How should kidney function be monitored during Sunvozertinib therapy?

Serum magnesium, calcium, potassium and sodium each cycle (and with symptoms); Stool frequency and volume status.

How can kidney injury from Sunvozertinib be prevented?

Aggressive diarrhea management and hydration Review concomitant medications that promote hyponatremia or Mg wasting

Who is at higher risk of kidney injury from Sunvozertinib?

Concurrent diuretics or other SIADH-inducing/Mg-wasting drugs; Significant treatment-related diarrhea; Baseline electrolyte abnormalities or CKD; Longer treatment duration (cumulative Mg wasting).

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Printable monograph

EGFR exon20 TKI

Sunvozertinib

Zegfrovy · SUNV

EGFR exon20 TKI · approved 2025 · 4 citations

Recent· through 2024

Fairly sourced6/9 · 5 signals

Not met: 4 citations
Not met: 12+ references
Met: Accrued over 10+ years (span: 13y)
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.

An EGFR exon-20 TKI whose renal story is electrolyte wasting more than structural injury.

MildEGFR exon-20 TKI

EGFR exon-20 insertion non-small cell lung cancer

§01

Signature kidney injury

Signature lesion

Electrolyte Disturbance

No established AKI rate. As with the EGFR-inhibitor class, the renal-relevant signal is electrolyte disturbance — particularly hypomagnesemia (renal Mg wasting) and diarrhea-driven losses, with a hyponatremia/SIADH-like pattern possible — rather than structural nephron injury. WU-KONG6 reported diarrhea and skin/EGFR-pathway toxicities as dominant; renal-specific events are not quantified.Source: Wang M et al., Lancet Respir Med 2023

Onset & rechallenge

Time to injurySubacute (~1–6 weeks)

Electrolyte changes within the first weeks to months; hypomagnesemia risk rises with treatment duration.

Distilled from: “Electrolyte changes can appear within the first weeks to months of therapy; hypomagnesemia risk rises with treatment duration.”

§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.

Electrolyte Disturbance#1 · Signaturequalitative — no citable incidence
Renal electrolyte derangement — magnesium/potassium/calcium wasting (cisplatin, anti-EGFR antibodies) or retention (FGFR-inhibitor hyperphosphatemia, tumor-lysis hyperkalemia/hyperphosphatemia).
SIADH / HyponatremiaSecondaryqualitative — no citable incidence
Inappropriate water retention at the collecting duct — high-dose cyclophosphamide.
Prerenal / Hemodynamic AKISecondaryqualitative — 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.

Incidence not quantified

SeverityMild

ReversibilityReversible

Evidence4 citations

Nephron map

Distal Tubule / Collecting DuctFine-tuning of Na, K, Mg, acid & water

Electrolyte Disturbance

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

§03

Kidney injury

Mechanism of kidney injury

EGFR is constitutively expressed in the distal convoluted tubule, where it sustains the magnesium channel TRPM6; EGFR blockade produces a TRPM6-dependent renal magnesium- (and calcium-) wasting state with hypomagnesemia and secondary hypokalemia. Class effects on distal/collecting-duct water handling can yield a euvolemic, SIADH-like hyponatremia, and diarrhea adds GI electrolyte loss and prerenal volume depletion. Direct tubular necrosis is not a described feature.

Clinical presentation

Hypomagnesemia (often the earliest finding) with hypocalcemia and hypokalemia; euvolemic, SIADH-pattern hyponatremia in some; diarrhea-related volume depletion; bland urinalysis; creatinine usually stable unless volume-depleted. Symptoms of Mg deficiency can be subtle (fatigue, cramps) or serious (arrhythmia, seizure).

Management

Correct electrolytes (replete magnesium — often parenterally as oral Mg is poorly absorbed and causes diarrhea; correct hypocalcemia/hypokalemia after Mg; manage sodium per SIADH principles with fluid restriction as appropriate), control diarrhea, and ensure euvolemia. Dose interrupt/reduce per protocol for severe toxicity. No structural renal lesion to treat.Lesion-level management framework

Risk factors

Concurrent diuretics or other SIADH-inducing/Mg-wasting drugs
Significant treatment-related diarrhea
Baseline electrolyte abnormalities or CKD
Longer treatment duration (cumulative Mg wasting)

Prevention

Aggressive diarrhea management and hydration
Review concomitant medications that promote hyponatremia or Mg wasting

Anticancer mechanism· how it treats cancer

Oral irreversible EGFR tyrosine kinase inhibitor with activity against EGFR exon-20 insertion mutations (and selected other EGFR mutations) while relatively sparing wild-type EGFR. Approved for previously treated locally advanced/metastatic NSCLC with EGFR exon-20 insertions.

Note · 2025 approval (initially via WU-KONG6 in China; subsequent US accelerated approval). Renal data are essentially absent; the SIADH/electrolyte framing is conservative EGFR-inhibitor-class reasoning, anchored to the well-established TRPM6 magnesium-wasting mechanism.

§04

Clinical depth

Renal dose adjustment

No dedicated renal dose adjustment established; sunvozertinib is hepatically metabolized (CYP3A) with low renal clearance, so mild-moderate impairment is not expected to require change. Limited data in severe impairment/dialysis.

Dialyzability & ESKD dosing

Not characterized; a highly protein-bound, non-renally cleared small molecule is unlikely to be appreciably dialyzed. No ESKD dosing guidance.

Differential diagnosis

Refractory hypokalemia/hypocalcemia that won't correct until magnesium is repleted points to EGFR-inhibitor TRPM6 Mg wasting. Distinguish SIADH-pattern hyponatremia (euvolemic, concentrated urine) from prerenal hyponatremia of diarrhea/volume depletion.

Monitoring

Serum magnesium, calcium, potassium and sodium each cycle (and with symptoms)
Stool frequency and volume status

Key trials & series

WU-KONG6 (Wang, Lancet Respir Med 2023) — pivotal phase 2 carrying the safety signal

Clinical pearls

EGFR inhibition wastes magnesium via TRPM6 in the distal tubule — check Mg, and replete it first, as hypokalemia/hypocalcemia are refractory until Mg is corrected.
The renal story is electrolytes, not creatinine — the kidney is structurally intact.

Beyond the kidney — non-renal toxicities· 3 organ systems

Class-level context for the major non-renal toxicities of the EGFR exon20 TKI class.

Dermatologic

Rash, HFS, SJS/TEN, vitiligo

Acneiform rash, paronychia

Gastrointestinal

Diarrhea, colitis, mucositis, perforation

Diarrhea

Pulmonary

Pneumonitis, ILD, effusions, hypertension

Interstitial lung disease (EGFR TKIs)

§05

References

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

Evidence accrual

4 references · 2011–2024 · 2 since 2022

Primary (non–case-report) references per year — a proxy for how actively the agent's renal literature is accruing. Recent years are highlighted. Reflects curation depth, not a systematic bibliometric count.

Guidelines & consensus· 13

Each recommendation below is this atlas's faithful summary of the source, not a quotation from it — follow the PubMed link for the wording the society published. Summaries may be superseded; consult the current full text and individualize to the patient.

General onco-nephrology references

ADQIThe nephrotoxic effects of anti-cancer therapies: consensus report of the 34th Acute Disease Quality Initiative workgroupNat Rev Nephrol 2026 · PMID 41361704Provides expert-based statements (modified Delphi) on preventing and managing cisplatin/platinum-associated AKI, including isotonic IV hydration, attention to volume status and concomitant nephrotoxins, and incorporates evidence that IV magnesium supplementation may reduce cisplatin-associated AKI; emphasizes risk stratification and standardized AKI definitions.SIRMSIRM-SIN-AIOM: appropriateness criteria for evaluation and prevention of renal damage in the patient undergoing contrast medium examinations-consensus statements from Italian College of Radiology (SIRM), Italian College of Nephrology (SIN) and Italian Association of Medical Oncology (AIOM)Radiol Med 2022 · PMID 35303246Recommends eGFR-based renal risk assessment and pre/post-contrast isotonic saline or sodium bicarbonate hydration; advises maintaining a 5-7 day interval between iodinated contrast administration and cisplatin in cancer patients to reduce additive nephrotoxicity.KDIGOKDIGO Controversies Conference on onco-nephrology: understanding kidney impairment and solid-organ malignancies, and managing kidney cancerKidney Int 2020 · PMID 33126977Identifies platinum compounds (especially cisplatin) as leading cytotoxic causes of acute tubular injury, AKI, and electrolyte/magnesium wasting; calls for interdisciplinary onco-nephrology care, accurate GFR estimation, and individualized drug dosing in patients with reduced kidney function.KDIGOKDIGO Controversies Conference on onco-nephrology: kidney disease in hematological malignancies and the burden of cancer after kidney transplantationKidney Int 2020 · PMID 33276867Addresses chemotherapy-associated AKI/CKD in hematologic cancer, GFR estimation and chemotherapy dosing in patients with reduced kidney function, and management priorities and research gaps for onco-nephrology care.ADDIKDIntegrating International Consensus Guidelines for Anticancer Drug Dosing in Kidney Dysfunction (ADDIKD) into everyday practiceEClinicalMedicine 2025 · PMID 40290844Provides GRADE-based, drug-specific dose-adjustment recommendations for anticancer agents in kidney dysfunction (illustrated for methotrexate, cisplatin, carboplatin and nivolumab); the recommendations build on Part 1's standardised CKD-EPI eGFR assessment rather than Cockcroft-Gault creatinine clearance.ADDIKDAligning kidney function assessment in patients with cancer to global practices in internal medicineEClinicalMedicine 2025 · PMID 40290845Three consensus recommendations: assess kidney function by GFR (measured GFR or CKD-EPI eGFR), classify it using KDIGO categories, and use this uniform approach to dose anticancer drugs — moving cancer medicine away from Cockcroft-Gault estimated creatinine clearance.ADDIKDA methodology for determining dosing recommendations for anticancer drugs in patients with reduced kidney functionEClinicalMedicine 2025 · PMID 40290846Establishes that, where RCT evidence is lacking, anticancer drug dosing recommendations in kidney dysfunction should be derived by critically appraising observational literature via GRADE combined with structured international multidisciplinary consensus voting.KDIGODiagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1)Crit Care 2013 · PMID 23394211Defines/stages AKI by serum creatinine and urine output; emphasizes avoiding nephrotoxins, maintaining euvolemia/perfusion, dose-adjusting drugs to kidney function, and monitoring high-risk patients — the framework applied to nephrotoxic anti-cancer agents.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Evaluation and Management of Chronic Kidney Disease: known knowns and known unknownsKidney Int 2024 · PMID 38519239Evaluate and risk-stratify CKD, manage to delay progression and its complications, and practise explicit medication management and drug stewardship — the framework the atlas's G1–G5 eGFR banding and every renal dose-adjustment recommendation sit inside. Because the guideline excludes dialysis and transplant recipients by its own statement of scope, its recommendations do not carry to those settings, where this atlas's dialyzability and post-transplant guidance rests on other sources.KDIGOExecutive summary of the KDIGO 2021 Guideline for the Management of Glomerular DiseasesKidney Int 2021 · PMID 34556300Provides the staging/treatment framework for drug-associated glomerular lesions (e.g., bisphosphonate- and interferon-related collapsing FSGS, VEGF-inhibitor podocytopathy/proteinuria), including immunosuppression and supportive RAAS-blockade strategies.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of ANCA-Associated VasculitisKidney Int 2024 · PMID 38388147Updates immunosuppressive induction (rituximab/cyclophosphamide), incorporates avacopan and lower-dose or glucocorticoid-sparing regimens — the management framework for drug- and checkpoint-inhibitor-associated ANCA/pauci-immune glomerulonephritis.KDIGOExecutive summary of the KDIGO 2024 Clinical Practice Guideline for the Management of Lupus NephritisKidney Int 2024 · PMID 38182299Updates first-line lupus nephritis therapy to combination immunosuppression with the addition of belimumab or a calcineurin inhibitor (voclosporin) — informs management of immune-complex/lupus-like glomerulonephritis encountered with immunotherapy.KDIGOExecutive summary of the KDIGO 2025 Clinical Practice Guideline for the Management of Immunoglobulin A Nephropathy (IgAN) and Immunoglobulin A Vasculitis (IgAV)Kidney Int 2025 · PMID 40975525Encourages liberal kidney biopsy and stricter proteinuria control (<0.5 g/d, ideally <0.3 g/d) with RAAS blockers, SGLT2 inhibitors, and targeted-release budesonide — the framework for IgA-dominant glomerular lesions, including those triggered by immune-modulating cancer therapy.

Where Sunvozertinib 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

Tamoxifen

Nolvadex · SERM

Profile

Hypercalcemia flare; rare hyponatremia.

SIADHLYTEPRE

Mild#1 · 86% phenotype match

Lazertinib

Lazcluze · EGFR TKI (3rd-gen)

Profile

2024 EGFR TKI; hyponatremia like osimertinib.

SIADHLYTE

Mild#2 · 84% phenotype match

Vinflunine

Javlor · Vinca alkaloid

Profile

Used because of renal impairment (cisplatin-unfit urothelial); CrCl-based dose bands; watch SIADH/hyponatremia.

LYTEPRESIADH

Mild#3 · 76% phenotype match

Sevabertinib

Hyrnuo · HER2/EGFR TKI

Profile

2025 reversible HER2/EGFR TKI; profuse diarrhea (84-91%) → prerenal AKI, plus EGFR-pathway renal magnesium wasting.

PRELYTE

Mild#4 · 73% phenotype match

Fedratinib

Inrebic · JAK2 inhibitor

Profile

JAK2 inhibitor; GI-loss prerenal azotemia and electrolyte disturbance.

LYTEPRE

Mild#5 · 73% phenotype match

Vismodegib

Erivedge · Hedgehog (SMO) inhibitor

Profile

Muscle spasms; hyponatremia reported.

SIADHLYTE

Mild#6 · 72% phenotype match

Compare Sunvozertinib 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 EGFR / HER2 inhibitors

Same-class agents ordered by their documented kidney-injury profile — atlas severity, an acute-kidney-injury FAERS signal, and how many injury types each is documented to cause. Agents nearer the top carry the lighter documented renal profile.

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.