How should kidney function be monitored during Sunitinib therapy?

Blood pressure at baseline and each visit/cycle (consider home monitoring early on); Urine protein (dipstick or urine protein-to-creatinine ratio) at baseline and periodically; CBC for anemia/thrombocytopenia and peripheral smear/LDH/haptoglobin if TMA suspected; Serum creatinine at baseline and serially during therapy.

How can kidney injury from Sunitinib be prevented?

Optimize/treat pre-existing hypertension before and during therapy

Who is at higher risk of kidney injury from Sunitinib?

Pre-existing hypertension; Pre-existing chronic kidney disease or proteinuria; Prior or concurrent VEGF-pathway therapy (e.g., bevacizumab); Solitary kidney / prior nephrectomy (common in RCC); Higher dose and continuous (vs intermittent) dosing schedules.

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Printable monograph

VEGFR TKI

Sunitinib

Sutent · Suni

VEGFR TKI · approved 2006 · 8 citations

Up to date· through 2026

Deeply sourced7/9 · 6 signals

Met: 8 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 18y)
Met: Beyond single case reports
Met: High-impact journal
Met: Landmark reference
Met: Current through 2026
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 whose anti-angiogenic action injures the glomerular endothelium and podocyte, producing near-ubiquitous hypertension, proteinuria, and, in severe cases, a renal-limited thrombotic microangiopathy.

ModerateVEGFR TKI

Metastatic/advanced renal cell carcinoma (first-line)Imatinib-resistant or intolerant gastrointestinal stromal tumor (GIST)Advanced pancreatic neuroendocrine tumorsAdjuvant therapy of high-risk RCC after nephrectomy

§01

Signature kidney injury

Signature lesion

Hypertension

Representative incidence21.6%

In a systematic review/meta-analysis of 4,999 patients across 13 trials, all-grade hypertension occurred in ~21.6% and high-grade hypertension in ~6.8% of sunitinib-treated patients, with a significantly increased risk of renal dysfunction versus controls (RR ~1.36); risk varied by tumor type and dosing schedule. Proteinuria is common but less consistently quantified, and severe glomerular lesions (thrombotic microangiopathy, nephrotic-range proteinuria) are reported mainly at the case-series level. Reported figures are class-consistent with other VEGF-pathway inhibitors.Source: Zhu, Acta Oncol 2009

Onset & rechallenge

Time to injuryVariable / unpredictable

Hypertension early (first cycle/weeks); proteinuria over weeks to months; biopsy-proven TMA on average ~2 years (range ~7-36 months) into therapy.

Distilled from: “Hypertension typically appears early (within the first treatment cycle/weeks); proteinuria develops over weeks to months, and biopsy-proven TMA in case series presented on average around 2 years (range ~7-36 months) into therapy.”

Long-term outlook & thresholds

Early-detection biomarkers

Blood pressure, by 24-h ambulatory or home monitoring through the first cycle — VEGF-withdrawal vasoconstriction — the earliest renal-vascular signal, and the one that decides whether full-dose therapy continues. The first cycle is where this happens: in a prospective ABPM study, 12 of the 14 patients who were normotensive at baseline (86%; the abstract prints 84%) needed antihypertensive treatment during cycle 1, while hypertension was infrequent afterwards and only 2 patients needed more medication later. Managing it properly is the point — 94% required no dose modification, and the authors argue ABPM plus guideline-directed treatment lets most patients stay on uninterrupted full dose. Read a rising pressure as a signal to treat, not to stop. Whether it also marks benefit is genuinely unsettled: this study found no correlation of hypertension with sunitinib efficacy, while a 770-patient multivariate analysis of sunitinib-treated mRCC patients found on-treatment hypertension (systolic >=140 mm Hg) independently associated with longer progression-free and overall survival (Donskov et al., Br J Cancer 2015, PMID 26492223). Do not present either as settled.PMID 21549588 (opens PubMed in a new tab)
Quantified proteinuria (24-h protein or protein–creatinine ratio) — Glomerular filtration-barrier injury — the presenting sign, and the one that precedes the TMA end of the spectrum. Measured before and 40 days into treatment in 20 patients, 24-hour proteinuria rose significantly, systolic and diastolic pressure rose significantly, and estimated GFR fell — so protein and pressure move together and early. Small and single-centre, and the authors say plainly that larger evidence is needed, so treat the direction as established and the magnitude as not. In the atlas's own biopsy material, proteinuria was often the first symptom of the anti-VEGF glomerular lesion and fell substantially when the drug was stopped.PMID 32270594 (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 · Signature21.6%PMID 18752081 (opens PubMed in a new tab)
All-grade hypertension 21.6% (95% CI 18.7-24.8%), high-grade 6.8%, in a meta-analysis of 4,999 patients on single-agent sunitinib; the signature and by far the most common renal-relevant toxicity of VEGF-pathway blockade.
Glomerular Injury / ProteinuriaSecondaryno population incidence denominator
Proteinuria is the commonest glomerular manifestation of VEGF-pathway inhibition and is regularly reported with sunitinib; podocyte VEGF blockade produces minimal-change/FSGS-like injury and nephrotic-range proteinuria in biopsy series. PMID 34838486 (opens PubMed in a new tab)
Thrombotic MicroangiopathyRareno population incidence denominator
Recognized severe vascular-glomerular lesion of VEGF blockade but occurring at case/biopsy-series level with sunitinib; biopsy-confirmed sunitinib-induced TMA with hypertension, nephrotic syndrome and AKI, reversible on drug withdrawal. PMID 39215250 (opens PubMed in a new tab)
Prerenal / Hemodynamic AKIRarequalitative — no citable incidence
Renal hypoperfusion from capillary leak and cytokine storm — IL-2 and CAR-T cytokine release syndrome.

Toxicity fingerprint

Tap a signature to trace where it strikes the nephron.

21.6%incidence

SeverityModerate

ReversibilityPartially reversible

Evidence8 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

Appears in 1 documented synergy combination

Mechanism of kidney injury

VEGF produced by podocytes maintains the health of the adjacent glomerular endothelium and its fenestrae. Sunitinib's VEGFR blockade removes this paracrine support, causing endothelial dysfunction, loss of fenestration, reduced nitric oxide and prostacyclin, and a rise in endothelin-1 — yielding systemic hypertension and a glomerular endotheliosis/thrombotic microangiopathy phenotype (subendothelial widening, mesangiolysis, capillary microthrombi, GBM double contours, foot-process effacement). Eremina and colleagues showed podocyte-specific VEGF deletion in mice reproduces a thrombotic glomerular injury — direct evidence that local glomerular VEGF reduction is sufficient to trigger the lesion. Hypertension and afferent vasoconstriction can also produce a reversible, largely hemodynamic ('pre-renal'-type) decline in GFR.

Clinical presentation

Most commonly new or worsening hypertension within the first cycles, often accompanied by proteinuria ranging from low-grade to nephrotic. More severe presentations include acute kidney injury with hypertension, nephrotic syndrome, microangiopathic hemolytic anemia/thrombocytopenia, and hematuria when overt thrombotic microangiopathy develops. Reversible serum creatinine rises occur and may reflect hemodynamic change rather than structural injury.

Management

Treat hypertension aggressively with standard agents (RAAS blockers are often preferred given concurrent proteinuria), and titrate as needed. For low-grade proteinuria, continue with closer monitoring; for nephrotic-range proteinuria, significant AKI, or suspected/biopsy-proven thrombotic microangiopathy, dose-reduce, interrupt, or discontinue sunitinib — hypertension, proteinuria, and renal function frequently improve or normalize after withdrawal, though some patients have incomplete recovery and rare progression to dialysis (especially if the drug is continued). Renal biopsy helps when the lesion or differential is unclear. Plasma exchange/eculizumab are generally not indicated for this VEGF-blockade ('secondary') TMA, for which drug cessation is the cornerstone.Lesion-level management framework

§ Receptor target map

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

9targeted

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

FGFRMETEGFRAXLTIE2RAF-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 hypertension
Pre-existing chronic kidney disease or proteinuria
Prior or concurrent VEGF-pathway therapy (e.g., bevacizumab)
Solitary kidney / prior nephrectomy (common in RCC)
Higher dose and continuous (vs intermittent) dosing schedules

Prevention

Optimize/treat pre-existing hypertension before and during therapy

Anticancer mechanism· how it treats cancer

Oral multitargeted receptor tyrosine kinase inhibitor blocking VEGFR-1/2/3, PDGFR-alpha/beta, KIT, FLT3, CSF1R, and RET. Anti-tumor activity in clear-cell renal cell carcinoma and imatinib-resistant GIST is driven largely by VEGFR/PDGFR blockade, which starves tumors of neovascularization.

Note · Incidence figures derive largely from RCC/GIST trial populations and meta-analysis; severe glomerular/TMA lesions are documented mainly through renal-biopsy case series, so those mechanistic and lesion-specific claims are appropriately hedged.

§04

Clinical depth

Renal dose adjustment

No specific renal dose adjustment is established for mild-to-moderate renal impairment; sunitinib pharmacokinetics are not markedly altered by reduced kidney function, and dosing is guided by tolerability/toxicity rather than eGFR. Standard metastatic RCC dosing is 50 mg daily on a 4-weeks-on/2-weeks-off schedule, with reductions (e.g., to 37.5 mg) for toxicity. Hold or reduce dose for severe hypertension, nephrotic-range proteinuria, or significant AKI.

Dialyzability & ESKD dosing

Sunitinib is highly protein-bound and has a large volume of distribution, so it is not expected to be appreciably removed by hemodialysis; supervised use in dialysis patients has been described, with dosing driven by tolerability rather than dialytic clearance.

Differential diagnosis

Distinguish VEGF-blockade thrombotic microangiopathy from primary/atypical HUS and TTP (ADAMTS13), and from hypertensive nephrosclerosis. A reversible hemodynamic creatinine rise (afferent vasoconstriction from hypertension) should be separated from structural glomerular injury. Proteinuria with bland sediment and hypertension favors the VEGF-pathway lesion; rarely, immune-complex/endocapillary glomerulonephritis and tubulointerstitial injury have been reported, and biopsy may be needed to differentiate.

Monitoring

Blood pressure at baseline and each visit/cycle (consider home monitoring early on)
Urine protein (dipstick or urine protein-to-creatinine ratio) at baseline and periodically
CBC for anemia/thrombocytopenia and peripheral smear/LDH/haptoglobin if TMA suspected
Serum creatinine at baseline and serially during therapy

Key trials & series

Phase III trial of 750 treatment-naive metastatic RCC patients showing sunitinib doubled progression-free survival vs interferon-alfa (established it as first-line standard of care)

Clinical pearls

Hypertension is the signature and earliest renal-vascular signal — it is so common it is sometimes used as a pharmacodynamic marker of VEGF-pathway target engagement.
The kidney lesion is a glomerular endothelial disease: think podocyte-VEGF withdrawal causing endotheliosis and a renal-limited TMA, not classic platelet-driven HUS/TTP.
Many RCC patients have a solitary kidney after nephrectomy, lowering renal reserve and raising the stakes of proteinuria and AKI.
A modest, reversible creatinine bump can be hemodynamic from hypertension rather than true structural injury — recheck after BP control before escalating.

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. Single-patient case reports are listed separately below, graded by strength. Citation metadata via PubMed / NLM.

Evidence accrual

7 references · 2008–2025 · 2 since 2023

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 · ModerateLate-Onset Normotensive Thrombotic Microangiopathy and Pyoderma Gangrenosum Following Nine Years of Sunitinib Therapy: A Case Report.Saiki R et al. · Kidney Med 2026 · PMID 41853329Biopsy-proven normotensive renal thrombotic microangiopathy with significant proteinuria and edema developing after nine years of sunitinib, with proteinuria improving on drug discontinuation — a delayed VEGF-inhibitor endothelial injury.

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

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

Boxed warning

WARNING: HEPATOTOXICITY Hepatotoxicity may be severe, and in some cases fatal. Monitor hepatic function and interrupt, dose reduce, or discontinue sunitinib recommended [see Warnings and Precautions (5.1)].

Renal impairment — from the label

No dose adjustment is recommended in patients with mild (CL cr 50 to 80 mL/min), moderate (CL cr 30 to < 50 mL/min), or severe (CL cr < 30 mL/min) renal impairment who are not on dialysis [see Clinical Pharmacology (12.3)] . No dose adjustment is recommended for patients with end-stage renal disease (ESRD) on hemodialysis [see Clinical Pharmacology (12.3)] .

What gets reported — FAERS

Everything below is FAERS — adverse events someone chose to report, about 39,094 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

Hypertensioncorroborated · ROR 4.75 — on the terms that name the lesion (ROR 4.73)
Glomerular Injury / Proteinuriacorroborated · ROR 4.44 — on the terms that name the lesion (ROR 4.15)
Thrombotic Microangiopathycorroborated · ROR 3.24
Prerenal / Hemodynamic AKINot queried in FAERS — No MedDRA term set is defined for this phenotype, so FAERS was never asked about it.

Hypertension

ROR 4.7595% CI 4.58–4.93· 3,176 reports

Glomerular Injury / Proteinuria

ROR 4.4495% CI 3.90–5.04· 238 reports

Thrombotic Microangiopathy

ROR 3.2495% CI 2.64–3.98· 93 reports

SIADH / Hyponatremia

ROR 2.6795% CI 2.42–2.95· 397 reports

Electrolyte Disturbance

ROR 2.1495% CI 1.99–2.30· 753 reports

Hemorrhagic Cystitis

ROR 2.0295% CI 1.79–2.29· 260 reports

FAERS outcomes & reporting trend· 29.8% of reports w/ death · 29.5% w/ hospitalization

29.8%

Reported with a death outcome

11,666 of 39,094 reports

29.5%

Reported with hospitalization

11,526 of 39,094 reports

Reports per year

Yearly FAERS report volume · most recent year is partial.

FAERS adverse-event signal — all organ systems· 9 systems · 39,094 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 0.5395% CI 0.45–0.63· 152 AKI reports ·AKI is reported less often than for other drugs (CI entirely below 1) — no disproportionate signal.

Gastrointestinal

Diarrhoea4,418Nausea3,122Vomiting2,210Stomatitis1,466Oral Pain1,147

General / constitutional

Fatigue4,192Asthenia2,463Weight Decreased1,589Malaise1,583Pain1,290

Metabolic & electrolyte

Decreased Appetite2,317Dehydration1,070

Blood & lymphatic

Platelet Count Decreased1,331Anaemia1,024Thrombocytopenia1,004

Vascular

Hypertension1,803Blood Pressure Increased1,279

Nervous system

Dysgeusia1,698Headache1,021

Skin

Palmar-Plantar Erythrodysaesthesia Syndrome1,455Rash1,023

Respiratory

Dyspnoea1,333

Musculoskeletal

Pain In Extremity1,330

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 Sunitinib 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 · 88% phenotype match

Axitinib

Inlyta · VEGFR TKI

Profile

Potent VEGFR-TKI; hypertension and proteinuria dominate.

HTNGLOMTMA

Moderate#2 · 88% phenotype match

Ziv-aflibercept

Zaltrap · VEGF trap

Profile

Hypertension and proteinuria like bevacizumab.

HTNGLOMTMA

Moderate#3 · 86% phenotype match

Bevacizumab

Avastin · Anti-VEGF antibody

Profile

Proteinuria, hypertension, glomerular TMA.

GLOMHTNTMA

Moderate#4 · 86% phenotype match

Ramucirumab

Cyramza · Anti-VEGFR2 antibody

Profile

Hypertension and proteinuria, class effect.

HTNGLOMTMA

Moderate#5 · 86% phenotype match

VEGFR TKIs (sunitinib · sorafenib · pazopanib · axitinib)

VEGFR TKI

Profile

Hypertension as an on-target marker; proteinuria.

HTNGLOMTMA

Moderate#6 · 86% phenotype match

Compare Sunitinib 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 Sunitinib’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 Sunitinib; 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 128 clinical records among all 166 PubMed matches, so counts are within-sample — bibliometric context, not an endorsement or a measure of clinical authority.