How should kidney function be monitored during Axitinib therapy?

Blood pressure at baseline and frequently during the first weeks, then regularly (home monitoring is useful); Urine protein at baseline and periodically (dipstick or urine protein-to-creatinine ratio); quantify if positive; CBC with smear and LDH/haptoglobin if thrombotic microangiopathy is suspected (anemia, thrombocytopenia, schistocytes); Serum creatinine at baseline and periodically during therapy.

How can kidney injury from Axitinib be prevented?

Optimize blood pressure before starting and control pre-existing hypertension Use guideline-based blood-pressure monitoring with prompt initiation/titration of antihypertensives (ACE inhibitors/ARBs are commonly preferred, also for their antiproteinuric effect) Follow protocol dose-titration rules that withhold dose escalation in patients with uncontrolled hypertension

Who is at higher risk of kidney injury from Axitinib?

Pre-existing or poorly controlled hypertension; Higher axitinib exposure / dose titration (effects are dose-related); Pre-existing chronic kidney disease or proteinuria; Concurrent or sequential use of other VEGF-pathway inhibitors; Underlying renal cell carcinoma with a single/remnant kidney after nephrectomy.

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Printable monograph

VEGFR TKI

Axitinib

Inlyta · Axi

VEGFR TKI · approved 2012 · 7 citations · FAERS AKI reporting ROR 1.41 (95% CI 1.23–1.63, 198 AKI reports)

Recent· through 2023

Deeply sourced8/9 · 7 signals

Met: 7 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 14y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2023
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 potent, selective second-generation VEGFR inhibitor whose renal signature is dose-related hypertension and proteinuria, with thrombotic microangiopathy at the severe end of the spectrum.

ModerateVEGFR tyrosine kinase inhibitor

Advanced (metastatic) renal cell carcinoma after failure of one prior systemic therapy (second-line monotherapy)First-line advanced renal cell carcinoma in combination with an immune checkpoint inhibitor (e.g., pembrolizumab or avelumab)

§01

Signature kidney injury

Signature lesion

Hypertension

Representative incidence40.4%

Hypertension is the dominant and best-quantified renal-relevant signal. In the randomized phase III AXIS trial, treatment-emergent all-causality hypertension occurred in 40.4% of axitinib-treated patients (vs 29.0% with sorafenib), with grade 3 hypertension in 15.3% and grade 4 in 0.3%. A real-world VEGFR-TKI cohort in metastatic RCC similarly found hypertension to be the single most common anti-angiogenesis-related adverse event (about 48.6% in TKI-naive patients across the class). Proteinuria is the next most common renal effect; across the VEGF-inhibitor class mild/asymptomatic proteinuria is reported in roughly 21% to 63% of patients, with heavy (nephrotic-range) proteinuria in up to about 6.5% of RCC patients, and axitinib-specific proteinuria rates have been higher in some populations (e.g., Japanese cohorts). Thrombotic microangiopathy and other glomerular lesions (FSGS-like injury, podocytopathy, hyaline occlusive glomerular microangiopathy) are reported at the severe, biopsy-level end of the spectrum but are not precisely quantified for axitinib specifically.Source: Rini, Target Oncol 2014 (AXIS hypertension analysis)

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Hypertension early (days to the first few weeks); proteinuria over weeks; severe glomerular lesions later and more variable.

Distilled from: “Hypertension typically emerges early, frequently within days to the first few weeks of starting therapy. Proteinuria tends to develop over weeks of continued exposure and is dose-related. Severe glomerular lesions (TMA, nephrotic syndrome) are usually later and more variable in timing.”

Long-term outlook & thresholds

Early-detection biomarkers

Blood pressure — VEGF-pathway vasoconstriction — this agent's most frequent toxicity. In the randomised phase III trial, treatment-emergent hypertension occurred in 40.4% of axitinib-treated patients versus 29.0% on sorafenib, with grade 3 in 15.3% and 10.7% respectively. The management read is as important as the rate: hypertension-related sequelae occurred in under 1% of axitinib patients, and roughly half of those with grade 3 or 4 hypertension continued treatment for nine months or more. So this is a number to treat and keep treating through, not a number to stop for.PMID 24595903 (opens PubMed in a new tab)
Urine protein at BASELINE, then quantified serially — Pre-existing filtration-barrier vulnerability — the strongest pre-treatment predictor of this drug's dose-limiting toxicity. The unusual row in this file: a marker that earns its place before the first dose. Baseline urine protein was associated with later development of proteinuria ≥2 g/24 h (hazard ratio 5.457 for baseline ≥1+ versus <1+), and it correlated MORE strongly with axitinib-related proteinuria than other baseline renal-function values or blood pressure — which is the direct argument for checking protein rather than creatinine here. That threshold matters because 28% of patients crossed it and required dose reduction, interruption or discontinuation, making proteinuria a major cause of stopping treatment. Generalise with care: 64 Japanese cytokine-refractory patients, whose 84% hypertension rate (70% grade ≥3) is roughly double the phase III figure, so this cohort is more toxicity-prone than the population most readers will treat.PMID 21889330 (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.

§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.

Hypertension#1 · Signature25%PMID 29353818 (opens PubMed in a new tab)
On-target VEGFR effect; axitinib safety meta-analysis reported high-grade (grade >=3) hypertension in ~24.9% (all-grade rates ~40%), the most common adverse event
Glomerular Injury / ProteinuriaSecondaryno population incidence denominator
VEGF-signaling inhibition (nephrin suppression/podocyte injury) causes proteinuria in ~21-63% overall, with heavy/nephrotic-range proteinuria up to ~6.5% in RCC patients PMID 20006922 (opens PubMed in a new tab)
Thrombotic MicroangiopathyRareno population incidence denominator
Glomerular thrombotic microangiopathy is the main VEGF-inhibition-associated kidney lesion but occurs at case-level frequency; no reliable axitinib-specific incidence PMID 20006922 (opens PubMed in a new tab)

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

40.4%incidence

SeverityModerate

ReversibilityPartially reversible

Evidence7 citations

Nephron map

GlomerulusFiltration barrier (podocytes + endothelium)

Vasculature / EndotheliumGlomerular & peritubular capillaries

Hypertension

Raised blood pressure — archetypally on-target loss of endothelial nitric oxide from VEGF-pathway blockade, studied as a pharmacodynamic marker of drug exposure. Other agents raise it too: vascular effects of BCR-ABL, BTK and RET inhibitors and of copanlisib; abiraterone's mineralocorticoid excess; androgen suppression or blockade.

§03

Kidney injury

Mechanism of kidney injury

Most renal toxicity is on-target VEGF-pathway inhibition acting on the glomerulus and vasculature. VEGF is constitutively produced by podocytes and is essential for the health of the glomerular endothelium and the slit-diaphragm protein nephrin; blocking VEGFR signaling downregulates or suppresses nephrin and injures glomerular endothelial cells, producing proteinuria and, in severe cases, a glomerular thrombotic microangiopathy (endothelial swelling, fibrin thrombi, mesangiolysis). The same loss of endothelial VEGF tone reduces nitric oxide and prostacyclin and causes rarefaction of the microvasculature, raising systemic vascular resistance and driving hypertension. Other reported glomerular patterns (focal segmental glomerulosclerosis, minimal-change-like podocytopathy) are thought to reflect podocyte injury from VEGF deprivation. These are class effects shared across VEGF/VEGFR inhibitors.

Clinical presentation

New or worsening hypertension, often within the first weeks of therapy, is the most common presentation and may be marked. Proteinuria ranges from asymptomatic dipstick/quantitative proteinuria detected on monitoring to overt nephrotic-range proteinuria with edema. The severe phenotype is a thrombotic microangiopathy or nephrotic syndrome with proteinuria, variable serum creatinine elevation, and sometimes microangiopathic hemolytic features; renal biopsy in such cases may show TMA, FSGS, or a hyaline occlusive glomerular microangiopathy pattern. Serum creatinine is often normal or only mildly elevated even with heavy proteinuria.

Management

Hypertension is managed with standard antihypertensive therapy (ACE inhibitors or ARBs are often favored, partly for antiproteinuric benefit), alongside axitinib dose interruption or reduction for grade 3 or persistent hypertension; in AXIS, hypertension led to dose interruption in 12.8%, dose reduction in 4.5%, and discontinuation in only 0.3%, and roughly half of patients with grade 3-4 hypertension continued treatment for 9 months or more. For significant or nephrotic-range proteinuria, hold or reduce the drug, add/optimize RAAS blockade, and refer to nephrology; proteinuria often improves but may persist after discontinuation. Suspected thrombotic microangiopathy or biopsy-proven severe glomerular injury generally warrants stopping the VEGF inhibitor; withdrawal frequently leads to improvement, and a short corticosteroid course has been used in selected biopsy-proven glomerular cases.Lesion-level management framework

§ Receptor target map

Which kinases Axitinib blocks — and where the blockade reaches the kidney

3targeted

VEGFR2 is the target with documented renal consequences across every VEGFR TKI; multi-kinase breadth beyond it (PDGFR-β, FGFR, and off-target receptor kinases) adds further renal and hypertensive liability. Select a lit receptor for its renal consequence.

VEGFR family

PDGFR

PDGFR-αPDGFR-β

Other receptor kinases

FGFRKITRETMETEGFRFLT3AXLCSF1RTIE2RAF-1/BRAF

VEGFR2 · renal target

Glomerular endothelial VEGFR2: loss of podocyte-derived paracrine VEGF signaling → fenestrae loss, nephrin downregulation, nitric-oxide depletion → hypertension, proteinuria, and thrombotic microangiopathy.

renal consequence (1)targetednot a target

Risk factors

Pre-existing or poorly controlled hypertension
Higher axitinib exposure / dose titration (effects are dose-related)
Pre-existing chronic kidney disease or proteinuria
Concurrent or sequential use of other VEGF-pathway inhibitors
Underlying renal cell carcinoma with a single/remnant kidney after nephrectomy

Prevention

Optimize blood pressure before starting and control pre-existing hypertension
Use guideline-based blood-pressure monitoring with prompt initiation/titration of antihypertensives (ACE inhibitors/ARBs are commonly preferred, also for their antiproteinuric effect)
Follow protocol dose-titration rules that withhold dose escalation in patients with uncontrolled hypertension

Anticancer mechanism· how it treats cancer

Axitinib is an oral, potent, selective second-generation small-molecule tyrosine kinase inhibitor that blocks vascular endothelial growth factor receptors VEGFR-1, VEGFR-2, and VEGFR-3 at subnanomolar concentrations. By interrupting VEGF-driven angiogenic signaling, it starves the tumor of neovascularization. Its high selectivity for the VEGFR family (relative to first-generation multi-kinase inhibitors) underlies both its antitumor potency and a renal/vascular toxicity profile dominated by on-target VEGF-pathway effects.

§04

Clinical depth

Renal dose adjustment

No renal dose adjustment is generally required across the range of baseline renal function studied, and patients with mild-to-severe renal impairment have been treated, though data in end-stage renal disease are very limited. Less than 1% of an administered dose is excreted unchanged in urine (axitinib is cleared primarily by hepatic CYP3A4/1A2 metabolism), so renal clearance is not a major elimination route. Dose modification in practice is driven by toxicity (e.g., uncontrolled hypertension, proteinuria) rather than by creatinine clearance, using protocol-based interruptions and reductions.

Dialyzability & ESKD dosing

Not well characterized. Axitinib is a small-molecule, highly protein-bound (>99%) oral TKI with predominantly hepatic clearance and minimal (<1%) urinary excretion of unchanged drug, so meaningful removal by hemodialysis is considered unlikely; specific dialysis-removal data are lacking.

Differential diagnosis

Distinguish VEGF-inhibitor hypertension/proteinuria (on-target, dose-related, often reversible) from pre-existing essential hypertension and diabetic or hypertensive nephropathy. In a patient with heavy proteinuria, declining filtration, or hematologic changes, consider drug-induced thrombotic microangiopathy versus other glomerular lesions (FSGS, minimal-change-like podocytopathy, hyaline occlusive glomerular microangiopathy) — biopsy distinguishes these. When axitinib is combined with an immune checkpoint inhibitor (e.g., pembrolizumab), also consider checkpoint-inhibitor acute interstitial nephritis or ICI-associated podocytopathy as an alternative or contributing cause of renal injury.

Monitoring

Blood pressure at baseline and frequently during the first weeks, then regularly (home monitoring is useful)
Urine protein at baseline and periodically (dipstick or urine protein-to-creatinine ratio); quantify if positive
CBC with smear and LDH/haptoglobin if thrombotic microangiopathy is suspected (anemia, thrombocytopenia, schistocytes)
Serum creatinine at baseline and periodically during therapy

Key trials & series

AXIS (Rini et al., Lancet 2011): randomized phase III of axitinib vs sorafenib as second-line therapy in metastatic RCC; longer PFS with axitinib (6.7 vs 4.7 months); hypertension among the most common adverse events
AXIS hypertension analysis (Rini et al., Target Oncol 2014): all-causality hypertension 40.4% with axitinib vs 29.0% with sorafenib; grade 3 in 15.3%; rarely led to discontinuation or cardiovascular sequelae

Clinical pearls

Hypertension is the headline renal-vascular toxicity and is more frequent with axitinib than with sorafenib (AXIS: 40.4% vs 29.0%).
Treatment-emergent hypertension/elevated diastolic BP has been explored as a potential pharmacodynamic biomarker of axitinib efficacy, but this remains investigational.
Heavy proteinuria can occur with a near-normal serum creatinine — monitor urine protein, not just creatinine.
Proteinuria and hypertension are class effects of VEGF-pathway blockade (shared with bevacizumab, sunitinib, sorafenib, pazopanib) driven by podocyte/glomerular-endothelial VEGF deprivation.
In axitinib + checkpoint-inhibitor regimens, new kidney injury has a broader differential that includes immune-mediated interstitial nephritis and podocytopathy.

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

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

Vascular

Hypertension, VTE/ATE, bleeding, aneurysm

Hypertension, arterial/venous thrombosis, bleeding, impaired wound healing

Cardiac

Cardiomyopathy, QT, ischemia, myocarditis

LV dysfunction; QT (some TKIs)

Gastrointestinal

Diarrhea, colitis, mucositis, perforation

Diarrhea, perforation/fistula

Dermatologic

Rash, HFS, SJS/TEN, vitiligo

Hand-foot skin reaction

§05

References

7 primary references — trials, cohorts, mechanism, and reviews. Citation metadata via PubMed / NLM.

Evidence accrual

7 references · 2009–2023 · 3 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.

FDA label — boxed warning & renal dosing· renal impairment

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

Renal impairment — from the label

No dedicated renal impairment trial for axitinib has been conducted. Based on the population pharmacokinetic analyses, no significant difference in axitinib clearance was observed in patients with pre-existing mild to severe renal impairment (15 mL/min ≤creatinine clearance [CLcr] <89 mL/min) [see Clinical Pharmacology (12.3) ] . No starting dose adjustment is needed for patients with pre-existing mild to severe renal impairment. Caution should be used in patients with end-stage renal disease (CLcr <15 mL/min).

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 19,365 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· 5 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

Glomerular Injury / Proteinuriacorroborated · ROR 8.44 — on the terms that name the lesion (ROR 4.96)
Hypertensioncorroborated · ROR 6.97 — on the terms that name the lesion (ROR 7.07)
Thrombotic MicroangiopathyNo 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.

Glomerular Injury / Proteinuria

ROR 8.4495% CI 7.39–9.64· 223 reports

Hypertension

ROR 6.9795% CI 6.67–7.29· 2,226 reports

Acute Interstitial Nephritis

ROR 2.3295% CI 1.70–3.16· 40 reports

SIADH / Hyponatremia

ROR 1.4095% CI 1.16–1.70· 104 reports

Electrolyte Disturbance

ROR 1.3595% CI 1.19–1.54· 238 reports

FAERS outcomes & reporting trend· 20.2% of reports w/ death · 25.8% w/ hospitalization

20.2%

Reported with a death outcome

3,907 of 19,365 reports

25.8%

Reported with hospitalization

4,995 of 19,365 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 19,365 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 1.4195% CI 1.23–1.63· 198 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

Renal Cancer359

Gastrointestinal

Diarrhoea2,578Nausea1,143Stomatitis593Vomiting576Constipation521

General / constitutional

Fatigue2,115Weight Decreased802Asthenia761Malaise533Pain518

Vascular

Hypertension1,326Blood Pressure Increased851

Respiratory

Dysphonia1,010Dyspnoea514

Metabolic & electrolyte

Decreased Appetite1,087Dehydration386

Nervous system

Headache604Dizziness334

Skin

Rash481Palmar-Plantar Erythrodysaesthesia Syndrome452

Musculoskeletal

Pain In Extremity453Arthralgia445

Guidelines & consensus· 17

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.

KDIGOManagement of Blood Pressure in Patients With Chronic Kidney Disease Not Receiving Dialysis: Synopsis of the 2021 KDIGO Clinical Practice GuidelineAnn Intern Med 2021 · PMID 34152826Recommends standardized office BP measurement and a target systolic BP <120 mm Hg for most CKD patients, with RAAS inhibitors first-line when albuminuria is present — the BP-management basis for anti-VEGF/TKI-induced hypertension and proteinuria.ESC2022 ESC Guidelines on cardio-oncology developed in collaboration with the European Hematology Association (EHA), the European Society for Therapeutic Radiology and Oncology (ESTRO) and the International Cardio-Oncology Society (IC-OS)Eur Heart J 2022 · PMID 36017568For VEGF/VEGFR inhibitors, perform baseline cardiovascular risk assessment, monitor blood pressure (weekly during the first cycle, then regularly) and treat to a target <140/90 mmHg with ACE inhibitors/ARBs and dihydropyridine calcium-channel blockers; manage VEGFi-associated hypertension and proteinuria with interruption/dose modification when severe.ESCEuropean Society of Cardiology quality indicators for the prevention and management of cancer therapy-related cardiovascular toxicity in cancer treatmentEur Heart J Qual Care Clin Outcomes 2022 · PMID 36316010Adherence quality indicators require documented baseline cardiovascular risk assessment and structured monitoring of cardiovascular complications (including hypertension) during cancer therapy such as VEGF-pathway inhibitors.UK Consensus PanelUsing bevacizumab to treat metastatic cancer: UK consensus guidelinesBr J Hosp Med (Lond) 2010 · PMID 21135762Assess and monitor blood pressure and proteinuria during bevacizumab therapy; treat emergent hypertension to standard targets and interrupt/discontinue the drug for uncontrolled hypertension, nephrotic-range proteinuria or other severe vascular toxicity.

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 Axitinib 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

Pazopanib

Votrient · VEGFR TKI

Profile

VEGFR-TKI; hypertension, proteinuria, TMA.

GLOMHTNTMA

Moderate#1 · 100% phenotype match

Ziv-aflibercept

Zaltrap · VEGF trap

Profile

Hypertension and proteinuria like bevacizumab.

HTNGLOMTMA

Moderate#2 · 98% phenotype match

Bevacizumab

Avastin · Anti-VEGF antibody

Profile

Proteinuria, hypertension, glomerular TMA.

GLOMHTNTMA

Moderate#3 · 98% phenotype match

Ramucirumab

Cyramza · Anti-VEGFR2 antibody

Profile

Hypertension and proteinuria, class effect.

HTNGLOMTMA

Moderate#4 · 98% phenotype match

VEGFR TKIs (sunitinib · sorafenib · pazopanib · axitinib)

VEGFR TKI

Profile

Hypertension as an on-target marker; proteinuria.

HTNGLOMTMA

Moderate#5 · 98% phenotype match

Nintedanib

Ofev · VEGFR/FGFR/PDGFR TKI

Profile

Proteinuria and rare TMA.

HTNTMAGLOM

Mild#6 · 92% phenotype match

Compare Axitinib 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 Anti-angiogenic (VEGF)

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 Axitinib’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 Axitinib; 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 47 clinical records among all 57 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.