What kind of kidney injury does Ruxolitinib 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, Thrombotic Microangiopathy.

How should kidney function be monitored during Ruxolitinib therapy?

CBC (platelets, neutrophils, hemoglobin) — dose is platelet-driven; Creatinine/eGFR to guide dosing; electrolytes and uric acid at initiation in high-burden disease; Infection surveillance (including reactivation: HBV, TB, herpes zoster).

How can kidney injury from Ruxolitinib be prevented?

TLS awareness/hydration at initiation in high-burden disease Renal dose adjustment per label Avoid abrupt cessation; taper when stopping

Who is at higher risk of kidney injury from Ruxolitinib?

Bulky/high-burden myelofibrosis (TLS risk at initiation); Pre-existing CKD (requires dose adjustment); Infection and cytopenia-related volume depletion; Abrupt discontinuation (withdrawal syndrome).

Back to explorer

Printable monograph

JAK1/2 inhibitor

Ruxolitinib

Jakafi · RUXO

JAK1/2 inhibitor · approved 2011 · 7 citations

Up to date· through 2026

Deeply sourced7/9 · 6 signals

Met: 7 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 11y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2026
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.

A JAK1/2 inhibitor for myelofibrosis whose kidney risks are tumor-lysis and dose-adjustment, not direct toxicity.

MildJAK1/2 inhibitor

MyelofibrosisPolycythemia veraGraft-versus-host disease

§01

Signature kidney injury

Signature lesion

Prerenal / Hemodynamic AKI

No established intrinsic nephrotoxicity. Over a decade of safety data show cytopenias and infections (including opportunistic) as the dominant toxicities. Renal concerns are indirect: rare tumor-lysis at treatment initiation in bulky myelofibrosis, the need for dose reduction in renal impairment, and a recognized ruxolitinib-withdrawal syndrome on abrupt cessation — rather than direct tubular injury.Source: Verstovsek et al., J Hematol Oncol 2023

Onset & rechallenge

Time to injuryVariable / unpredictable

Tumor-lysis risk is confined to the first cycles and a withdrawal syndrome occurs within days of stopping, but otherwise there is no defined renal onset.

Distilled from: “Any tumor-lysis risk is early (first cycles); withdrawal syndrome occurs within days of stopping; otherwise no defined renal onset.”

§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).
Thrombotic MicroangiopathyRarequalitative — no citable incidence
Independent predictor of transplant-associated TMA in a GVHD cohort; a transplant-context signal.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

Incidence not quantified

SeverityMild

ReversibilityReversible

Evidence7 citations

Nephron map

Glomerulus

Vasculature / Endothelium

Distal Tubule / Collecting Duct

Prerenal / Hemodynamic AKI

Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

§03

Kidney injury

Mechanism of kidney injury

No characterized direct nephron injury. Plausible renal stress is indirect: tumor-lysis-type metabolic derangements early after starting therapy in high-burden disease (urate/phosphate intratubular deposition), infection/cytopenia-related complications causing prerenal/ischemic AKI, and a ruxolitinib-withdrawal syndrome (cytokine rebound with hemodynamic instability, occasionally a capillary-leak-like picture) on abrupt discontinuation.

Clinical presentation

Usually a bland renal picture; if tumor lysis occurs, hyperuricemia/hyperphosphatemia with creatinine rise; prerenal AKI in the setting of infection or volume depletion; abrupt-withdrawal symptom flare with hemodynamic compromise.

Management

Supportive; standard tumor-lysis management if it occurs, treat infections, correct prerenal factors, and adjust dose for renal function. For withdrawal syndrome, resume ruxolitinib and provide hemodynamic support. No drug-specific renal therapy; intrinsic nephrotoxicity has not been established.Lesion-level management framework

Risk factors

Bulky/high-burden myelofibrosis (TLS risk at initiation)
Pre-existing CKD (requires dose adjustment)
Infection and cytopenia-related volume depletion
Abrupt discontinuation (withdrawal syndrome)

Prevention

TLS awareness/hydration at initiation in high-burden disease
Renal dose adjustment per label
Avoid abrupt cessation; taper when stopping

Anticancer mechanism· how it treats cancer

Oral ATP-competitive JAK1/JAK2 inhibitor that dampens dysregulated JAK-STAT signaling (driven by JAK2 V617F and related mutations), reducing splenomegaly, inflammatory cytokines and constitutional symptoms. Approved for intermediate/high-risk myelofibrosis, polycythemia vera, and acute/chronic graft-versus-host disease.

Note · Clinician-flagged as an emerging topic. Well-established agent but with no significant direct renal toxicity; the prerenal/TLS framing is conservative and supported by the long-term safety review.

§04

Clinical depth

Renal dose adjustment

Renal dosing is required: the starting dose is reduced in moderate-to-severe renal impairment and in ESKD. In myelofibrosis/PV with platelets 100-150 x10^9/L and moderate-to-severe impairment (CrCl 15-59), and in dialysis-dependent ESKD, the label specifies reduced starting doses; in ESKD on hemodialysis, give a single reduced dose after dialysis on dialysis days. Avoid initiating if CrCl <15 mL/min and not on dialysis. Always titrate to platelets and response.

Dialyzability & ESKD dosing

Ruxolitinib itself is not removed by hemodialysis - dialysate recovery of the parent drug was negligible - but removal of some ACTIVE METABOLITES cannot be ruled out, which matters because ESKD raises the combined parent-plus-active-metabolite exposure about 1.6-fold. Dose AFTER dialysis on hemodialysis days. Highly protein-bound, hepatically (CYP3A4) metabolized small molecule.

Differential diagnosis

Distinguish early tumor-lysis AKI, infection/cytopenia-related prerenal AKI, and withdrawal-syndrome hemodynamic AKI from any unrelated intrinsic renal disease; the drug is rarely the direct nephrotoxic cause.

Monitoring

CBC (platelets, neutrophils, hemoglobin) — dose is platelet-driven
Creatinine/eGFR to guide dosing; electrolytes and uric acid at initiation in high-burden disease
Infection surveillance (including reactivation: HBV, TB, herpes zoster)

Key trials & series

COMFORT-I/II — registrational myelofibrosis trials (clinical context)
10-year safety review (Verstovsek, J Hematol Oncol 2023) — cytopenia/infection-dominant profile

Clinical pearls

Don't stop ruxolitinib abruptly — withdrawal can precipitate a cytokine-rebound, capillary-leak-like crisis; taper instead.
The renal risks are TLS at start and dosing logistics, not a tubulopathy.
Ruxolitinib was an independent predictor of transplant-associated TMA in a GVHD cohort, not explained by GVHD severity — a transplant-context signal, not a general ruxolitinib-TMA claim.

§05

References

5 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

5 references · 2015–2023 · 4 since 2021

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 · LimitedRuxolitinib-associated Karyomegalic Interstitial Nephritis Without FAN1 Mutation: Expanding the Etiology to JAK Inhibitors.Aldana S et al. · Nephron 2026 · PMID 42139177First reported case of karyomegalic interstitial nephritis with acute kidney injury attributed to prolonged ruxolitinib, with renal function improving after drug withdrawal.CaseC · LimitedSevere Hypocalcemia During JAK1/2 Inhibitor Therapy for Myelofibrosis in a Patient with Liver Cirrhosis.Kurumazaki M et al. · Intern Med 2025 · PMID 39814384Severe hypocalcemia developing during ruxolitinib therapy, attributed in part to impaired vitamin D activation from renal/hepatic insufficiency, illustrating a drug-related electrolyte derangement.

FDA label — boxed warning & renal dosing· renal impairment

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

Renal impairment — from the label

Reduce JAKAFI/JAKAFI XR starting dose or avoid treatment as recommended. ( 2.7 , 8.6 )

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 71,241 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

Thrombotic Microangiopathycorroborated · ROR 3.65
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.
Electrolyte DisturbanceNo 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.

Thrombotic Microangiopathy

ROR 3.6595% CI 3.17–4.21· 190 reports

Crystal / Obstructive Nephropathy

ROR 1.6795% CI 1.50–1.87· 315 reports

Hemorrhagic Cystitis

ROR 1.6295% CI 1.47–1.79· 380 reports

FAERS outcomes & reporting trend· 13.8% of reports w/ death · 19.1% w/ hospitalization

13.8%

Reported with a death outcome

9,813 of 71,241 reports

19.1%

Reported with hospitalization

13,602 of 71,241 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 7 systems · 71,241 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 0.7995% CI 0.72–0.88· 412 AKI reports ·AKI is reported less often than for other drugs (CI entirely below 1) — no disproportionate signal.

General / constitutional

Fatigue6,114Asthenia2,531Weight Increased1,996Pain1,856Malaise1,601

Blood & lymphatic

Anaemia3,094Haemoglobin Decreased2,961Platelet Count Decreased2,700Platelet Count Increased1,536Thrombocytopenia1,365

Nervous system

Dizziness2,494Headache2,425

Gastrointestinal

Diarrhoea2,683Nausea2,155

Immune / infection

Pneumonia2,170

Respiratory

Dyspnoea1,987

Skin

Pruritus1,808

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 Ruxolitinib 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

Avapritinib

Ayvakit · KIT / PDGFRA inhibitor

Profile

Edema, intracranial bleeding and cognitive effects.

PRELYTE

Mild#1 · 83% phenotype match

Quizartinib

Vanflyta · FLT3 inhibitor

Profile

2023 AML FLT3 inhibitor; tumor lysis and QT.

PRELYTE

Mild#2 · 83% phenotype match

Midostaurin

Rydapt · FLT3 / multikinase inhibitor

Profile

Tumor lysis, edema and QT in AML/mastocytosis.

PRELYTE

Mild#3 · 72% phenotype match

Imetelstat

Rytelo · Telomerase inhibitor

Profile

2024 MDS agent; tumor lysis risk.

PRELYTE

Mild#4 · 72% phenotype match

Zanidatamab

Ziihera · HER2 bispecific antibody

Profile

2024 biliary-tract HER2 bispecific; renal data emerging.

PRELYTE

Mild#5 · 72% 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#6 · 72% phenotype match

Compare Ruxolitinib 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 Other kinase 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.

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 Ruxolitinib’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 Ruxolitinib; 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 27 clinical records among all 34 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.