional

Fatigue78Pyrexia38Asthenia32Malaise19

Respiratory

Cough26Dyspnoea20

Immune / infection

Pneumonia41

Blood & lymphatic

Febrile Neutropenia18Neutropenia17

Skin

Rash34

Nervous system

Headache26

Metabolic & electrolyte

Decreased Appetite23

Musculoskeletal

Arthralgia21

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 Duvelisib 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

Idelalisib

Zydelig · PI3Kδ inhibitor

Profile

Immune-mediated colitis → volume-depletion prerenal AKI; transaminitis.

PREAIN

Mild#1 · 100% phenotype match

Pexidartinib

Turalio · CSF1R inhibitor

Profile

Boxed hepatotoxicity; secondary renal effects.

PRE

Mild#2 · 53% phenotype match

Sacituzumab govitecan

Trodelvy · Antibody-drug conjugate (Trop-2/SN-38)

Profile

Diarrhea-driven prerenal AKI; emerging direct signals.

PREAINATN

Moderate#3 · 53% phenotype match

Elotuzumab

Empliciti · Anti-SLAMF7 mAb

Profile

Kidney-neutral antibody; unchanged PK in severe impairment and dialysis; no renal dose adjustment.

PRE

Mild#4 · 53% phenotype match

Tisotumab vedotin

Tivdak · Antibody-drug conjugate (tissue factor/MMAE)

Profile

Ocular/bleeding toxicity dominates; renal involvement essentially unreported.

PRE

Mild#5 · 53% phenotype match

Elacestrant

Orserdu · Oral selective estrogen-receptor degrader (SERD)

Profile

2023 oral SERD; nausea-dominant, minimal intrinsic nephrotoxicity.

PRE

Mild#6 · 53% phenotype match

Compare Duvelisib 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 PI3K / AKT inhibitors

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.

1Duvelisib· this agentPRE — Prerenal / Hemodynamic AKIMild
2GedatolisibLYTE — Electrolyte DisturbanceMild
3IdelalisibPRE — Prerenal / Hemodynamic AKIMild
4CopanlisibHTN — HypertensionModerate
5CapivasertibPRE — Prerenal / Hemodynamic AKIModerate
6AlpelisibPRE — Prerenal / Hemodynamic AKIModerate
7InavolisibLYTE — Electrolyte DisturbanceFAERS AKIModerate

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.