What kind of kidney injury does Fedratinib cause?

Electrolyte Disturbance — Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia). Other reported patterns: Prerenal / Hemodynamic AKI.

Is kidney injury from Fedratinib reversible?

Reversible. Typical onset: GI adverse events appear early — typically within the first one to two treatment cycles — and tend to diminish over time with supportive care and dose management; the associated electrolyte and creatinine changes track these early GI events. Reduced clearance in renal impairment is present from the first dose (higher exposure independent of time on drug)..

How should kidney function be monitored during Fedratinib therapy?

Thiamine (vitamin B1) level at baseline and periodically; reassess in at-risk or symptomatic patients; Serum creatinine / eGFR and electrolytes (potassium, magnesium, sodium) at baseline and during treatment; CBC for anemia and thrombocytopenia (exposure-driven in renal impairment); Liver transaminases, bilirubin and amylase/lipase (label-recommended labs); Clinical assessment of GI symptoms and hydration status, plus neurologic assessment for encephalopathy.

How can kidney injury from Fedratinib be prevented?

Supplement thiamine (vitamin B1) and correct deficiency before and during therapy Prophylactic and early antiemetic/antidiarrheal therapy to limit GI fluid and electrolyte loss Correct potassium, magnesium and sodium before dosing and during treatment Reduce the starting dose to 200 mg once daily in severe renal impairment (CrCl 15-29 mL/min) Encourage adequate hydration and oral intake; take doses with food to improve GI tolerability

Who is at higher risk of kidney injury from Fedratinib?

Moderate-to-severe renal impairment (higher fedratinib exposure; severe impairment mandates dose reduction); Uncontrolled nausea, vomiting or diarrhea causing ongoing fluid and electrolyte loss; Baseline thiamine deficiency or poor nutritional status / reduced oral intake; Concomitant diuretics or other drugs that deplete potassium or magnesium; Elderly or low-body-weight patients; Co-administration of strong CYP3A4 inhibitors (raise exposure) or inducers (lower it).

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Printable monograph

JAK2 inhibitor

Fedratinib

Inrebic · FED

JAK2 inhibitor · approved 2019 · 7 citations

Aging evidence· through 2020

Thinly sourced3/9 · 3 signals

Met: 7 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 5y)
Met: Beyond single case reports
Not met: Peer-reviewed sources
Met: Landmark reference
Not met: Current through 2020
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 selective JAK2 inhibitor for myelofibrosis that is not a direct nephrotoxin — its kidney relevance is a renally-influenced exposure that rises in kidney impairment (mandating dose reduction) compounded by heavy GI fluid-and-electrolyte loss.

MildJAK2 inhibitor

Intermediate-2 or high-risk primary or secondary (post-polycythemia vera / post-essential thrombocythemia) myelofibrosisJAK-inhibitor-naive patients and those previously treated with (relapsed/refractory or intolerant to) ruxolitinib

§01

Signature kidney injury

Signature lesion

Electrolyte Disturbance

There is no established incidence of direct fedratinib-induced kidney injury; the renal story is pharmacokinetic and GI-driven rather than a discrete nephrotoxic lesion. In the pivotal placebo-controlled JAKARTA phase 3 trial, gastrointestinal symptoms were among the most common adverse events and "increased levels of serum creatinine" was reported as a common laboratory abnormality — but neither a rate of clinically significant AKI nor a discrete electrolyte-depletion incidence was separately quantified, so a headline nephrotoxicity percentage cannot be stated without overstating the evidence. The dedicated phase 1 renal-impairment study found systemic exposure (AUC) roughly 1.9-fold higher in severe renal impairment, which is the basis for a mandated dose reduction rather than an injury rate.Source: Pardanani et al., JAMA Oncol 2015 (JAKARTA)

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Reduced clearance in renal impairment is present from the first dose — higher exposure independent of time on drug. GI adverse events appear early, within the first one to two treatment cycles, and the associated electrolyte and creatinine changes track those early GI events; that GI timing is the drug's known class pattern rather than a finding of the cited single-dose study.

Distilled from: “In single-dose renal- and hepatic-impairment studies, fedratinib exposure was higher with renal impairment, present from the first dose independent of time on drug (PMID 32449142). The early GI onset (first one to two cycles) is fedratinib's established class pattern, not established by that single-dose PK study.” · PMID 32449142 (opens PubMed in a new tab)

§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.

Electrolyte Disturbance#1 · Signaturequalitative — 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 AKISecondaryqualitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

§03

Kidney injury

Mechanism of kidney injury

Two intertwined, indirect mechanisms rather than a primary tubular or glomerular toxin. (1) Renally-influenced clearance: population pharmacokinetics identify creatinine clearance as a statistically significant covariate on fedratinib apparent clearance, so reduced kidney function raises drug exposure (a dedicated renal-impairment study found AUC ~1.5-fold higher in moderate and ~1.9-fold in severe impairment; population PK put the moderate increase near 37%), amplifying downstream toxicity unless the dose is cut. (2) GI-mediated fluid and electrolyte loss: frequent nausea, vomiting and diarrhea reduce intake and drive volume contraction with potassium and magnesium loss, which can precipitate prerenal/hemodynamic AKI. Serum-creatinine rises observed in trials may partly reflect this hemodynamic effect (and possibly altered tubular creatinine handling) rather than proven structural GFR loss. A separate, non-renal but thematically linked concern is thiamine (vitamin B1) deficiency and Wernicke encephalopathy, plausibly aggravated by the same GI losses/reduced intake — the drug's black-box warning.

Clinical presentation

Rather than a classic nephrotoxic syndrome, the picture is an at-risk patient: gastrointestinal upset (nausea, vomiting, diarrhea) with reduced oral intake and volume contraction, whose biochemical footprint is hypokalemia, hypomagnesemia and a rising serum creatinine (often modest and reversible with rehydration). In kidney impairment the higher fedratinib exposure can manifest as more pronounced GI and hematologic (anemia, thrombocytopenia) toxicity. The most feared associated event is Wernicke-type encephalopathy (confusion, ophthalmoplegia, ataxia) from thiamine deficiency — a neurologic emergency, not a renal one, but part of the same GI-loss theme.

Management

Manage GI toxicity aggressively with antiemetics and antidiarrheals and by taking the dose with food; replete potassium and magnesium and restore intravascular volume for prerenal creatinine rises. Dose-interrupt or reduce for severe/persistent GI events, significant creatinine elevation, or cytopenias per label thresholds. For any encephalopathy, hold fedratinib immediately and give parenteral thiamine. In renal impairment, use the reduced dose and monitor exposure-driven toxicity (GI, hematologic); there is no specific antidote and no established renal-replacement removal strategy. Re-escalate cautiously once toxicity resolves.Lesion-level management framework

Risk factors

Moderate-to-severe renal impairment (higher fedratinib exposure; severe impairment mandates dose reduction)
Uncontrolled nausea, vomiting or diarrhea causing ongoing fluid and electrolyte loss
Baseline thiamine deficiency or poor nutritional status / reduced oral intake
Concomitant diuretics or other drugs that deplete potassium or magnesium
Elderly or low-body-weight patients
Co-administration of strong CYP3A4 inhibitors (raise exposure) or inducers (lower it)

Prevention

Supplement thiamine (vitamin B1) and correct deficiency before and during therapy
Prophylactic and early antiemetic/antidiarrheal therapy to limit GI fluid and electrolyte loss
Correct potassium, magnesium and sodium before dosing and during treatment
Reduce the starting dose to 200 mg once daily in severe renal impairment (CrCl 15-29 mL/min)
Encourage adequate hydration and oral intake; take doses with food to improve GI tolerability

Anticancer mechanism· how it treats cancer

Oral, selective small-molecule inhibitor of Janus kinase 2 (JAK2), including the JAK2V617F mutant that drives constitutive JAK/STAT signaling in myeloproliferative neoplasms. Blocking JAK2-mediated phosphorylation of STAT5 curbs malignant myeloid proliferation, reduces splenomegaly and improves constitutional symptoms; it also has secondary off-target activity against FLT3 and BRD4.

Note · Fedratinib has no established direct nephrotoxic lesion, so the kidney narrative here is pharmacokinetic (renally-influenced clearance → dose reduction) and indirect (GI fluid/electrolyte loss → prerenal AKI, plus thiamine-deficiency/Wernicke risk). FDA approval was August 2019. Claims are hedged to the available evidence.

§04

Clinical depth

Renal dose adjustment

Mild renal impairment (CrCl 60-89 mL/min): no dose adjustment. Moderate impairment (CrCl 30-59 mL/min): the standard 400 mg once-daily dose may be used but with monitoring and dose reduction as needed, since exposure is ~37% higher on population PK. Severe impairment (CrCl 15-29 mL/min): reduce to 200 mg once daily — a dedicated phase 1 study found ~1.9-fold higher AUC. End-stage renal disease was included in that same phase 1 study, but it yielded no ESRD dosing recommendation, so no ESRD/dialysis dose is defined. Separately, reduce the dose (or avoid) with concomitant strong CYP3A4 inhibitors.

Dialyzability & ESKD dosing

Not established and unlikely to be meaningfully dialyzable. Fedratinib is extensively protein-bound with a large volume of distribution and a long (~41 h) effective half-life; the dedicated impairment study did not identify hemodialysis as a clearance route, and no dosing recommendation exists for dialysis patients. Dosing is driven by exposure and tolerability, not by dialytic removal.

Differential diagnosis

Distinguish a prerenal/hemodynamic creatinine rise from GI volume loss (improves promptly with rehydration) from true intrinsic AKI. Consider that fedratinib's reported serum-creatinine elevations may be a laboratory or hemodynamic signal rather than a fall in true GFR — confirm with cystatin C or the trajectory if the clinical picture does not fit. Separate thiamine-deficiency Wernicke encephalopathy from other causes of altered mental status (hepatic encephalopathy, sepsis, CNS disease). Attribute electrolyte disturbances to GI losses and concomitant drugs rather than to a specific tubulopathy, since fedratinib is not a recognized direct tubular toxin. Anemia and thrombocytopenia are usually disease- or exposure-related cytopenias, not a renal process.

Monitoring

Thiamine (vitamin B1) level at baseline and periodically; reassess in at-risk or symptomatic patients
Serum creatinine / eGFR and electrolytes (potassium, magnesium, sodium) at baseline and during treatment
CBC for anemia and thrombocytopenia (exposure-driven in renal impairment)
Liver transaminases, bilirubin and amylase/lipase (label-recommended labs)
Clinical assessment of GI symptoms and hydration status, plus neurologic assessment for encephalopathy

Key trials & series

JAKARTA (phase 3, Pardanani, JAMA Oncol 2015): double-blind, placebo-controlled; 400 mg once daily achieved a 36% spleen response vs 1% with placebo; common adverse events were anemia, gastrointestinal symptoms and increased serum creatinine/transaminases; encephalopathy occurred in 4 women on 500 mg.
JAKARTA-2 (phase 2, Harrison, Lancet Haematol 2017): single-arm study in ruxolitinib-relapsed/intolerant myelofibrosis; 55% spleen response; suspected Wernicke encephalopathy cases contributed to a clinical hold on development.
Dedicated phase 1 renal/hepatic impairment PK study (Ogasawara, Cancer Chemother Pharmacol 2020): AUC 1.9- and 1.5-fold higher in severe and moderate renal impairment; basis for the 200 mg dose in severe impairment.
Population PK analysis (Ogasawara, Cancer Chemother Pharmacol 2019): creatinine clearance a significant covariate on clearance; mild and moderate renal impairment associated with 10% and 37% higher exposure.

Clinical pearls

Fedratinib is not a classic nephrotoxin — its kidney relevance is dosing (renally-influenced clearance) plus GI-driven electrolyte and volume loss, not a discrete tubular or glomerular lesion.
The one hard renal rule: severe renal impairment (CrCl 15-29) mandates cutting the dose to 200 mg because exposure runs ~1.9-fold higher; moderate impairment warrants monitoring with reduction as needed.
Check thiamine before and during therapy and give parenteral thiamine (and hold the drug) at any hint of encephalopathy — the black-box Wernicke risk is the defining safety issue and is plausibly compounded by GI losses.
A modest, reversible creatinine bump reported in trials may be hemodynamic or a laboratory signal rather than true GFR loss — rehydrate and recheck before abandoning an effective therapy.
GI toxicity is early and usually wanes; proactive antiemetics/antidiarrheals and electrolyte (K/Mg) repletion prevent the downstream prerenal AKI and electrolyte depletion.

Where it strikes· nephron segments & injury signatures

Nephron segments

Distal Tubule / Collecting Duct

Fine-tuning of Na, K, Mg, acid & water

Injury signatures

Electrolyte Disturbance Prerenal / Hemodynamic AKI

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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 · 2015–2020 · 5 since 2018

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.

FDA label — boxed warning & renal dosing· boxed warning · renal impairment

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

Boxed warning

WARNING: ENCEPHALOPATHY INCLUDING WERNICKE'S Serious and fatal encephalopathy, including Wernicke's, has occurred in patients treated with INREBIC. Wernicke's encephalopathy is a neurologic emergency. Assess thiamine levels in all patients prior to starting INREBIC. Do not start INREBIC in patients with thiamine deficiency; replete thiamine prior to treatment initiation. While on treatment all patients should receive prophylaxis with daily oral thiamine and should have thiamine levels assessed as clinically indicated. If encephalopathy is suspected, immediately discontinue INREBIC and initiate parenteral thiamine. Monitor until symptoms resolve or improve and thiamine levels normalize [see Dosage and Administration (2.6) , Warnings and Precautions (5.1) and Adverse Reactions (6.1) ] . WARNING: ENCEPHALOPATHY INCLUDING WERNICKE'S See full prescribing information for complete boxed warning. Serious and fatal encephalopathy, including Wernicke's, has occurred in patients treated with INREBIC. Wernicke's encephalopathy is a neurologic emergency. Assess thiamine levels in all patients prior to starting INREBIC. Do not start INREBIC in patients with thiamine deficiency; replete thiamine prior to treatment initiation. While on treatment all patients should receive prophylaxis with daily oral thiamine and should have thiamine levels assessed as clinically indicated. If encephalopathy…

Renal impairment — from the label

Reduce INREBIC dose when administered to patients with severe renal impairment (CL cr 15 mL/min to 29 mL/min by Cockcroft-Gault) [see Dosage and Administration (2.5) and Clinical Pharmacology (12.3) ] . No modification of the starting dose is recommended for patients with mild to moderate renal impairment (CL cr 30 mL/min to 89 mL/min by Cockcroft-Gault). Due to potential increase of exposure, patients with preexisting moderate renal impairment require more intensive safety monitoring, and if necessary, dose modifications based on adverse reactions [see Dosage and Administration (2.6) ].

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 1,322 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· 14.3% of reports w/ death · 19.5% w/ hospitalization

14.3%

Reported with a death outcome

189 of 1,322 reports

19.5%

Reported with hospitalization

258 of 1,322 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 1,322 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 2026-08-08.

Disproportionality (acute kidney injury):ROR 1.3695% CI 0.79–2.34· 13 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Gastrointestinal

Diarrhoea143Nausea118Vomiting71Constipation59Abdominal Discomfort36

General / constitutional

Fatigue113Asthenia51Pain32Malaise30Weight Decreased25

Blood & lymphatic

Haemoglobin Decreased54Platelet Count Decreased49Anaemia40White Blood Cell Count Increased27

Skin

Pruritus43

Nervous system

Dizziness39

Respiratory

Dyspnoea27

Immune / infection

Pneumonia26

Musculoskeletal

Muscle Spasms25

Guidelines & consensus· 12

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 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 Fedratinib 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

Darolutamide

Nubeqa · Androgen receptor inhibitor (ARSI)

Profile

Not nephrotoxic; exposure rises in severe renal impairment, so consider dose adaptation.

LYTEPRE

Mild#1 · 78% phenotype match

Glasdegib

Daurismo · Hedgehog (SMO) inhibitor

Profile

QT prolongation and muscle spasms; AML.

PRELYTE

Mild#2 · 77% phenotype match

Sevabertinib

Hyrnuo · HER2/EGFR TKI

Profile

2025 reversible HER2/EGFR TKI; profuse diarrhea (84-91%) → prerenal AKI, plus EGFR-pathway renal magnesium wasting.

PRELYTE

Mild#3 · 77% phenotype match

Avapritinib

Ayvakit · KIT / PDGFRA inhibitor

Profile

Edema, intracranial bleeding and cognitive effects.

PRELYTE

Mild#4 · 77% phenotype match

Gedatolisib

Revtorpyk · Pan-PI3K inhibitor

Profile

2026 IV pan-PI3K + mTORC1/2 (breast); on-target hyperglycemia and low-grade Na/K/Mg drift — creatinine up 14% vs 8% control, grade 3-4 rare.

LYTEPRE

Mild#5 · 77% phenotype match

Midostaurin

Rydapt · FLT3 / multikinase inhibitor

Profile

Tumor lysis, edema and QT in AML/mastocytosis.

PRELYTE

Mild#6 · 77% phenotype match

Compare Fedratinib 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.