Is kidney injury from Pemetrexed reversible?

Partially reversible. Typical onset: Delayed / cumulative; risk rises after ~10 cycles..

How should kidney function be monitored during Pemetrexed therapy?

Check serum creatinine/eGFR and recalculate CrCl (Cockcroft-Gault) before EVERY cycle; withhold if CrCl falls below 45 mL/min.; Confirm folic acid and B12 supplementation are in place and adherent before each cycle (under-supplementation predicts severe toxicity).; Screen and document NSAID and other nephrotoxin exposure at each visit; reinforce the peri-dose NSAID hold window.; Monitor CBC (nadir counts) and mucositis as surrogate markers of impaired renal clearance, since accumulation manifests first as marrow/mucosal toxicity.; With prolonged or cumulative (maintenance) exposure, trend eGFR over time and assess electrolytes, urine osmolality and polyuria for tubulopathy (NDI, RTA)..

How can kidney injury from Pemetrexed be prevented?

Folic acid + vitamin B12 supplementation Dose-hold for declining eGFR

Who is at higher risk of kidney injury from Pemetrexed?

High cumulative dose / prolonged maintenance; Pre-existing CKD; Concurrent nephrotoxins.

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Printable monograph

Antifolate

Pemetrexed

Alimta · Pem

Antifolate · approved 2004 · 10 citations · FAERS AKI reporting ROR 4.89 (95% CI 4.62–5.17, 1,299 AKI reports)

Up to date· through 2026

Deeply sourced8/9 · 7 signals

Met: 10 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 20y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2026
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 slow burn — cumulative tubular toxicity that surfaces after many cycles.

ModerateMultitargeted antifolate

NSCLC (non-squamous)Mesothelioma

§01

Signature kidney injury

Signature lesion

Chronic Interstitial Nephropathy

Representative incidence21%

Clinically relevant eGFR decline (≥25%) in ~21%; ~8% discontinue for nephrotoxicity. Cumulative-dose dependent.Source: de Rouw et al., Lung Cancer 2020

Onset & rechallenge

Time to injuryDelayed (>6 weeks / cumulative)

Cumulative — renal risk rises after roughly 10 cycles of exposure.

Distilled from: “Delayed / cumulative; risk rises after ~10 cycles.”

Long-term outlook & thresholds

Renal recoveryOften partial recovery

Acute pemetrexed ATN may recover, but cumulative/maintenance exposure drives insidious CKD upstaging with tubular dysfunction (nephrogenic diabetes insipidus, renal tubular acidosis) that is often only partially reversible after the drug is stopped.PMID 41614227 (opens PubMed in a new tab)

CKD trajectory.: In a 222-patient territory-wide mesothelioma cohort, 47 (21.2%) had CKD upstaging, 31 (14.0%) showed renal progression (>30 mL/min eGFR drop) and 18 (8.1%) developed AKI.

Cumulative-dose threshold

~10 cycles of exposure

Renal risk rises after roughly 10 cycles; clinically relevant eGFR decline (>=25%) occurs in ~21% and ~8% discontinue for nephrotoxicity.PMID 32505078 (opens PubMed in a new tab)

Early-detection biomarkers

Cystatin C (serum) — Glomerular filtration / drug clearance. Pemetrexed exposure is dictated by kidney function; cystatin C-based eGFR is a validated renal-function biomarker studied for more precise pemetrexed clearance prediction and dosing, less confounded by muscle mass than creatinine.PMID 39365467 (opens PubMed in a new tab)

Long-term outcome and threshold data distilled from the agent's cited literature — educational, not a substitute for the primary sources.

Recovery across agents

§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.

Chronic Interstitial Nephropathy#1 · Signature21%PMID 32505078 (opens PubMed in a new tab)
Clinically relevant (≥25%) eGFR decline in 21% during pemetrexed therapy — cumulative and dose-dependent (≥10 cycles: adjusted OR 5.66); a chronic tubulointerstitial injury that is often only partially reversible
Acute Tubular NecrosisSecondaryno population incidence denominator
Acute tubular injury/AKI reported in ~21% (6/29) of a single-center NSCLC cohort (baseline eGFR >45); biopsy-documented ATN with interstitial fibrosis in case reports PMID 24986522 (opens PubMed in a new tab)
Electrolyte DisturbanceRareno population incidence denominator
Tubular electrolyte disturbances (nephrogenic diabetes insipidus, distal renal tubular acidosis, hypophosphatemia/hypokalemia) reported mainly at case level, not systematically quantified PMID 35190107 (opens PubMed in a new tab)
SIADH / HyponatremiaRarequalitative — no citable incidence
Exposure-correlated severe hyponatremia in a prospective PK cohort, with events during single-agent maintenance.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

21%incidence

SeverityModerate

ReversibilityPartially reversible

Evidence10 citations

Nephron map

Proximal Tubule

Distal Tubule / Collecting Duct

InterstitiumSupporting tissue around the tubules

Chronic Interstitial Nephropathy

Slow, cumulative tubulointerstitial scarring — fibrosis, tubular atrophy and glomerulosclerosis with no discrete acute phase. The nitrosourea (carmustine/lomustine) lesion and delayed radioligand (radiation) nephropathy; often irreversible and detected only as a creeping creatinine months to years later.

§03

Kidney injury

Deep divePemetrexed tubular nephrotoxicityPemetrexed leaves the body through the kidney, so the tubule sees the drug at every cycle — and the injury accumulates quietly, cycle by cycle, into a tubulointerstitial scar that often does not heal once the drug is finally stopped.Appears in 1 documented synergy combination

Mechanism of kidney injury

Thought to be taken up into proximal tubular cells via the reduced folate carrier and organic anion transporters, producing direct tubular toxicity and chronic tubulointerstitial damage that accumulates with prolonged maintenance dosing.

Clinical presentation

Slowly progressive eGFR decline, sometimes renal tubular acidosis, hypophosphatemia and nephrogenic diabetes insipidus — insidious rather than abrupt AKI.

Management

Discontinue or dose-adjust; supportive care.Lesion-level management framework

Risk factors

High cumulative dose / prolonged maintenance
Pre-existing CKD
Concurrent nephrotoxins

Prevention

Folic acid + vitamin B12 supplementation
Dose-hold for declining eGFR

Anticancer mechanism· how it treats cancer

Multitargeted antifolate inhibiting thymidylate synthase, DHFR and GARFT. Non-squamous NSCLC and mesothelioma, often as maintenance therapy.

Note · Increasingly relevant as immuno-chemotherapy prolongs pemetrexed exposure.

§04

Clinical depth

Renal dose adjustment

Pemetrexed is predominantly renally cleared, and the FDA label contraindicates initiation when CrCl is below 45 mL/min (Cockcroft-Gault) because reduced clearance drives severe myelosuppression and mucositis; there is no validated reduced-dose regimen below this threshold. In patients with CrCl 45-79 mL/min no dose reduction is specified, but avoid NSAIDs around dosing (hold short-half-life NSAIDs 2 days before to 2 days after, longer-half-life agents ~5 days) since they impair tubular clearance and amplify toxicity. Mandatory folic acid (350-1000 mcg/day starting ~1 week pre-treatment) and IM vitamin B12 (1 mg every ~9 weeks) supplementation is required to blunt overall toxicity.

Dialyzability & ESKD dosing

Limited data; pemetrexed is moderately protein-bound (~81%) with a low molecular weight, so it is theoretically partly dialyzable, but it is not used in dialysis-dependent patients and no established schedule exists. Because the drug is contraindicated below CrCl 45 mL/min, dosing in ESKD/HD is essentially uncharacterized and should be avoided outside specialist judgment.

Differential diagnosis

Acute pemetrexed nephrotoxicity is typically ATN with a non-oliguric rise in creatinine, distinguished from cisplatin co-administration (also ATN with Mg wasting) chiefly by exposure pattern and reversibility. Chronic/cumulative use produces a tubulointerstitial picture with reported nephrogenic diabetes insipidus (polyuria, hypotonic urine resistant to desmopressin) and distal renal tubular acidosis — features that help separate it from prerenal volume depletion and from immune-checkpoint interstitial nephritis (sterile pyuria, white-cell casts) when those agents are combined.

Monitoring

Check serum creatinine/eGFR and recalculate CrCl (Cockcroft-Gault) before EVERY cycle; withhold if CrCl falls below 45 mL/min.
Confirm folic acid and B12 supplementation are in place and adherent before each cycle (under-supplementation predicts severe toxicity).
Screen and document NSAID and other nephrotoxin exposure at each visit; reinforce the peri-dose NSAID hold window.
Monitor CBC (nadir counts) and mucositis as surrogate markers of impaired renal clearance, since accumulation manifests first as marrow/mucosal toxicity.
With prolonged or cumulative (maintenance) exposure, trend eGFR over time and assess electrolytes, urine osmolality and polyuria for tubulopathy (NDI, RTA).

Key trials & series

JMDB (Scagliotti, JCO 2008) — phase III cisplatin plus pemetrexed first-line in advanced NSCLC; the registrational efficacy trial that also established the platinum-doublet renal/toxicity profile requiring CrCl-based dosing.
EMPHACIS (Vogelzang, JCO 2003) — phase III cisplatin/pemetrexed in mesothelioma; demonstrated that mandatory folic acid and B12 supplementation markedly reduced toxicity, shaping the current supplementation requirement.
PARAMOUNT (Paz-Ares, Lancet Oncol 2012) — phase III continuation-maintenance pemetrexed in NSCLC; prolonged exposure surfaced cumulative renal/laboratory toxicity informing the chronic-nephrotoxicity concern.

Clinical pearls

The hard rule: do not start pemetrexed if CrCl < 45 mL/min — reduced clearance causes life-threatening myelosuppression and mucositis, which are the earliest clinical signals of drug accumulation.
NSAIDs are the classic avoidable hit — they cut tubular secretion of pemetrexed; observe the peri-dose hold window, especially in any degree of renal impairment.
Folate/B12 supplementation is non-negotiable and renal-protective in effect; missed supplementation is a leading driver of severe toxicity.
Cumulative/maintenance dosing can cause an insidious CKD with tubular dysfunction — watch for nephrogenic diabetes insipidus (polyuria) and renal tubular acidosis, which are often only partially reversible after stopping.
Renal injury is amplified when pemetrexed is paired with cisplatin; aggressive hydration, Mg repletion, and avoiding additional nephrotoxins matter most in the doublet.
Severe hyponatremia tracks pemetrexed exposure (AUC) in a prospective PK cohort, with urine osmolality exceeding serum suggesting SIADH and further events during single-agent maintenance.

Beyond the kidney — non-renal toxicities· 4 organ systems

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

Gastrointestinal

Diarrhea, colitis, mucositis, perforation

Mucositis and diarrhea

Hepatic / Liver

Transaminitis, hepatitis, VOD/SOS

Transaminitis (methotrexate)

Hematologic

Cytopenias, thrombosis, TMA

Myelosuppression

Pulmonary

Pneumonitis, ILD, effusions, hypertension

Methotrexate / gemcitabine pneumonitis

§05

References

9 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

9 references · 2006–2026 · 2 since 2024

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 · ModerateAcute Tubular Necrosis and Interstitial Nephritis during Pemetrexed Therapy.Michels J et al. · Case Rep Oncol 2009 · PMID 20740145Biopsy-proven acute tubular necrosis with interstitial fibrosis and persistent chronic renal insufficiency following pemetrexed monotherapy.

Conference abstracts & journal reports· 1 non-PubMed

Non-PubMed sources — conference abstracts (e.g. ASN Kidney Week, badged Abstract) and case reports from non-indexed field journals (e.g. Journal of Onco-Nephrology, badged Journal). Included for completeness; weigh below peer-reviewed PubMed citations.

AbstractAcute Interstitial Nephritis Induced by Pemetrexed in a Patient with Metastatic Adenocarcinoma of the LungOmer M, Vela Parada X · ASN Kidney Week 2025 / JASN 2025Acute interstitial nephritis attributed to maintenance pemetrexed — an unusual renal presentation given pemetrexed's classic acute tubular / proximal-tubular toxicity, widening its lesion spectrum to include AIN.

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

Pemetrexed is primarily excreted by the kidneys. Decreased renal function results in reduced clearance and greater exposure (AUC) to pemetrexed compared with patients with normal renal function [see Warnings and Precautions ( 5.2 , 5.6 ) and Clinical Pharmacology ( 12.3 )] . No dosage is recommended for patients with creatinine clearance less than 45 mL/min [see Dosage and Administration ( 2.3 )] .

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 37,889 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· 7 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

Acute Tubular Necrosiscorroborated · ROR 16.55
Electrolyte Disturbancecorroborated · ROR 3.09 — on the terms that name the lesion (ROR 5.61)
SIADH / Hyponatremiacorroborated · ROR 3.04 — on the terms that name the lesion (ROR 2.35)
Chronic Interstitial NephropathyNot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Acute Tubular Necrosis

ROR 16.5595% CI 14.70–18.63· 284 reports

Acute Interstitial Nephritis

ROR 16.3195% CI 14.95–17.79· 530 reports

Glomerular Injury / Proteinuria

ROR 4.8995% CI 4.32–5.54· 254 reports

Electrolyte Disturbance

ROR 3.0995% CI 2.90–3.28· 1,042 reports

SIADH / Hyponatremia

ROR 3.0495% CI 2.76–3.34· 437 reports

Thrombotic Microangiopathy

ROR 2.8795% CI 2.31–3.58· 80 reports

Fanconi Syndrome

ROR 1.7395% CI 1.06–2.83· 16 reports

FAERS outcomes & reporting trend· 19% of reports w/ death · 47.5% w/ hospitalization

19%

Reported with a death outcome

7,188 of 37,889 reports

47.5%

Reported with hospitalization

17,979 of 37,889 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 8 systems · 37,889 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 4.8995% CI 4.62–5.17· 1,299 AKI reports ·AKI is reported disproportionately more often than for other drugs (CI entirely above 1) — a hypothesis-generating signal, not proof of causation.

Renal & urinary

Acute Kidney Injury1,299Renal Failure747

Blood & lymphatic

Anaemia2,133Pancytopenia1,773Neutropenia1,745Thrombocytopenia1,631Febrile Neutropenia1,240

Gastrointestinal

Nausea1,906Diarrhoea1,824Vomiting1,417

General / constitutional

Fatigue1,444Pyrexia1,283Asthenia1,182

Respiratory

Dyspnoea1,339Interstitial Lung Disease905Pneumonitis762Pleural Effusion681

Skin

Rash1,289

Immune / infection

Pneumonia1,260

Metabolic & electrolyte

Decreased Appetite1,065

Guidelines & consensus· 14

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.

ADQIConventional cytotoxic chemotherapy-associated nephrotoxicity: consensus report of the 34th Acute Disease Quality Initiative (ADQI) WorkgroupKidney Int 2026 · PMID 41881107Cisplatin is identified as a leading cytotoxic nephrotoxin; the workgroup details preventive measures (adequate isotonic hydration, correction of volume depletion, avoidance of concurrent nephrotoxins, attention to electrolyte/magnesium wasting) and management of cisplatin-associated AKI, with a research agenda for knowledge gaps.

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 Pemetrexed 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

Fotemustine

Muphoran · Nitrosourea (alkylating)

Profile

Class delayed cumulative tubulointerstitial/ATN; usually mild; acute signal often really cisplatin.

CINATNLYTE

Moderate#1 · 77% phenotype match

Pentostatin

Nipent · Purine analog (ADA inhibitor)

Profile

Renally cleared; dose-related acute kidney injury.

ATNLYTESIADH

Moderate#2 · 76% phenotype match

Nimustine (ACNU)

Nidran · Nitrosourea (alkylating)

Profile

Water-soluble nitrosourea; renal risk inferred at class level; cumulative delayed tubulointerstitial injury; DLT is myelosuppression.

CINATNLYTE

Moderate#3 · 76% phenotype match

Vemurafenib

Zelboraf · BRAF inhibitor

Profile

Strongest renal offender of the BRAF/MEK class: proximal tubular injury/Fanconi and early AKI.

ATNFANCLYTE

Moderate#4 · 68% phenotype match

Lutetium-177 PSMA-617 (vipivotide)

Pluvicto · Radioligand therapy (PSMA)

Profile

PSMA-targeted radioligand for prostate cancer; renal radiation exposure and xerostomia.

CINLYTE

Moderate#5 · 62% phenotype match

Azacitidine

Vidaza · Hypomethylating agent

Profile

Proximal (type 2) RTA / Fanconi-like tubulopathy; overt AKI uncommon.

FANCATNLYTE

Moderate#6 · 56% phenotype match

Compare Pemetrexed 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 Antimetabolites

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 Pemetrexed’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 Pemetrexed; 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 81 clinical records among all 111 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.