Diagnostic challenge of systemic amyloidosis mimicking EGFR-TKI toxicity in lung adenocarcinoma: a case report

Introduction

Lung adenocarcinoma with epidermal growth factor receptor (EGFR) mutations benefits significantly from targeted therapies using tyrosine kinase inhibitors (TKIs) (1). First-generation EGFR-TKIs such as gefitinib and third-generation inhibitors like osimertinib have revolutionized treatment outcomes for these patients. Despite their efficacy, EGFR-TKIs can cause various adverse effects, ranging from common dermatological reactions to rare systemic complications (2).

Amyloidosis is a disorder characterized by the extracellular deposition of insoluble protein fibrils, ultimately leading to progressive organ dysfunction (3). In amyloid light chain (AL) amyloidosis, monoclonal plasma cell disorders produce abnormal immunoglobulin light chains that misfold and aggregate to form amyloid deposits (3). These plasma cells originate from B cells, and the disease is therefore fundamentally linked to B-cell lineage abnormalities, particularly clonal expansions that give rise to excessive production of amyloidogenic light chains (4). The kidneys are among the most commonly affected organs, often presenting with nephrotic-range proteinuria or progressive renal insufficiency (3,5). Cardiac involvement, marked by amyloid infiltration of the myocardium, leads to restrictive cardiomyopathy and heart failure (3,6). Concurrent involvement of both the heart and kidneys is associated with a significantly poorer prognosis.

We present a case of a patient with lung adenocarcinoma who developed both cardiac and renal dysfunction during long-term EGFR-TKI therapy. Although initially suspected to be a drug-related adverse effect, further evaluation revealed the underlying AL-type amyloidosis. We present this article in accordance with the CARE reporting checklist (available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2025-913/rc).

Case presentation

A 67-year-old East Asian female was diagnosed with lung adenocarcinoma harboring an EGFR exon 19 deletion in 2013 and underwent left upper lobectomy. Final pathological staging following surgical resection was stage IIB (pT1bN1). The patient remained disease-free until 2018 when recurrence was detected and gefitinib was initiated. In January 2023, disease progression was noted, and molecular testing revealed the T790M resistance mutation, and treatment was switched to osimertinib.

In April 2024, more than one year after initiating osimertinib, the patient presented with generalized edema. Laboratory investigations revealed mildly elevated cardiac enzyme [Troponin I 86 pg/mL (normal range, 2.3–17.5 pg/mL); N-terminal pro-B-type natriuretic peptide (NT-proBNP) 717 pg/mL (normal range <125 pg/mL)], severe proteinuria (dipstick 3+) and hypoalbuminemia [1.2 g/dL (normal range, 4.0–5.0 g/dL)], consistent with nephrotic syndrome [urine protein-to-creatinine ratio (UPCR) 5,679 mg/g (nephrotic-range proteinuria defined as >3,500 mg/g)] (Figure 1). Cardiac evaluation with magnetic resonance imaging (MRI) and echocardiography initially suggested myocarditis. The echocardiogram revealed global hypokinesia of the left ventricle, with a left ventricular ejection fraction of approximately 50%, consistent with mild left ventricular systolic dysfunction.

Figure 1 Trends in UPCR, Troponin I, and NT-proBNP levels over time. Serial measurements of UPCR (mg/g), Troponin I (pg/mL), and NT-proBNP (pg/mL) levels from June 2024 to January 2025. The marked elevations in UPCR and NT-proBNP were consistent with worsening renal and cardiac dysfunction, respectively, contributing to the subsequent diagnosis of systemic amyloidosis. NT-proBNP, N-terminal pro-B-type natriuretic peptide; UPCR, urinary protein-to-creatinine ratio.

Given the concern for drug-induced toxicity, osimertinib was discontinued for several weeks. As proteinuria showed partial improvement and there was no evidence of cancer progression, the treatment was cautiously reinitiated with lazertinib (Figure 2). However, despite two months of treatment with lazertinib, the patient’s symptoms persisted, and both the UPCR and cardiac enzyme levels continued to rise without improvement. To further investigate the underlying cause, a kidney biopsy was performed in October 2024. Histopathological examination revealed features consistent with amyloidosis (Figure 3). Congo red staining demonstrated characteristic apple-green birefringence under polarized light, confirming the diagnosis of amyloidosis. Immunohistochemistry showed lambda light chain predominance, establishing a diagnosis of AL-type amyloidosis. Subsequent bone marrow biopsy and cytogenetic analysis revealed an underlying plasma cell dyscrasia with monoclonal gammopathy. In collaboration with cardiology and radiology departments, a re-evaluation of the patient’s echocardiogram and cardiac MRI was conducted. Although endocardial late gadolinium enhancement (LGE)—a classic imaging finding in cardiac amyloidosis—was not observed, it was noted that early-stage disease may lack such enhancement and can present with subtle or absent signal abnormalities. Additional findings, including elevated native T1 values (>1,300 ms), septal wall thickening, and pericardial effusion, suggested possible cardiac involvement of amyloidosis (Figure 4).

Figure 2 Clinical timeline and treatment history. After undergoing LUL lobectomy in 2013, the patient experienced recurrence in 2018 and was treated with gefitinib. Following progression and identification of the T790M mutation in 2023, treatment was switched to osimertinib. In 2024, the patient developed nephrotic syndrome and heart failure, initially attributed to drug-induced toxicity. Despite switching to lazertinib, proteinuria and symptom of edema continued. Subsequent kidney and bone marrow biopsies confirmed AL-type amyloidosis, ultimately leading to the initiation of hemodialysis by the end of 2024. ADC, adenocarcinoma; AL, amyloid light chain; BM, bone marrow; EGFR, epidermal growth factor receptor; LUL, left upper lobe; PD, progressive disease.

Figure 3 Histopathological, immunofluorescence, and electron microscopy findings from a renal biopsy of amyloidosis. (A) Hematoxylin and eosin staining shows amorphous deposits in the glomerular capillary loops (red arrow). These deposits distort normal glomerular architecture, leading to mesangial expansion and thickened glomerular basement membranes (×400). (B) Congo red staining highlights the amyloid deposits as salmon-pink areas (red arrows), characteristic of amyloidosis (×400). (C) Immunofluorescence for κ light chains shows positive staining within glomeruli (×400). (D) Immunofluorescence for λ light chains shows stronger and more dominant staining than κ, indicating λ light chain-dominant amyloid deposition (×400). (E) Electron microscopy shows diffusely thickened and irregular glomerular basement membranes (yellow arrow) with dense accumulations of fibrillary materials (×10,000). (F) Higher magnification electron microscopy reveals randomly oriented, non-branching fibrils measuring approximately 8–10 nm in diameter, consistent with amyloid fibrils. The mesangial regions are expanded with nodular fibril accumulation, and the epithelial foot processes are markedly effaced (×60,000).

Figure 4 Echocardiographic and cardiac MRI findings in a patient with cardiac amyloidosis. (A) Parasternal long-axis view on transthoracic echocardiography shows marked septal wall thickening (yellow arrows) and small pericardial effusion (red arrows). (B) Apical four-chamber view demonstrating concentric left ventricular wall thickening (yellow arrow) and pericardial effusion (red arrow). (C) Bull’s-eye plot of global longitudinal strain reveals relative apical sparing (“cherry-on-top” pattern), a characteristic strain distribution in cardiac amyloidosis. (D) Cine cardiac MRI without evident endocardial late gadolinium enhancement (yellow arrow). Although this classic finding of cardiac amyloidosis is not observed here, early-stage disease may lack such enhancement and can present with subtle or absent signal abnormalities. (E) Native T1 mapping demonstrates diffuse elevation of myocardial T1 values (>1,300 ms), indicating increased myocardial extracellular volume due to amyloid deposition. (F) Diastolic frame of cine MRI shows prominent septal thickening and pericardial effusion (yellow arrow), further supporting the diagnosis of cardiac amyloidosis. MRI, magnetic resonance imaging.

To further evaluate the cause of persistent renal dysfunction, whole genome sequencing (WGS) was performed on both peripheral blood and kidney tissue samples. Targeted analysis of B cell-related genes showed mutations in several key regulators of B cell activation and plasma cell differentiation. Most of these mutations were detected exclusively in the kidney tissue (Figure 5).

Figure 5 Oncoplot target analysis of B cell-related genes in blood and kidney. Target analysis shows enrichment of somatic mutations exclusively in the kidney tissue. Blood samples showed only mutation for ATAD5 gene.

Despite supportive management, the patient’s renal function progressively deteriorated, and she initiated regular hemodialysis for end-stage renal disease in December 2024. Although her edema partially improved following dialysis, her overall clinical condition remained poor due to the combined burden of renal and cardiac amyloidosis. Notably, there was no evidence of lung cancer progression during this period, and cancer-directed therapy had been discontinued.

All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration and its subsequent amendments. This study was approved by the Clinical Research Ethics Committee of the Chungnam National University Hospital (Approval No. CNUH 2020-11-043). Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Discussion

This case describes a patient with lung adenocarcinoma who developed severe edema along with renal and cardiac dysfunction during treatment with osimertinib. Although these manifestations were initially presumed to be adverse effects of targeted therapy, subsequent evaluations identified underlying AL-type amyloidosis involving both the heart and kidneys. This case highlights the diagnostic challenges associated with systemic diseases emerging during targeted cancer therapy and emphasizes the importance of not attributing multisystem dysfunction solely to drug toxicity in patients receiving EGFR-TKIs. Early recognition and comprehensive evaluation are essential to ensure timely diagnosis and appropriate management of concurrent systemic conditions.

Despite supportive management, the patient’s renal function progressively deteriorated, eventually requiring maintenance hemodialysis for end-stage renal disease. Her overall clinical condition remained poor because of the combined burden of renal and cardiac amyloidosis, which is known to carry a poor prognosis. As there was no evidence of lung cancer progression during this period, EGFR inhibitor therapy was permanently discontinued, primarily due to advanced organ dysfunction and poor performance status related to systemic amyloidosis rather than cancer progression itself.

EGFR-TKIs are the standard treatment for EGFR mutation-positive lung adenocarcinoma (7). By inhibiting the enzymatic activity of mutant EGFR proteins, these agents block downstream signaling pathways that promote cancer cell proliferation and survival (7,8). Despite their therapeutic benefits, these agents are known to cause a range of adverse effects, most commonly involving the skin and gastrointestinal tract (9,10). Osimertinib, a third-generation EGFR-TKI, has been associated with cardiotoxicity, including QT interval prolongation (11,12) and reduced left ventricular ejection fraction (11,13-15), as well as myocarditis (16). Several pharmacokinetic and exposure-response studies suggest that higher plasma trough concentrations of osimertinib are associated with an increased risk of adverse events (17,18), with a proposed toxicity risk threshold around ~250–300 ng/mL (19,20). Nevertheless, therapeutic drug monitoring of osimertinib is not routinely available in most clinical settings, and proposed thresholds still require prospective validation. While various toxicities related to EGFR-TKIs have been well described, there have been no reports or studies linking EGFR-TKI therapy to the development of amyloidosis.

Following recurrence after surgery, the patient had been treated with the first-generation EGFR-TKI, gefitinib, for five years without experiencing any notable adverse effects. After the emergence of the EGFR T790M mutation, the treatment was switched to the third-generation EGFR-TKI, osimertinib. Approximately 15 months after initiating osimertinib, the patient developed new-onset symptoms, including generalized edema. While gefitinib is associated with a low incidence of cardiotoxicity, cardiotoxic effects related to osimertinib have been reported in up to 21.64% of cases (21). In this case, the temporal association between symptom onset and the initiation of osimertinib raised suspicion of drug-induced toxicity. Echocardiography revealed global left ventricular dysfunction, further supporting the possibility of osimertinib-induced cardiotoxicity. Moreover, cardiac MRI did not demonstrate the typical subendocardial LGE that is characteristically observed in cardiac amyloidosis (3,6), making osimertinib-induced myocarditis the initial diagnosis. The simultaneous deterioration in renal function and the presence of proteinuria were also considered potentially attributable to osimertinib-related nephrotoxicity. Consequently, osimertinib was changed to lazertinib, another third-generation EGFR-TKI, due to its lower risk of cardiac and renal adverse effects (22,23). However, the patient’s edema and proteinuria progressively worsened despite the change in therapy. Ongoing concern regarding the persistent and aggravating symptoms prompted a comprehensive evaluation, including a kidney biopsy, which ultimately revealed the true underlying pathology. Given the patient’s overall condition, cardiac biopsy was not pursued, and the diagnosis of cardiac amyloidosis was made based on imaging and clinical findings without histological confirmation.

Notably, in imaging studies, patients with early cardiac involvement of amyloidosis may not exhibit the typical subendocardial LGE on cardiac MRI. In early stages, the disease may present with subtle or absent signal abnormalities, and an elevation in native T1 values often precedes the development of LGE (24,25). This imaging nuance contributed to the diagnostic challenge in confirming cardiac amyloidosis in this case.

Although cardiotoxicity associated with osimertinib has been relatively well documented, its nephrotoxic potential has been rarely reported (26,27). Furthermore, existing reports suggest that renal dysfunction during osimertinib treatment is often attributable to alternative underlying conditions or pseudorenal dysfunction rather than direct drug toxicity (28,29). In addition, previously reported studies of osimertinib-induced cardiotoxicity typically developed approximately six months after treatment initiation (30-33), whereas in this case, symptoms emerged more than one year after starting osimertinib. Despite switching to lazertinib, which has a more favorable cardiac and renal safety profile (22,23), the patient’s symptoms continued to progress. Taken together, these findings made osimertinib-induced toxicity less likely and prompted further diagnostic evaluation to identify other potential etiologies.

In this case, WGS was performed on both peripheral blood and kidney tissue to elucidate the mechanism underlying the patient’s renal dysfunction. Given that AL-type amyloidosis originates from clonal plasma cells of B-cell lineage, we performed a targeted analysis of B cell-related genes. As shown in Figure 5, oncoplot analysis revealed a marked enrichment of somatic mutations in B cell-related genes exclusively within the kidney tissue. This finding suggests localized clonal activity of B cell lineage and supports the hypothesis that the renal dysfunction was primarily driven by AL-type amyloidosis rather than drug-induced nephrotoxicity. Furthermore, the clear disparity in mutation burden between the kidney and peripheral blood indicates that these genomic alterations are more likely attributable to localized pathophysiological processes—such as light chain deposition or chronic inflammation—rather than systemic, nonspecific effects of osimertinib. Chronic disorders like renal amyloidosis are known to involve tissue-specific clonal expansion and microenvironmental remodeling, which may contribute to the observed somatic mutation burden in the affected organ (34). Collectively, these findings suggest that the patient’s renal dysfunction was predominantly attributable to the underlying disease process itself rather than to osimertinib-related toxicity.

This case highlights the importance of maintaining a broad differential diagnosis when new organ dysfunction arises during EGFR-TKI therapy. While drug-related toxicity should be considered, the possibility of rare systemic disorders such as amyloidosis must not be underestimated—particularly when symptoms persist despite changes in medication. In addition, other systemic conditions that may clinically resemble amyloidosis—such as sarcoidosis, light-chain deposition disease, and connective-tissue-related nephropathy—should also be considered in the differential diagnosis, as they can similarly present with multi-organ involvement and renal dysfunction. Timely recognition and accurate diagnosis are essential to guide appropriate management and prevent delays in care. Furthermore, this report adds value by incorporating WGS to differentiate between drug-induced nephrotoxicity and disease-related organ damage. The use of WGS to uncover a clonal B cell-driven renal amyloidosis process illustrates how genomic analysis can enhance diagnostic precision in clinically ambiguous scenarios. Although the patient’s advanced age and overall condition precluded aggressive treatment, identifying the underlying etiology was crucial for symptom control and for facilitating informed clinical decisions.

Conclusions

This case highlights the diagnostic challenges in distinguishing drug-induced toxicity from rare systemic diseases in patients receiving targeted cancer therapy. While adverse drug reactions for cancer treatments are a common concern, clinicians must remain vigilant for rare but serious systemic diseases such as amyloidosis, especially when symptoms are atypical or progressive. Accurate and timely identification of the underlying etiology is essential for guiding appropriate personalized management strategies and supporting informed clinical decisions.

Acknowledgments

None.

Footnote

Reporting Checklist: The authors have completed the CARE reporting checklist. Available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2025-913/rc

Peer Review File: Available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2025-913/prf

Funding: This work was supported by the National Research Foundation of Korea (NRF) grant funded by the Korean Government (MSIT) (No. 2022R1A2C2010148). This research was supported by a grant of the Korea Health Technology R&D Project through the Korea Health Industry Development Institute (KHIDI), funded by the Ministry of Health & Welfare, Republic of Korea (Grant Nos. RS-2020-KH088690 and RS-2024-00440671).

Conflicts of Interest: All authors have completed the ICMJE uniform disclosure form (available at https://tlcr.amegroups.com/article/view/10.21037/tlcr-2025-913/coif). H.Y.K. serves as the CEO of NGeneS Inc., but this role is unrelated to the submitted work. The other authors have no conflicts of interest to declare.

Ethical Statement: The authors are accountable for all aspects of the work in ensuring that questions related to the accuracy or integrity of any part of the work are appropriately investigated and resolved. All procedures performed in this study were in accordance with the ethical standards of the institutional and/or national research committee(s) and with the Helsinki Declaration and its subsequent amendments. This study was approved by the Clinical Research Ethics Committee of the Chungnam National University Hospital (Approval No. CNUH 2020-11-043). Written informed consent was obtained from the patient for publication of this case report and accompanying images. A copy of the written consent is available for review by the editorial office of this journal.

Open Access Statement: This is an Open Access article distributed in accordance with the Creative Commons Attribution-NonCommercial-NoDerivs 4.0 International License (CC BY-NC-ND 4.0), which permits the non-commercial replication and distribution of the article with the strict proviso that no changes or edits are made and the original work is properly cited (including links to both the formal publication through the relevant DOI and the license). See: https://creativecommons.org/licenses/by-nc-nd/4.0/.

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