Axitinib
Inlyta · VEGFR TKI
Potent VEGFR-TKI; hypertension and proteinuria dominate.
HTNGLOMTMA
Moderate#1 · 100% phenotype match
Pazopanib
Votrient · Pazo
VEGFR TKI · approved 2009 · 9 citations
Recent· through 2024
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 2024
- 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 VEGFR tyrosine kinase inhibitor that throttles glomerular VEGF housekeeping signaling, producing the class triad of hypertension, proteinuria, and occasional renal-limited thrombotic microangiopathy.
ModerateVEGFR tyrosine kinase inhibitor
Advanced renal cell carcinomaAdvanced soft-tissue sarcoma (after prior chemotherapy)
§01
Signature kidney injury
Signature lesion
Representative incidence15%
Proteinuria is common but usually low-grade, and reported any-grade rates span roughly 15% to 80% depending on the population and how proteinuria was ascertained. In a pooled secondary analysis of two phase III trials of pazopanib or sunitinib in metastatic RCC (n=1392, Sorich 2016), any-grade proteinuria occurred in 15.0% and grade 3/4 in 3.7% — a trial adverse-event figure covering both agents, not a pazopanib-specific rate. In a single-center first-line mRCC cohort, proteinuria was reported in 80% of the pazopanib-treated patients (Land 2016), most grade 1-2 and managed with continued monitoring at the same dose. Assume proteinuria is the expectation rather than the exception on pazopanib and schedule urine protein monitoring accordingly. Hypertension is one of the most frequent class effects, with severe (grade 3-4) hypertension a recognized class risk. Thrombotic microangiopathy is rare and largely case-level; biopsy-proven renal-limited and systemic TMA/TTP-like presentations have been reported.Source: Sorich, Br J Cancer 2016 (pooled phase III, pazopanib or sunitinib); pazopanib-specific cohort reports 80% (Land, J Oncol Pharm Pract 2016)
Onset & rechallenge
Time to injurySubacute (~1–6 weeks)
Proteinuria and hypertension within weeks to a few months; TMA case reports within the first weeks to ~2 months.
Distilled from: “Proteinuria and hypertension typically emerge within weeks to a few months of starting therapy; TMA case reports describe onset within the first weeks to ~2 months.”
Long-term outlook & thresholds
Early-detection biomarkers
- Quantified urine protein at baseline and each cycle — Glomerular filtration-barrier injury — this agent's signature renal lesion. In a 129-patient first-line metastatic RCC cohort, 80% of the pazopanib arm developed proteinuria (35 patients; the abstract's n counts those with proteinuria, not the arm), and the grading is what makes it actionable rather than alarming: most events were grade 1–2, and at peak proteinuria 80% of those 35 (n = 28) were managed with continued monitoring at the same dose, while treatment modification or discontinuation is reserved for grade 3–4. Pooled phase III data put any-grade proteinuria at 15.0% and grade 3/4 at 3.7%, and identify pre-existing grade 1 proteinuria, baseline systolic pressure, diabetes, Asian ethnicity and prior nephrectomy as independent predictors — so a baseline measurement stratifies as well as anchors. The same pooled analysis found grade 3/4 proteinuria associated with IMPROVED overall survival, which is the recurring caution of this class: the toxicity partly marks exposure to a working drug.PMID 25505255 (opens PubMed in a new tab)
- Blood pressure — VEGF-pathway vasoconstriction, and on this agent the pressure and the proteinuria are linked rather than independent. Across 13 trials and 1,651 patients on single-agent pazopanib, all-grade hypertension ran 35.9% and high-grade 6.5%. The clinically useful discrimination is where pazopanib differs from its peers: its all-grade risk is substantially higher than sorafenib (RR 1.99) and sunitinib (RR 2.20), while its HIGH-grade risk is statistically indistinguishable from either — so expect to treat more hypertension on this drug without expecting more severe hypertension. Baseline systolic pressure is also an independent predictor of later proteinuria on this agent, so the two rows here inform each other.PMID 23178953 (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.
Proteinuria from VEGF-signaling inhibition: mild/asymptomatic in ~21-63%, heavy (nephrotic-range) in up to ~6.5% of RCC patients; reflects glomerular podocyte/slit-diaphragm injury. PMID 20006922 (opens PubMed in a new tab)
Hypertension is among the most common adverse events with pazopanib in the pivotal phase III RCC trial; prospectively documented BP rise within 4 weeks of therapy. PMID 20100962 (opens PubMed in a new tab)
Uncommon; biopsy-proven drug-induced thrombotic microangiopathy reported at the case level (VEGF-inhibitor endothelial injury). PMID 33850692 (opens PubMed in a new tab)
Toxicity fingerprint
Tap a signature to trace where it strikes the nephron.
15%incidence
SeverityModerate
ReversibilityPartially reversible
Evidence9 citations
Nephron map
GlomerulusFiltration barrier (podocytes + endothelium)
Vasculature / Endothelium
Glomerular Injury / Proteinuria
Damage to the filtration barrier — podocyte injury, FSGS and protein leak from VEGF and mTOR blockade.
§03
Kidney injury
Mechanism of kidney injury
Inhibition of VEGFR2 signaling disrupts the constitutive paracrine VEGF-A signal from podocytes to the glomerular endothelium that maintains the fenestrated filtration barrier. Loss of this housekeeping signal causes endothelial dysfunction, reduced nitric oxide and prostacyclin (driving hypertension), podocyte and endothelial injury (proteinuria, sometimes nephrotic-range, with minimal-change/FSGS-like or endotheliosis patterns), and in some patients a localized thrombotic microangiopathy. A biopsy of a pazopanib-treated patient with nephrotic syndrome showed glomerular endothelial injury with podocyte changes that resolved on drug withdrawal.
Clinical presentation
Most often new or worsening hypertension and asymptomatic dipstick/quantified proteinuria detected on routine monitoring; occasionally nephrotic-range proteinuria with edema. TMA may present with a rising creatinine, hypertension, and bland or nephrotic urine, with or without systemic microangiopathic hemolysis (thrombocytopenia, schistocytes); reported cases span renal-limited TMA in a transplant graft to a systemic TTP-like syndrome with acute kidney injury.
Management
Manage hypertension proactively per standard antihypertensive guidance (ACE inhibitors/ARBs are commonly favored for concurrent proteinuria). For low-grade proteinuria, continue at the same dose with monitoring; for grade 3-4 or nephrotic-range proteinuria, interrupt, dose-reduce, or discontinue. For suspected TMA, hold/discontinue pazopanib; case reports describe improvement after withdrawal, and ADAMTS13-low presentations have responded to plasma exchange. Discontinuation often leads to partial or full resolution of proteinuria and renal function.Lesion-level management framework
§ Receptor target map
Which kinases Pazopanib blocks — and where the blockade reaches the kidney
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
Other receptor kinases
FGFRRETMETEGFRFLT3AXLCSF1RTIE2RAF-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 (3)targetednot a target
Risk factors
- Pre-existing proteinuria
- Pre-existing/baseline hypertension
- Diabetes
- Prior nephrectomy (common in RCC)
- Asian ethnicity (per pooled analysis)
- Reduced renal reserve / solitary kidney
- Concurrent calcineurin inhibitor or kidney transplant (TMA susceptibility)
Prevention
- Optimize blood pressure before and during treatment
Anticancer mechanism· how it treats cancer
Oral multi-targeted tyrosine kinase inhibitor of VEGFR-1/2/3, PDGFR-alpha/beta, and c-KIT; blocks tumor angiogenesis by interrupting VEGF-driven endothelial proliferation and vascular sprouting.
Note · Pazopanib-specific renal evidence is dominated by class-level cohort/trial proteinuria-hypertension data plus biopsy-level case reports for TMA and podocyte/endothelial injury; mechanistic and TMA claims are hedged accordingly.
§04
Clinical depth
Renal dose adjustment
No starting-dose adjustment is generally required for mild-to-moderate renal impairment; data in patients with CrCl <30 mL/min are limited. Pazopanib undergoes predominantly hepatic metabolism (CYP3A4) with minimal renal excretion, so renal impairment is not the principal pharmacokinetic driver; dose modification is guided more by hepatic function and toxicity (including proteinuria) than by GFR.
Dialyzability & ESKD dosing
Not meaningfully dialyzable — pazopanib is highly protein-bound (>99%) and largely hepatically cleared, so hemodialysis is not expected to remove appreciable drug.
Differential diagnosis
Distinguish VEGF-inhibitor effect from pre-existing hypertensive/diabetic nephropathy, RCC-related paraneoplastic glomerulopathy, contrast- or other nephrotoxin-associated AKI, and prerenal azotemia from GI losses. TMA must be separated from primary TTP (ADAMTS13 activity), atypical HUS, and calcineurin-inhibitor-associated TMA in transplant recipients.
Monitoring
- Urinalysis / urine protein-to-creatinine ratio at baseline and periodically
- Blood pressure (often weekly early, then routinely)
- CBC with smear and LDH/haptoglobin if TMA suspected
Key trials & series
- VEG105192 / COMPARZ-era phase III RCC programs (pooled for proteinuria risk analysis, Sorich 2016)
- BIONIKK phase II (VEGFR-TKI arm including pazopanib; grade 3-4 hypertension and a TMA death noted in TKI recipients)
Clinical pearls
- The hypertension-proteinuria pairing is a direct on-target marker of effective VEGF pathway blockade, not an idiosyncratic reaction.
- Most pazopanib proteinuria is grade 1-2 and can be monitored without dose change; reserve interruption/discontinuation for grade 3-4 or nephrotic-range disease.
- On-therapy proteinuria was associated with improved overall survival in the pooled mRCC analysis — a possible pharmacodynamic signal, not a reason to ignore it.
- Renal TMA can be biopsy-proven and renal-limited (normal platelets/smear) — a rising creatinine on a VEGFR-TKI warrants suspicion even without systemic hemolysis.
- A pazopanib-associated TTP-like case had transiently undetectable ADAMTS13 that normalized after plasma exchange, blurring the TMA/TTP boundary.
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
8 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
8 references · 2016–2024 · 2 since 2022Primary (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.
- 1.LandmarkTherapeutic Inhibition of VEGF Signaling and Associated Nephrotoxicities.Estrada CC, Maldonado A, Mallipattu SK · J Am Soc Nephrol · 2019 · PMID 30642877Authoritative mechanistic review establishing that VEGFR tyrosine kinase inhibition preferentially causes glomerulopathy (minimal change/FSGS) plus hypertension and proteinuria, with TMA also described — the mechanistic backbone for this profile.
- 2.Risk factors of proteinuria in renal cell carcinoma patients treated with VEGF inhibitors: a secondary analysis of pooled clinical trial dataSorich MJ, Rowland A, Kichenadasse G, Woodman RJ, Mangoni AA · Br J Cancer · 2016 · PMID 27228299Pooled phase III data (n=1392, pazopanib or sunitinib) quantifying any-grade proteinuria at 15.0% and grade 3/4 at 3.7%, defining risk factors and the survival association — source of the headline incidence.
- 3.Proteinuria with first-line therapy of metastatic renal cell cancerLand JD, Chen AH, Atkinson BJ, Cauley DH, Tannir NM · J Oncol Pharm Pract · 2016 · PMID 25505255Retrospective review of 129 patients prospectively enrolled in a phase II trial, reporting proteinuria in 80% of pazopanib-treated mRCC patients, mostly low-grade and managed with continued monitoring — supports incidence and management framing.
- 4.Pazopanib-induced Endothelial Injury with Podocyte ChangesMaruyama K, Nakagawa N, Suzuki A, Kabara M, Matsuki M, Shindo M, Ogawa Y, Hasebe N · Intern Med · 2017 · PMID 29269661Biopsy-proven case of pazopanib nephrotic syndrome showing glomerular endothelial injury with podocyte changes that resolved on withdrawal — direct histologic basis for the glomerular signature mechanism.
- 5.Thrombotic Microangiopathy Associated with Pazopanib in a Kidney Transplant RecipientKalla S, Ellis RJ, Campbell SB, Doucet B, Isbel N, Tie B, Jegatheesan D · J Kidney Cancer VHL · 2021 · PMID 33850692First reported biopsy-proven case of pazopanib-attributed renal TMA (in a transplant graft), with nephrotic-range proteinuria and graft dysfunction improving after drug cessation — supports the TMA signature.
- 6.Thrombotic Thrombocytopenic Purpura Associated with PazopanibSyed U, Wahlberg KJ, Douce DR, Sprague JR · Case Rep Hematol · 2018 · PMID 30057830Case of pazopanib-associated systemic TMA/TTP-like syndrome with AKI, schistocytes, and transiently undetectable ADAMTS13 responding to plasma exchange — illustrates the systemic end of the TMA spectrum.
- 7.A case of pazopanib-induced acute kidney injury, reversible hair depigmentation and radiation recall dermatitisLi J, Li Z, Su T · Ren Fail · 2023 · PMID 37264782Case report documenting pazopanib-associated acute kidney injury, supporting the broader renal-injury spectrum beyond proteinuria/hypertension.
- 8.Ocular and systemic vascular endothelial growth factor ligand inhibitor use and nephrotoxicity: an updateRangaswamy D, Nagaraju SP, Bhojaraja MV, Swaminathan SM, Prabhu RA, Rao IR, Shenoy SV · Int Urol Nephrol · 2024 · PMID 38498275Recent comprehensive review of VEGF-inhibitor renal adverse effects (hypertension, proteinuria, renal dysfunction, TMA, electrolyte disturbances) contextualizing pazopanib within the class.
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.
FDA label — boxed warning & renal dosing· boxed warning · renal impairment
Quoted verbatim from this agent's current FDA label (May 2026) — not paraphrased or interpreted. Full label on DailyMed .
Boxed warning
WARNING: HEPATOTOXICITY Severe and fatal hepatotoxicity has been observed in clinical trials. Monitor hepatic function and interrupt, reduce, or discontinue dosing as recommended [see Warnings and Precautions (5.1)]. WARNING: HEPATOTOXICITY See full prescribing information for complete boxed warning. Severe and fatal hepatotoxicity has been observed in clinical trials. Monitor hepatic function and interrupt, reduce, or discontinue dosing as recommended. (5.1)
Renal impairment — from the label
No dose adjustment is recommended for patients with renal impairment. Pazopanib has not been studied in patients with severe renal impairment or in patients undergoing peritoneal dialysis or hemodialysis.
What gets reported — FAERS
Everything below is FAERS — adverse events someone chose to report, about 26,904 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· 6 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 6.88 — on the terms that name the lesion (ROR 5.57)
- Hypertensioncorroborated · ROR 4.54 — on the terms that name the lesion (ROR 4.84)
- Thrombotic Microangiopathycorroborated · ROR 1.56
Glomerular Injury / Proteinuria
ROR 6.8895% CI 6.08–7.79· 253 reports
Hypertension
ROR 4.5495% CI 4.34–4.74· 2,098 reports
Thrombotic Microangiopathy
ROR 1.5695% CI 1.10–2.22· 31 reports
SIADH / Hyponatremia
ROR 1.4295% CI 1.20–1.67· 146 reports
Electrolyte Disturbance
ROR 1.3995% CI 1.25–1.54· 339 reports
Hemorrhagic Cystitis
ROR 1.3395% CI 1.11–1.59· 118 reports
FAERS outcomes & reporting trend· 25.8% of reports w/ death · 22.4% w/ hospitalization
25.8%
Reported with a death outcome
6,942 of 26,904 reports
22.4%
Reported with hospitalization
6,030 of 26,904 reports
Reports per year
- 2015: 3,630 reports
- 2016: 2,597 reports
- 2017: 2,672 reports
- 2018: 2,555 reports
- 2019: 2,281 reports
- 2020: 1,676 reports
- 2021: 1,342 reports
- 2022: 991 reports
- 2023: 855 reports
- 2024: 473 reports
- 2025: 317 reports
- 2026: 185 reports
Yearly FAERS report volume · most recent year is partial.
FAERS adverse-event signal — all organ systems· 8 systems · 26,904 reports
Bars rank systems by summed reaction-term mentions (a report counts once per term it names) — an ordinal “more vs less reported” cue, not a tally of distinct reports. Renal & urinary first. As of 2026-10-01.
Disproportionality (acute kidney injury):ROR 0.9095% CI 0.78–1.04· 176 AKI reports ·no disproportionate AKI reporting signal (CI spans 1).
Gastrointestinal
Diarrhoea3,606Nausea2,419Vomiting1,405Abdominal Pain518Abdominal Pain Upper490
General / constitutional
Fatigue2,490Asthenia932Malaise903Weight Decreased882Pain677
Vascular
Hypertension1,263Blood Pressure Increased786
Nervous system
Headache717Dysgeusia504Dizziness417
Metabolic & electrolyte
Decreased Appetite1,438
Respiratory
Dyspnoea845
Skin
Rash499
Musculoskeletal
Pain In Extremity415
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 Pazopanib 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.
Phenotype-similar agents· the numbered markers on the map above
Profile
Ziv-aflibercept
Zaltrap · VEGF trap
Hypertension and proteinuria like bevacizumab.
HTNGLOMTMA
Moderate#2 · 98% phenotype match
Bevacizumab
Avastin · Anti-VEGF antibody
Proteinuria, hypertension, glomerular TMA.
GLOMHTNTMA
Moderate#3 · 98% phenotype match
Ramucirumab
Cyramza · Anti-VEGFR2 antibody
Hypertension and proteinuria, class effect.
HTNGLOMTMA
Moderate#4 · 98% phenotype match
VEGFR TKIs (sunitinib · sorafenib · pazopanib · axitinib)
VEGFR TKI
Hypertension as an on-target marker; proteinuria.
HTNGLOMTMA
Moderate#5 · 98% phenotype match
Nintedanib
Ofev · VEGFR/FGFR/PDGFR TKI
Proteinuria and rare TMA.
HTNTMAGLOM
Mild#6 · 93% phenotype match
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.
- 1NintedanibHTN — HypertensionMild
- 2CabozantinibHTN — HypertensionModerate
- 3RegorafenibHTN — HypertensionModerate
- 4TivozanibHTN — HypertensionModerate
- 5FruquintinibHTN — HypertensionModerate
- 6Pazopanib· this agentGLOM — Glomerular Injury / ProteinuriaModerate
- 7RamucirumabHTN — HypertensionModerate
- 8VandetanibHTN — HypertensionModerate
- 9VEGFR TKIs (sunitinib · sorafenib · pazopanib · axitinib)HTN — HypertensionModerate
- 10Ziv-afliberceptHTN — HypertensionModerate
- 11SorafenibHTN — HypertensionModerate
- 12SunitinibHTN — HypertensionModerate
- 13LenvatinibHTN — HypertensionFAERS AKIModerate
- 14AxitinibHTN — HypertensionFAERS AKIModerate
- 15BevacizumabGLOM — Glomerular Injury / ProteinuriaFAERS AKIModerate
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 Pazopanib’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 Pazopanib; the PMIDs beside each name are up to three of their most recent papers on it, not the full count.
- Sleijfer, Stefan — their work on Pazopanib, on PubMed (opens in a new tab)2 papers · 572 citesPMID 30831041 (opens PubMed in a new tab)PMID 19451427 (opens PubMed in a new tab)
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 41 clinical records among all 50 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.