Severe Hyperferritinemia with Preserved Transferrin Saturation in Genetically Confirmed X-Linked Alport Syndrome: A Case Report

Severe Hyperferritinemia with Preserved Transferrin Saturation in Genetically Confirmed X-Linked Alport Syndrome: A Case Report | Research Square window.SnipcartSettings = { analytics: { enabled: false } }; (function() { var accessVector = localStorage.getItem('access_vector') || ''; window.dataLayer = window.dataLayer || []; if (accessVector) { window.dataLayer.push({ user: { profile: { profileInfo: { snid: accessVector } } } }); } })(); (function(w,d,s,l,i){w[l]=w[l]||[];w[l].push({'gtm.start':new Date().getTime(),event:'gtm.js'});var f=d.getElementsByTagName(s)[0],j=d.createElement(s),dl=l!='dataLayer'?'&l='+l:'';j.async=true;j.src='https://www.googletagmanager.com/gtm.js?id='+i+dl;f.parentNode.insertBefore(j,f);})(window,document,'script','dataLayer','GTM-K279D39R'); Browse Preprints In Review Journals COVID-19 Preprints AJE Video Bytes Research Tools Research Promotion AJE Professional Editing AJE Rubriq About Preprint Platform In Review Editorial Policies Our Team Advisory Board Help Center Sign In Submit a Preprint Cite Share Download PDF Case Report Severe Hyperferritinemia with Preserved Transferrin Saturation in Genetically Confirmed X-Linked Alport Syndrome: A Case Report Tuba Uyanık This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-8970844/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 7 You are reading this latest preprint version Abstract Background Alport syndrome is an X-linked inherited kidney disease caused by mutations in type IV collagen genes (COL4A3, COL4A4, and COL4A5) that affect the glomerular basement membrane and can lead to sensorineural hearing loss and eye abnormalities. This disease, which can cause hematuria, proteinuria, and in more severe cases chronic kidney disease, is characterized by bilateral and high-frequency sensorineural hearing loss, eye dysfunction, and in rare cases, aortic aneurysm; however, abnormalities in iron metabolism are not commonly described. Case Presentation: We report a case of persistent and marked hyperferritinemia in a patient with genetically confirmed Alport syndrome, without blood transfusion, significant inflammation, or hereditary hemochromatosis. In 2016, a patient whose etiology of proteinuria and hematuria was investigated showed no abnormalities in iron parameters in laboratory tests performed at that time, while as of 2021, serum ferritin levels were found to be > 1000 µg/L. Abdominal ultrasound and MRI scans revealed severe hepatosplenomegaly. Minimal increases in infection and inflammation markers did not explain this severely elevated ferritin level. Hemochromatosis gene mutations were tested in several different laboratories, and no mutations were detected. Conclusion This case suggests a possible dysregulation of iron metabolism in a patient diagnosed with Alport syndrome, beyond the inflammation associated with conventional chronic kidney disease. The interaction between collagen IV mutations and systemic inflammation and iron regulatory pathways may require more detailed investigation. Alport syndrome hyperferritinemia iron metabolism chronic kidney disease inflammation Figures Figure 1 Introduction Alport syndrome results from mutations in type IV collagen genes (COL4A3, COL4A4, and COL4A5), leading to structural abnormalities of the glomerular basement membrane and progressive chronic kidney disease ( 1 ). It causes hematuria and progressive proteinuria in the kidneys and is characterized by extrarenal manifestations, including sensorineural hearing loss. Ferritin is an acute phase reactant that increases in response to oxidative stress and cytokine release ( 2 ). In severe hyperferritinemia (> 1000 ng/mL), exclusion of hereditary hemochromatosis, transfusion-induced iron overload, malignancies, liver diseases, or macrophage activation syndromes is necessary ( 3 ). The relationship between collagen IV mutations and systemic iron metabolism is not yet fully defined. Here, we report a genetically confirmed case of X-linked Alport syndrome presenting with persistent hyperferritinemia exceeding 2000 ng/mL despite preserved transferrin saturation and negative HFE mutation analysis, suggesting a potential secondary iron redistribution phenotype. Case Presentation A 38-year-old female patient presented to the hospital in 2016 with a spontaneous miscarriage at the seventh week of her first pregnancy. Complete urinalysis at that time revealed 1 + proteinuria. Quantitative evaluation showed a 24-hour urinary protein excretion of 1540 mg/day. Serum creatinine and estimated glomerular filtration rate (eGFR) were within normal limits. Renal ultrasonography measured the dimensions of the right kidney at 150 x 35 mm and the left kidney at 91 x 32 mm, with preserved parenchymal thickness (12 mm on both sides). Kidney contours and localization were normal, and no pelvicalyceal enlargement was observed. Initial immunological evaluation showed ANA 1+, ANCA negative, normal immunoglobulin A, G, and M levels, normal complement C3, and decreased C4 (15 mg/dL). Suspicion of lupus nephritis arose due to persistent proteinuria and isolated complement deficiency. Kidney biopsy revealed findings suggestive of focal segmental glomerulosclerosis without chronic tubulointerstitial damage or global glomerulosclerosis. Renal function was preserved throughout the follow-up period. A dynamic upper abdominal MRI performed in August 2021 showed hepatomegaly (long axis of the right lobe 206 mm) and splenomegaly (long axis of the spleen 132 mm). Decreased T1 and T2 signal intensities were observed in both the liver and spleen, raising suspicion of iron accumulation or hematological pathology. An abdominal scan performed in October 2025 revealed hepatomegaly with a craniocaudal liver diameter of 185 mm and splenomegaly with a spleen long axis of 130 mm. Liver parenchymal density was decreased in both T1 and T2 weighted sequences, without focal solid or cystic lesions. On November 27, 2025, a custom liver and heart iron quantification MRI (T2*) showed a significant decrease in liver T2* values ​​(1.5–1.8 ms), consistent with severe hepatic iron accumulation. Cardiac T2* values ​​were measured as 30–35 ms in the interventricular septum and free wall, remaining within normal limits and ruling out myocardial iron accumulation. Serial ferritin levels, which had been increasing since 2019, were above 2000 ng/mL in 2021 (Fig. 1). Despite severe hyperferritinemia, transferrin saturation remained within the normal range. Inflammatory markers (CRP, ESR) and transaminases were normal. HFE mutation analysis performed in 2021 and 2025 was negative. Due to persistently high ferritin levels and radiological evidence of severe hepatic iron deposition, weekly therapeutic phlebotomy was initiated, and deferasirox treatment was administered when ferritin levels remained significantly elevated. In 2025, a diagnosis of progressive bilateral sensorineural hearing loss, confirmed by audiometry, was made. Given the combination of renal involvement and hearing loss, genetic testing was performed, and a pathogenic COL4A5 mutation consistent with X-linked Alport syndrome was identified. Initially, low-dose angiotensin-converting enzyme inhibitor therapy was initiated due to persistent proteinuria; however, treatment was discontinued due to hyperkalemia and hypotension. To reduce the progression of renal disease, SGLT2 inhibitor therapy, which has been shown to be effective in previous studies, was initiated. The patient, who visited the outpatient clinic for kidney function tests during the second week of SGLT2 inhibitor treatment, showed no increase in creatinine levels, and proteinuria measured in spot urine had decreased to 700 mg/day. Discussion Type IV collagen mutations lead to structural disruption of the glomerular basement membrane, causing progressive renal damage and sterile inflammation in the kidney ( 4 ). In Alport-associated nephropathy, activated macrophages exhibit a pro-inflammatory phenotype, leading to cytokine release. IL-6 increases hepcidin synthesis, and hepcidin degrades ferroportin, reducing iron release into circulation ( 5 ). Persistent macrophage activation and hepcidin-mediated iron retention may therefore lead to hyperferritinemia ( 6 ). Chronic kidney injury can further contribute to this process ( 7 ). Another potential contributing mechanism may be alterations in erythropoiesis associated with inflammation, leading to functional iron deficiency and increased intracellular iron retention despite preserved transferrin saturation ( 8 ). The relationship between collagen IV mutations and systemic iron metabolism is not yet fully defined, and excessive and persistent hyperferritinemia in Alport syndrome has not been described in the literature. It is unclear whether this results from inflammatory disease activity, hepcidin-induced iron retention, or a previously unknown immunometabolic phenotype within Alport syndrome. Recognizing this pattern is clinically important because in nephrology practice, severe hyperferritinemia is often interpreted as primary iron overload. In patients with hereditary nephropathy, misclassification can lead to unnecessary investigations or inappropriate long-term treatment strategies. This case highlights the importance of integrating transferrin saturation, genetic assessment, and quantitative MRI findings when interpreting significantly elevated ferritin levels. Key laboratory and imaging findings are summarized in Table 1 . Table 1 Key Laboratory and Imaging Findings Parameter Finding Peak ferritin > 2000 ng/mL (persistent) Transferrin saturation 21–32% (normal range) Hemoglobin Normocytic, stable HFE mutation Negative Liver T2* MRI Severe hepatic iron deposition (1.5–1.8 ms) Cardiac T2* MRI Normal Audiometry Bilateral sensorineural hearing loss Genetic testing Pathogenic COL4A5 mutation Further prospective studies are needed to clarify whether this represents a reproducible immunometabolic phenotype within collagen IV–associated nephropathy. Conclusion This case describes persistent hyperferritinemia with radiologically confirmed severe hepatic iron accumulation in a patient with genetically confirmed X-linked Alport syndrome, without transfusion exposure or hereditary hemochromatosis. The co-occurrence of renal involvement, bilateral and progressive sensorineural hearing loss, hepatosplenomegaly, and severe hyperferritinemia suggests that chronic basement membrane damage may affect systemic iron metabolism in addition to structural glomerular pathology. These findings are consistent with a macrophage-mediated secondary iron redistribution process, representing an immunometabolic dimension in Alport syndrome. Clarifying this situation is also clinically important because in such patients, severe hyperferritinemia can be misinterpreted as primary iron overload, ultimately leading to unnecessary or incorrect interventions. Further studies are needed to clarify whether dysregulated iron metabolism in collagen IV-related nephropathies reflects inflammatory disease activity, reticuloendothelial iron retention, or a contributing pathogenic mechanism. Increased awareness of this potential relationship could improve the diagnostic evaluation of unexplained hyperferritinemia in hereditary glomerular disorders. The main educational implications of this case are summarized in Table 2 . Table 2 Teaching Points Teaching Points Severe hyperferritinemia with normal transferrin saturation should prompt evaluation for secondary iron redistribution mechanisms. In hereditary nephropathies, chronic sterile inflammation may contribute to altered iron metabolism. Hepatic T2* MRI is useful for distinguishing patterns of iron deposition. Negative HFE mutation analysis does not exclude non-classical iron accumulation patterns. Alport syndrome may rarely present with systemic iron dysregulation. Abbreviations MRI Magnetic Resonance Imaging HFE Hereditary Haemochromatosis Protein ANA Anti Nuclear Antibody ANCA Anti Neutrophil Cytoplasmic Antibody CRP C-Reactive Protein ESR Erythrocyte Sedimentation Rate SGLT2 inhibitors Sodium-Glucose Co-transporter 2 inhibitors Declarations Ethics approval and consent to participate Ethical approval was not required for this case report according to institutional policy. Written informed consent was obtained from the patient for participation in this study. Consent for publication Written informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal. Availability of data and materials All data generated or analysed during this study are included in this published article. Competing interests The author declares that she has no competing interests. Funding The author received no specific funding for this work. Authors’ contributions TU conceptualized the study, collected the clinical data, analysed the findings, and wrote the manuscript. The author read and approved the final manuscript. Acknowledgements Not applicable. References Warady BA, Agarwal R, Bangalore S, Chapman A, Levin A, Stenvinkel P, Toto RD, Chertow GM. Alport syndrome classification and management. Kidney Med. 2020;2(5):639–49. 10.1016/j.xkme.2020.05.014 . Mahroum N, Alghory A, Kiyak Z, Alwani A, Seida R, Alrais M, Shoenfeld Y. Ferritin—from iron, through inflammation and autoimmunity, to COVID-19. J Autoimmun. 2022;126:102778. 10.1016/j.jaut.2021.102778 . Fauter M, Mainbourg S, El Jammal T, Guerber A, Zaepfel S, Henry T, Gerfaud-Valentin M, Sève P, Jamilloux Y. Extreme hyperferritinemia: causes and prognosis. J Clin Med. 2022;11(18):5438. 10.3390/jcm11185438 . Quinlan C, Rheault MN. Genetic basis of type IV collagen disorders of the kidney. Clin J Am Soc Nephrol. 2021;16(7):1101–9. 10.2215/CJN.19171220 . Sandnes M, Ulvik RJ, Vorland M, Reikvam H. Hyperferritinemia—A clinical overview. J Clin Med. 2021;10(9):2008. 10.3390/jcm10092008 . Speer T, Dimmeler S, Schunk SJ, Fliser D, Ridker PM. Targeting innate immunity-driven inflammation in CKD and cardiovascular disease. Nat Rev Nephrol. 2022;18(12):762–78. 10.1038/s41581-022-00621-9 . Ogolla CO, Karani LW, Musyoki S, Maruti P. Impact of iron deficiency and erythropoiesis-stimulating agents on anemia in CKD progression. Int J Nephrol. 2025;2025:2567637. 10.1155/ijne/2567637 . Marques O, Weiss G, Muckenthaler MU. The role of iron in chronic inflammatory diseases: from mechanisms to treatment options in anemia of inflammation. Blood. 2022;140(19):2011–2023. 10.1182/blood.2021013472 . PMID: 35994752. Additional Declarations No competing interests reported. Supplementary Files CAREchecklistEnglish20131.pdf Cite Share Download PDF Status: Under Review Version 1 posted Reviews received at journal 04 Apr, 2026 Reviewers agreed at journal 03 Apr, 2026 Reviewers invited by journal 25 Mar, 2026 Editor assigned by journal 23 Mar, 2026 Editor invited by journal 02 Mar, 2026 Submission checks completed at journal 28 Feb, 2026 First submitted to journal 28 Feb, 2026 You are reading this latest preprint version Research Square lets you share your work early, gain feedback from the community, and start making changes to your manuscript prior to peer review in a journal. As a division of Research Square Company, we’re committed to making research communication faster, fairer, and more useful. We do this by developing innovative software and high quality services for the global research community. Our growing team is made up of researchers and industry professionals working together to solve the most critical problems facing scientific publishing. Also discoverable on Platform About Our Team In Review Editorial Policies Advisory Board Help Center Resources Author Services Accessibility API Access RSS feed Manage Cookie Preferences © Research Square 2026 | ISSN 2693-5015 (online) Privacy Policy Terms of Service Do Not Sell My Personal Information {"props":{"pageProps":{"initialData":{"identity":"rs-8970844","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":612169804,"identity":"e78ccc31-0f67-4cc4-bbea-0dafe8ea90d5","order_by":0,"name":"Tuba Uyanık","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAABFElEQVRIiWNgGAWjYFACHjDJ2ADhSRjwg6iEAnwaYFrYoFokQZoTDIjXwmBgcABM4dZiL5F78MOPisOy/fI9ZhI/d1gYG59fnfjhgQGDPL/YAey2SOQlS/acOWw8s43HTLL3jISZ2Y23myWADjOcOTsBh5YcA2nGtrTEDcd4zCR42yRszG6c3QDSkmBwG6cW49+M/9IS9wO1SP4FajGecXbzDwJazKQZG2wSN7DxmEkDbTEz4O/dht+WM+/SLHuOAc0+llZsLdsmYSxxg3ebRYKBBE6/sLfnHr7xo0ZCtr/58Mabb9vqDPv7z26++aPCRp5fGrsWZMAiAaYkwColCCoHAeYPYIr/AFGqR8EoGAWjYOQAAA/PWz6i0PcSAAAAAElFTkSuQmCC","orcid":"","institution":"Kastamonu University Faculty of Medicine","correspondingAuthor":true,"prefix":"","firstName":"Tuba","middleName":"","lastName":"Uyanık","suffix":""}],"badges":[],"createdAt":"2026-02-25 19:38:12","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-8970844/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-8970844/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":105574465,"identity":"4fcc0651-6e87-40f8-8239-35551e7a22df","added_by":"auto","created_at":"2026-03-27 13:35:07","extension":"jpeg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":152669,"visible":true,"origin":"","legend":"\u003cp\u003eSee image above for figure legend.\u003c/p\u003e","description":"","filename":"Figure1FerritinLinearBMC.jpeg","url":"https://assets-eu.researchsquare.com/files/rs-8970844/v1/dda4acada63c8bc93af9ee12.jpeg"},{"id":105728127,"identity":"b23efb92-0e49-43bc-adba-500e170af748","added_by":"auto","created_at":"2026-03-30 11:09:58","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":533257,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8970844/v1/50d94c82-f8aa-4d5a-a423-d56fc4721186.pdf"},{"id":105574385,"identity":"2047e5b2-207a-4216-bdc2-9bb822769076","added_by":"auto","created_at":"2026-03-27 13:34:45","extension":"pdf","order_by":1,"title":"","display":"","copyAsset":false,"role":"supplement","size":211197,"visible":true,"origin":"","legend":"","description":"","filename":"CAREchecklistEnglish20131.pdf","url":"https://assets-eu.researchsquare.com/files/rs-8970844/v1/c436321136832064b9080ee8.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"\u003cp\u003eSevere Hyperferritinemia with Preserved Transferrin Saturation in Genetically Confirmed X-Linked Alport Syndrome: A Case Report\u003c/p\u003e","fulltext":[{"header":"Introduction","content":"\u003cp\u003eAlport syndrome results from mutations in type IV collagen genes (COL4A3, COL4A4, and COL4A5), leading to structural abnormalities of the glomerular basement membrane and progressive chronic kidney disease (\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e). It causes hematuria and progressive proteinuria in the kidneys and is characterized by extrarenal manifestations, including sensorineural hearing loss.\u003c/p\u003e \u003cp\u003eFerritin is an acute phase reactant that increases in response to oxidative stress and cytokine release (\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e). In severe hyperferritinemia (\u0026gt;\u0026thinsp;1000 ng/mL), exclusion of hereditary hemochromatosis, transfusion-induced iron overload, malignancies, liver diseases, or macrophage activation syndromes is necessary (\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eThe relationship between collagen IV mutations and systemic iron metabolism is not yet fully defined. Here, we report a genetically confirmed case of X-linked Alport syndrome presenting with persistent hyperferritinemia exceeding 2000 ng/mL despite preserved transferrin saturation and negative HFE mutation analysis, suggesting a potential secondary iron redistribution phenotype.\u003c/p\u003e"},{"header":"Case Presentation","content":"\u003cp\u003eA 38-year-old female patient presented to the hospital in 2016 with a spontaneous miscarriage at the seventh week of her first pregnancy. Complete urinalysis at that time revealed 1\u0026thinsp;+\u0026thinsp;proteinuria. Quantitative evaluation showed a 24-hour urinary protein excretion of 1540 mg/day. Serum creatinine and estimated glomerular filtration rate (eGFR) were within normal limits. Renal ultrasonography measured the dimensions of the right kidney at 150 x 35 mm and the left kidney at 91 x 32 mm, with preserved parenchymal thickness (12 mm on both sides). Kidney contours and localization were normal, and no pelvicalyceal enlargement was observed. Initial immunological evaluation showed ANA 1+, ANCA negative, normal immunoglobulin A, G, and M levels, normal complement C3, and decreased C4 (15 mg/dL). Suspicion of lupus nephritis arose due to persistent proteinuria and isolated complement deficiency. Kidney biopsy revealed findings suggestive of focal segmental glomerulosclerosis without chronic tubulointerstitial damage or global glomerulosclerosis. Renal function was preserved throughout the follow-up period.\u003c/p\u003e \u003cp\u003eA dynamic upper abdominal MRI performed in August 2021 showed hepatomegaly (long axis of the right lobe 206 mm) and splenomegaly (long axis of the spleen 132 mm). Decreased T1 and T2 signal intensities were observed in both the liver and spleen, raising suspicion of iron accumulation or hematological pathology.\u003c/p\u003e \u003cp\u003eAn abdominal scan performed in October 2025 revealed hepatomegaly with a craniocaudal liver diameter of 185 mm and splenomegaly with a spleen long axis of 130 mm. Liver parenchymal density was decreased in both T1 and T2 weighted sequences, without focal solid or cystic lesions. On November 27, 2025, a custom liver and heart iron quantification MRI (T2*) showed a significant decrease in liver T2* values ​​(1.5\u0026ndash;1.8 ms), consistent with severe hepatic iron accumulation. Cardiac T2* values ​​were measured as 30\u0026ndash;35 ms in the interventricular septum and free wall, remaining within normal limits and ruling out myocardial iron accumulation.\u003c/p\u003e \u003cp\u003eSerial ferritin levels, which had been increasing since 2019, were above 2000 ng/mL in 2021 (Fig.\u0026nbsp;1). Despite severe hyperferritinemia, transferrin saturation remained within the normal range. Inflammatory markers (CRP, ESR) and transaminases were normal.\u003c/p\u003e \u003cp\u003eHFE mutation analysis performed in 2021 and 2025 was negative. Due to persistently high ferritin levels and radiological evidence of severe hepatic iron deposition, weekly therapeutic phlebotomy was initiated, and deferasirox treatment was administered when ferritin levels remained significantly elevated. In 2025, a diagnosis of progressive bilateral sensorineural hearing loss, confirmed by audiometry, was made. Given the combination of renal involvement and hearing loss, genetic testing was performed, and a pathogenic COL4A5 mutation consistent with X-linked Alport syndrome was identified. Initially, low-dose angiotensin-converting enzyme inhibitor therapy was initiated due to persistent proteinuria; however, treatment was discontinued due to hyperkalemia and hypotension. To reduce the progression of renal disease, SGLT2 inhibitor therapy, which has been shown to be effective in previous studies, was initiated. The patient, who visited the outpatient clinic for kidney function tests during the second week of SGLT2 inhibitor treatment, showed no increase in creatinine levels, and proteinuria measured in spot urine had decreased to 700 mg/day.\u003c/p\u003e"},{"header":"Discussion","content":"\u003cp\u003eType IV collagen mutations lead to structural disruption of the glomerular basement membrane, causing progressive renal damage and sterile inflammation in the kidney (\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e). In Alport-associated nephropathy, activated macrophages exhibit a pro-inflammatory phenotype, leading to cytokine release. IL-6 increases hepcidin synthesis, and hepcidin degrades ferroportin, reducing iron release into circulation (\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e).\u003c/p\u003e \u003cp\u003ePersistent macrophage activation and hepcidin-mediated iron retention may therefore lead to hyperferritinemia (\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e). Chronic kidney injury can further contribute to this process (\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e). Another potential contributing mechanism may be alterations in erythropoiesis associated with inflammation, leading to functional iron deficiency and increased intracellular iron retention despite preserved transferrin saturation (\u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eThe relationship between collagen IV mutations and systemic iron metabolism is not yet fully defined, and excessive and persistent hyperferritinemia in Alport syndrome has not been described in the literature. It is unclear whether this results from inflammatory disease activity, hepcidin-induced iron retention, or a previously unknown immunometabolic phenotype within Alport syndrome.\u003c/p\u003e \u003cp\u003eRecognizing this pattern is clinically important because in nephrology practice, severe hyperferritinemia is often interpreted as primary iron overload. In patients with hereditary nephropathy, misclassification can lead to unnecessary investigations or inappropriate long-term treatment strategies. This case highlights the importance of integrating transferrin saturation, genetic assessment, and quantitative MRI findings when interpreting significantly elevated ferritin levels.\u003c/p\u003e \u003cp\u003eKey laboratory and imaging findings are summarized in Table\u0026nbsp;\u003cspan refid=\"Tab1\" class=\"InternalRef\"\u003e1\u003c/span\u003e.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab1\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eKey Laboratory and Imaging Findings\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"2\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c2\" colnum=\"2\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eParameter\u003c/p\u003e \u003c/th\u003e \u003cth align=\"left\" colname=\"c2\"\u003e \u003cp\u003eFinding\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003ePeak ferritin\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e\u0026gt;\u0026thinsp;2000 ng/mL (persistent)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTransferrin saturation\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003e21\u0026ndash;32% (normal range)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHemoglobin\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eNormocytic, stable\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHFE mutation\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eNegative\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eLiver T2* MRI\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eSevere hepatic iron deposition (1.5\u0026ndash;1.8 ms)\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eCardiac T2* MRI\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eNormal\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAudiometry\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003eBilateral sensorineural hearing loss\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eGenetic testing\u003c/p\u003e \u003c/td\u003e \u003ctd align=\"left\" colname=\"c2\"\u003e \u003cp\u003ePathogenic COL4A5 mutation\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e \u003cp\u003eFurther prospective studies are needed to clarify whether this represents a reproducible immunometabolic phenotype within collagen IV\u0026ndash;associated nephropathy.\u003c/p\u003e"},{"header":"Conclusion","content":"\u003cp\u003eThis case describes persistent hyperferritinemia with radiologically confirmed severe hepatic iron accumulation in a patient with genetically confirmed X-linked Alport syndrome, without transfusion exposure or hereditary hemochromatosis.\u003c/p\u003e \u003cp\u003eThe co-occurrence of renal involvement, bilateral and progressive sensorineural hearing loss, hepatosplenomegaly, and severe hyperferritinemia suggests that chronic basement membrane damage may affect systemic iron metabolism in addition to structural glomerular pathology.\u003c/p\u003e \u003cp\u003eThese findings are consistent with a macrophage-mediated secondary iron redistribution process, representing an immunometabolic dimension in Alport syndrome. Clarifying this situation is also clinically important because in such patients, severe hyperferritinemia can be misinterpreted as primary iron overload, ultimately leading to unnecessary or incorrect interventions.\u003c/p\u003e \u003cp\u003eFurther studies are needed to clarify whether dysregulated iron metabolism in collagen IV-related nephropathies reflects inflammatory disease activity, reticuloendothelial iron retention, or a contributing pathogenic mechanism. Increased awareness of this potential relationship could improve the diagnostic evaluation of unexplained hyperferritinemia in hereditary glomerular disorders.\u003c/p\u003e \u003cp\u003eThe main educational implications of this case are summarized in Table\u0026nbsp;\u003cspan refid=\"Tab2\" class=\"InternalRef\"\u003e2\u003c/span\u003e.\u003c/p\u003e \u003cp\u003e \u003cdiv class=\"gridtable\"\u003e\u003ctable float=\"Yes\" id=\"Tab2\" border=\"1\"\u003e \u003ccaption language=\"En\"\u003e \u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e \u003cdiv class=\"CaptionContent\"\u003e \u003cp\u003eTeaching Points\u003c/p\u003e \u003c/div\u003e \u003c/caption\u003e \u003ccolgroup cols=\"1\"\u003e \u003cdiv align=\"left\" class=\"colspec\" colname=\"c1\" colnum=\"1\"\u003e\u003c/div\u003e \u003cthead\u003e \u003ctr\u003e \u003cth align=\"left\" colname=\"c1\"\u003e \u003cp\u003eTeaching Points\u003c/p\u003e \u003c/th\u003e \u003c/tr\u003e \u003c/thead\u003e \u003ctbody\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eSevere hyperferritinemia with normal transferrin saturation should prompt evaluation for secondary iron redistribution mechanisms.\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eIn hereditary nephropathies, chronic sterile inflammation may contribute to altered iron metabolism.\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eHepatic T2* MRI is useful for distinguishing patterns of iron deposition.\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eNegative HFE mutation analysis does not exclude non-classical iron accumulation patterns.\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003ctr\u003e \u003ctd align=\"left\" colname=\"c1\"\u003e \u003cp\u003eAlport syndrome may rarely present with systemic iron dysregulation.\u003c/p\u003e \u003c/td\u003e \u003c/tr\u003e \u003c/tbody\u003e \u003c/colgroup\u003e \u003c/table\u003e\u003c/div\u003e \u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cdiv class=\"DefinitionList\"\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eMRI\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eMagnetic Resonance Imaging\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eHFE\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eHereditary Haemochromatosis Protein\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eANA\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eAnti Nuclear Antibody\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eANCA\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eAnti Neutrophil Cytoplasmic Antibody\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eCRP\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eC-Reactive Protein\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eESR\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eErythrocyte Sedimentation Rate\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003cdiv class=\"DefinitionListEntry\"\u003e \u003cdiv class=\"Term\"\u003eSGLT2 inhibitors\u003c/div\u003e \u003cdiv class=\"Description\"\u003e \u003cp\u003eSodium-Glucose Co-transporter 2 inhibitors\u003c/p\u003e \u003c/div\u003e \u003c/div\u003e \u003c/div\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eEthical approval was not required for this case report according to institutional policy. Written informed consent was obtained from the patient for participation in this study.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConsent for publication\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eWritten informed consent was obtained from the patient for publication of this case report and any accompanying images. A copy of the written consent is available for review by the Editor-in-Chief of this journal.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eAll data generated or analysed during this study are included in this published article.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe author declares that she has no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eThe author received no specific funding for this work.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors\u0026rsquo; contributions\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eTU conceptualized the study, collected the clinical data, analysed the findings, and wrote the manuscript. The author read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e\u003c/p\u003e\n\u003cp\u003eNot applicable.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eWarady BA, Agarwal R, Bangalore S, Chapman A, Levin A, Stenvinkel P, Toto RD, Chertow GM. Alport syndrome classification and management. Kidney Med. 2020;2(5):639\u0026ndash;49. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1016/j.xkme.2020.05.014\u003c/span\u003e\u003cspan address=\"10.1016/j.xkme.2020.05.014\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMahroum N, Alghory A, Kiyak Z, Alwani A, Seida R, Alrais M, Shoenfeld Y. Ferritin\u0026mdash;from iron, through inflammation and autoimmunity, to COVID-19. J Autoimmun. 2022;126:102778. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1016/j.jaut.2021.102778\u003c/span\u003e\u003cspan address=\"10.1016/j.jaut.2021.102778\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFauter M, Mainbourg S, El Jammal T, Guerber A, Zaepfel S, Henry T, Gerfaud-Valentin M, S\u0026egrave;ve P, Jamilloux Y. Extreme hyperferritinemia: causes and prognosis. J Clin Med. 2022;11(18):5438. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.3390/jcm11185438\u003c/span\u003e\u003cspan address=\"10.3390/jcm11185438\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eQuinlan C, Rheault MN. Genetic basis of type IV collagen disorders of the kidney. Clin J Am Soc Nephrol. 2021;16(7):1101\u0026ndash;9. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.2215/CJN.19171220\u003c/span\u003e\u003cspan address=\"10.2215/CJN.19171220\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSandnes M, Ulvik RJ, Vorland M, Reikvam H. Hyperferritinemia\u0026mdash;A clinical overview. J Clin Med. 2021;10(9):2008. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.3390/jcm10092008\u003c/span\u003e\u003cspan address=\"10.3390/jcm10092008\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eSpeer T, Dimmeler S, Schunk SJ, Fliser D, Ridker PM. Targeting innate immunity-driven inflammation in CKD and cardiovascular disease. Nat Rev Nephrol. 2022;18(12):762\u0026ndash;78. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1038/s41581-022-00621-9\u003c/span\u003e\u003cspan address=\"10.1038/s41581-022-00621-9\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eOgolla CO, Karani LW, Musyoki S, Maruti P. Impact of iron deficiency and erythropoiesis-stimulating agents on anemia in CKD progression. Int J Nephrol. 2025;2025:2567637. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1155/ijne/2567637\u003c/span\u003e\u003cspan address=\"10.1155/ijne/2567637\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eMarques O, Weiss G, Muckenthaler MU. The role of iron in chronic inflammatory diseases: from mechanisms to treatment options in anemia of inflammation. Blood. 2022;140(19):2011\u0026ndash;2023. \u003cspan class=\"ExternalRef\"\u003e\u003cspan class=\"RefSource\"\u003e10.1182/blood.2021013472\u003c/span\u003e\u003cspan address=\"10.1182/blood.2021013472\" targettype=\"DOI\" class=\"RefTarget\"\u003e\u003c/span\u003e\u003c/span\u003e. PMID: 35994752.\u003c/span\u003e\u003c/li\u003e\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":false,"hideJournal":false,"highlight":"","institution":"","isAcceptedByJournal":false,"isAuthorSuppliedPdf":false,"isDeskRejected":"","isHiddenFromSearch":false,"isInQc":false,"isInWorkflow":false,"isPdf":false,"isPdfUpToDate":true,"isWithdrawnOrRetracted":false,"journal":{"display":true,"email":"[email protected]","identity":"bmc-nephrology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bnep","sideBox":"Learn more about [BMC Nephrology](http://bmcnephrol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bnep/default.aspx","title":"BMC Nephrology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true},"keywords":"Alport syndrome, hyperferritinemia, iron metabolism, chronic kidney disease, inflammation","lastPublishedDoi":"10.21203/rs.3.rs-8970844/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-8970844/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003ch2\u003eBackground\u003c/h2\u003e \u003cp\u003eAlport syndrome is an X-linked inherited kidney disease caused by mutations in type IV collagen genes (COL4A3, COL4A4, and COL4A5) that affect the glomerular basement membrane and can lead to sensorineural hearing loss and eye abnormalities. This disease, which can cause hematuria, proteinuria, and in more severe cases chronic kidney disease, is characterized by bilateral and high-frequency sensorineural hearing loss, eye dysfunction, and in rare cases, aortic aneurysm; however, abnormalities in iron metabolism are not commonly described.\u003c/p\u003e\u003ch2\u003eCase Presentation:\u003c/h2\u003e \u003cp\u003eWe report a case of persistent and marked hyperferritinemia in a patient with genetically confirmed Alport syndrome, without blood transfusion, significant inflammation, or hereditary hemochromatosis. In 2016, a patient whose etiology of proteinuria and hematuria was investigated showed no abnormalities in iron parameters in laboratory tests performed at that time, while as of 2021, serum ferritin levels were found to be \u0026gt;\u0026thinsp;1000 \u0026micro;g/L. Abdominal ultrasound and MRI scans revealed severe hepatosplenomegaly. Minimal increases in infection and inflammation markers did not explain this severely elevated ferritin level. Hemochromatosis gene mutations were tested in several different laboratories, and no mutations were detected.\u003c/p\u003e\u003ch2\u003eConclusion\u003c/h2\u003e \u003cp\u003eThis case suggests a possible dysregulation of iron metabolism in a patient diagnosed with Alport syndrome, beyond the inflammation associated with conventional chronic kidney disease. The interaction between collagen IV mutations and systemic inflammation and iron regulatory pathways may require more detailed investigation.\u003c/p\u003e","manuscriptTitle":"Severe Hyperferritinemia with Preserved Transferrin Saturation in Genetically Confirmed X-Linked Alport Syndrome: A Case Report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-03-27 13:11:17","doi":"10.21203/rs.3.rs-8970844/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"editorInvitedReview","content":"","date":"2026-04-04T07:48:19+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"119256942206475729167083249914180283162","date":"2026-04-03T16:58:28+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-03-25T12:35:41+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-03-23T10:48:21+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2026-03-02T06:34:27+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-02-28T21:57:25+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Nephrology","date":"2026-02-28T21:53:38+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"[email protected]","identity":"bmc-nephrology","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":false,"externalIdentity":"bnep","sideBox":"Learn more about [BMC Nephrology](http://bmcnephrol.biomedcentral.com/)","snPcode":"","submissionUrl":"https://www.editorialmanager.com/bnep/default.aspx","title":"BMC Nephrology","twitterHandle":"BMC_series","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"em","reportingPortfolio":"BMC Series","inReviewEnabled":true,"inReviewRevisionsEnabled":true}}],"origin":"","ownerIdentity":"fbd1616e-56a1-4e27-b1bf-e34ae9b8750a","owner":[],"postedDate":"March 27th, 2026","published":true,"recentEditorialEvents":[],"rejectedJournal":[],"revision":"","amendment":"","status":"under-review","subjectAreas":[],"tags":[],"updatedAt":"2026-03-27T13:11:17+00:00","versionOfRecord":[],"versionCreatedAt":"2026-03-27 13:11:17","video":"","vorDoi":"","vorDoiUrl":"","workflowStages":[]},"version":"v1","identity":"rs-8970844","journalConfig":"researchsquare"},"__N_SSP":true},"page":"/article/[identity]/[[...version]]","query":{"redirect":"/article/rs-8970844","identity":"rs-8970844","version":["v1"]},"buildId":"XKTyCvWXoU3ODBz1xrDgd","isFallback":false,"isExperimentalCompile":false,"dynamicIds":[84888],"gssp":true,"scriptLoader":[]}