What kind of kidney injury does Pemigatinib cause?

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

Is kidney injury from Pemigatinib reversible?

Reversible. Typical onset: Early — within the first cycles..

How should kidney function be monitored during Pemigatinib therapy?

Serum phosphate at baseline and periodically (more often during up-titration/early cycles); Serum calcium and calcium-phosphate product; Ophthalmologic exams for retinal detachment/serous retinopathy; routine creatinine.

How can kidney injury from Pemigatinib be prevented?

Low-phosphate diet when phosphate rises Protocol-based dose modification (14-days-on / 7-days-off schedule)

Who is at higher risk of kidney injury from Pemigatinib?

Pre-existing CKD; High calcium-phosphate product; Concurrent vitamin D / phosphate intake.

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Printable monograph

FGFR inhibitor

Pemigatinib

Pemazyre · Pemi

FGFR inhibitor · approved 2020 · 9 citations

Up to date· through 2025

Fairly sourced5/9 · 5 signals

Met: 9 citations
Not met: 12+ references
Not met: Accrued over 10+ years (span: 8y)
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.

An FGFR1/2/3 inhibitor for cholangiocarcinoma — hyperphosphatemia is its near-universal class signature.

ModerateFGFR inhibitor

FGFR2-fusion/rearrangement cholangiocarcinoma

§01

Signature kidney injury

Signature lesion

Electrolyte Disturbance

Representative incidence60%

Hyperphosphatemia is the most common adverse event in the pivotal FIGHT-202 trial, affecting roughly 60% of patients (any grade), with low rates of severe events; it is on-target and managed with monitoring, diet, and binders.Source: Abou-Alfa et al., Lancet Oncol 2020

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Early — within the first cycles.

Distilled from: “Early — within the first cycles.”

§02

Renal toxicities, ranked

This agent's defining kidney lesion — its #1 signature. 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).

§03

Kidney injury

Mechanism of kidney injury

On-target FGFR1 inhibition disrupts FGF23-mediated suppression of proximal-tubular phosphate reabsorption (NaPi-2a/2c), increasing reabsorption and raising serum phosphate. Prolonged hyperphosphatemia with a high calcium-phosphate product risks nephrocalcinosis and ectopic/vascular calcification.

Clinical presentation

Asymptomatic hyperphosphatemia on routine monitoring; may co-occur with hypophosphatemia after dose interruption (a 'rebound') or hypocalcemia, and an elevated calcium-phosphate product. Soft-tissue mineralization risk if persistent; alopecia, dysgeusia, and nail changes are common non-renal effects.

Management

Phosphate binders (e.g. sevelamer) and dietary restriction for phosphate >5.5 mg/dL; interrupt and dose-reduce for higher/persistent levels per label, and discontinue for persistent hyperphosphatemia despite optimal therapy. Monitor for nephrocalcinosis with prolonged elevation.Lesion-level management framework

Risk factors

Pre-existing CKD
High calcium-phosphate product
Concurrent vitamin D / phosphate intake

Prevention

Low-phosphate diet when phosphate rises
Protocol-based dose modification (14-days-on / 7-days-off schedule)

Anticancer mechanism· how it treats cancer

Selective FGFR1/2/3 inhibitor blocking oncogenic FGFR signaling; approved for FGFR2-fusion/rearrangement-positive cholangiocarcinoma.

Note · Nephrocalcinosis is a theoretical/uncommon risk of sustained hyperphosphatemia; the dominant signal is reversible on-target hyperphosphatemia.

§04

Clinical depth

Renal dose adjustment

No starting-dose change for mild or moderate renal impairment (eGFR 30-89). Severe impairment (eGFR 15-29) carries a specific label reduction: 9 mg on whichever schedule the indication designates, down from 13.5 mg. ESRD on intermittent hemodialysis needs no adjustment per label. Beyond those bands, dosing is driven by the phosphate-guided algorithm (and the intermittent 14-days-on/7-days-off schedule) rather than a CrCl rule.

Dialyzability & ESKD dosing

Highly protein-bound oral small molecule; not expected to be appreciably dialyzed. The label carries a dedicated ESRD-on-intermittent-hemodialysis cohort and recommends no dosage adjustment there — which is also the strongest support for the non-dialyzable verdict. The phosphate biomarker, however, is confounded in ESKD.

Differential diagnosis

On-target FGFR-inhibitor hyperphosphatemia vs CKD-related hyperphosphatemia vs tumor lysis (with hyperuricemia/hyperkalemia/AKI). The early, dose-related, isolated phosphate elevation without AKI points to the drug.

Monitoring

Serum phosphate at baseline and periodically (more often during up-titration/early cycles)
Serum calcium and calcium-phosphate product
Ophthalmologic exams for retinal detachment/serous retinopathy; routine creatinine

Key trials & series

FIGHT-202 (registrational FGFR2-fusion cholangiocarcinoma)
FIGHT-302 (first-line cholangiocarcinoma)

Clinical pearls

Hyperphosphatemia is the FGFR-class signature; expect it, monitor phosphate, and treat with diet/binders before changing dose.
Watch for rebound hypophosphatemia during the planned 7-day drug-free interval.
Sustained elevation risks nephrocalcinosis — track the calcium-phosphate product, not phosphate alone.

Where it strikes· nephron segments & injury signatures

Nephron segments

Proximal Tubule

Bulk reabsorption + drug uptake (OCT2, OATs)

Injury signatures

Electrolyte Disturbance

Beyond the kidney — non-renal toxicities· 2 organ systems

Class-level context for the major non-renal toxicities of the FGFR inhibitor class.

Ophthalmic

Keratopathy, uveitis, retinopathy

Central serous retinopathy

Dermatologic

Rash, HFS, SJS/TEN, vitiligo

Nail/skin changes, hand-foot syndrome

§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 · 2017–2024 · 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· 3

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 · LimitedManagement and mechanism of calciphylaxis in a patient treated with the FGFR inhibitor pemigatinib-a case report.Chandana SR et al. · J Gastrointest Oncol 2024 · PMID 38482230Pemigatinib-associated calciphylaxis from FGF23-pathway hyperphosphatemia occurring without advanced renal failure, detailing the phosphate dysregulation mechanism of FGFR inhibition.CaseC · LimitedHyperphosphatemic Tumoral Calcinosis With Pemigatinib Use.Puar A et al. · AACE Clin Case Rep 2022 · PMID 36189136Pemigatinib inhibition of FGF23 caused marked hyperphosphatemia (serum phosphorus 7.5 mg/dL, intact FGF23 1216 pg/mL) with ectopic tumoral calcinosis, the signature electrolyte (phosphate) wasting/handling derangement of FGFR inhibitors.CaseC · LimitedCalcinosis Cutis With Selective Fibroblast Growth Factor Receptor Inhibitors: A Case Report and Review of Literature.Ghimire B et al. · Cureus 2025 · PMID 40486452Pemigatinib-induced hyperphosphatemia (normal calcium) drove calcinosis cutis, managed with phosphate binders and electrolyte correction, illustrating the drug's disordered renal phosphate handling.

FDA label — boxed warning & renal dosing· renal impairment

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

Renal impairment — from the label

Reduce the recommended dosage of PEMAZYRE for patients with severe renal impairment (eGFR 15 to 29 mL/min/1.73 m 2 , estimated by MDRD equation) [see Dosage and Administration ( 2.5 ) and Clinical Pharmacology ( 12.3 )] . No dosage adjustment is recommended for patients with mild or moderate renal impairment (eGFR 30 to 89 mL/min/1.73 m 2 ). No dosage adjustment is recommended for patients with end-stage renal disease (eGFR < 15 mL/min/1.73 m 2 ) who are receiving intermittent hemodialysis [ see Clinical Pharmacology ( 12.3 )] .

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 821 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· 1 signal

Only significant signals appear (95% CI lower bound above 1) — a phenotype missing here was tested and did not reach significance, except Prerenal / Hemodynamic AKI, Pseudo-AKI, Renal Cysts, Chronic Interstitial Nephropathy — outside the clinician-reviewed MedDRA term map, never queried — and ATN and AIN, queried but biopsy-bound: real cases are filed as generic “acute kidney injury”, so their absence is not a negative. As of 2026-10-01.

What reporting says about this profile's documented lesions

Electrolyte Disturbancecorroborated · ROR 2.3 — but the naming terms alone are not disproportionate, so this rests on terms merely consistent with the lesion

Electrolyte Disturbance

ROR 2.3095% CI 1.42–3.72· 17 reports

FAERS outcomes & reporting trend· 17.5% of reports w/ death · 24% w/ hospitalization

17.5%

Reported with a death outcome

144 of 821 reports

24%

Reported with hospitalization

197 of 821 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 821 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 1.0195% CI 0.45–2.25· 6 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).

Renal & urinary

Renal Impairment17

Gastrointestinal

Diarrhoea43Nausea41Constipation39Stomatitis34Dry Mouth33

Skin

Alopecia63Nail Disorder30Dry Skin25Palmar-Plantar Erythrodysaesthesia Syndrome22

General / constitutional

Fatigue79Pain29

Metabolic & electrolyte

Hyperphosphataemia51Decreased Appetite35

Eye

Dry Eye30

Musculoskeletal

Arthralgia24

Nervous system

Taste Disorder21

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 Pemigatinib 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

Erdafitinib

Balversa · FGFR inhibitor

Profile

Hyperphosphatemia is an on-target class effect.

LYTE

Moderate#1 · 100% phenotype match

Futibatinib

Lytgobi · FGFR inhibitor

Profile

Hyperphosphatemia, class effect.

LYTE

Moderate#2 · 100% phenotype match

Infigratinib

Truseltiq · FGFR inhibitor

Profile

Hyperphosphatemia — on-target FGFR class effect; nephrocalcinosis risk.

LYTEXTAL

Moderate#3 · 73% phenotype match

Denosumab

Xgeva · Anti-RANKL antibody

Profile

Severe hypocalcemia in low GFR; not directly nephrotoxic.

LYTE

Moderate#4 · 66% phenotype match

Necitumumab

Portrazza · Anti-EGFR antibody

Profile

Severe hypomagnesemia, class effect.

LYTE

Moderate#5 · 66% phenotype match

Nedaplatin

Aqupla · Platinum agent

Profile

Second-gen platinum with reduced renal toxicity vs cisplatin.

ATNLYTE

Moderate#6 · 65% phenotype match

Compare Pemigatinib 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 FGFR 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.

1ErdafitinibLYTE — Electrolyte DisturbanceModerate
2FutibatinibLYTE — Electrolyte DisturbanceModerate
3Pemigatinib· this agentLYTE — Electrolyte DisturbanceModerate
4InfigratinibLYTE — Electrolyte DisturbanceModerate

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.