Severe Adenovirus Pneumonia Associated with Biopsy-Evaluated Acute Kidney Injury in an Immunocompetent Adult: 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 Adenovirus Pneumonia Associated with Biopsy-Evaluated Acute Kidney Injury in an Immunocompetent Adult: A Case Report Nazife Nur Özer Şensoy, Yavuz Ayar This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-9050096/v1 This work is licensed under a CC BY 4.0 License Status: Under Review Version 1 posted 15 You are reading this latest preprint version Abstract Background Adenovirus infection is typically self-limited in immunocompetent individuals. Severe pneumonia with renal involvement is uncommon and predominantly reported in immunocompromised hosts. Acute kidney injury (AKI) during viral infections may occur through inflammatory or tubular mechanisms even in the absence of immune-complex–mediated glomerular disease. Case Presentation A previously healthy young woman presented with severe pneumonia. Upper respiratory tract PCR was positive for adenovirus, while blood and urine cultures were negative. Laboratory findings showed marked systemic inflammation (CRP 256 mg/L; procalcitonin 15 ng/mL). Serum creatinine was elevated to 4.0 mg/dL prior to antibiotic therapy. Urinalysis revealed leukocyturia, microscopic hematuria, and subnephrotic proteinuria (860 mg/24 h). Due to persistent renal dysfunction, a kidney biopsy was performed. Light microscopy demonstrated preserved glomerular architecture without proliferative or crescentic changes. Immunofluorescence staining was negative for IgG, IgA, IgM, C3, and C1q. Mild tubular alterations, including focal granular-hyaline casts, were observed, without specific vascular pathology. Overall findings were compatible with infection-associated acute kidney injury. Mini-pulse corticosteroid therapy and empirical broad-spectrum antibiotics were administered. Renal function subsequently improved. Conclusion Severe adenovirus infection may be associated with acute kidney injury even in immunocompetent adults. In the absence of immune-complex deposition or overt glomerular pathology, renal dysfunction may reflect infection-associated tubular injury or systemic inflammatory mechanisms. Adenovirus Acute kidney injury Viral infection Kidney biopsy Immunocompetent patient Case report Figures Figure 1 Figure 2 İNTRODUCTİON Adenovirus infections are generally mild and self-limited in immunocompetent adults [ 1 ]. Severe pulmonary involvement is uncommon and occurs more frequently in immunocompromised individuals and transplant recipients [ 2 ]. Renal complications associated with adenovirus are rare and have been described predominantly in immunosuppressed populations [ 3 ]. Acute kidney injury (AKI) during viral infections may result from multiple mechanisms, including systemic inflammatory response, hemodynamic alterations, or tubular injury. Immune-complex–mediated glomerular disease is uncommon in adenovirus infection, particularly in immunocompetent adults. Reports describing biopsy-evaluated renal involvement in this population remain limited [ 4 ]. Here, we describe a case of severe adenovirus pneumonia complicated by biopsy-evaluated acute kidney injury in a previously healthy woman. CASE PRESENTATION A previously healthy young woman with no history of chronic disease, immunodeficiency, or recent drug exposure was admitted with severe pneumonia. Chest computed tomography demonstrated bilateral ground-glass opacities and consolidations consistent with severe viral pneumonia (Fig. 1 ). A comprehensive upper respiratory tract PCR panel was performed. SARS-CoV-2 (COVID-19), influenza A/B, respiratory syncytial virus, parainfluenza virus, and other common respiratory pathogens were negative; adenovirus was the only detected pathogen. Blood and urine cultures were also negative. Laboratory evaluation revealed marked systemic inflammation (C-reactive protein 256 mg/L; procalcitonin 15 ng/mL). At admission, serum creatinine was elevated to 4,0 mg/dL from previously normal baseline levels. Notably, renal dysfunction developed prior to the initiation of antibiotic therapy. Urinalysis demonstrated leukocyturia (7 leukocytes per high-power field), microscopic hematuria (5 erythrocytes per high-power field), and subnephrotic proteinuria (860 mg/24 h), without clinical features suggestive of primary glomerular disease Due to persistent renal dysfunction and absence of an alternative explanation, a percutaneous kidney biopsy was performed. Light microscopy demonstrated preserved glomerular architecture without proliferative or crescentic changes. Immunofluorescence staining was negative for IgG, IgA, IgM, C3, and C1q. Mild tubular alterations, including focal granular-hyaline casts, were observed. No granuloma formation, immune-complex deposition, or specific vascular pathology was identified. Overall, the findings were compatible with infection-associated acute kidney injury. (Fig. 2 ) Mini-pulse corticosteroid therapy was initiated in the setting of persistent renal dysfunction and systemic inflammation. Broad-spectrum antibiotics were administered empirically according to infectious disease recommendations. Renal function progressively improved during follow-up. DISCUSSION Acute kidney injury (AKI) during systemic infections may result from multiple mechanisms, including hemodynamic instability, systemic inflammatory response, cytokine-mediated tubular stress, or less commonly immune-mediated processes [ 5 ]. Drug-induced acute interstitial nephritis represents a frequent cause of biopsy-proven AKI; however, infection-associated renal injury may occur even in the absence of drug exposure [ 6 ]. Adenovirus-associated renal involvement has predominantly been described in immunocompromised individuals, particularly hematopoietic stem cell and solid organ transplant recipients, where direct viral cytopathic effects have been demonstrated in renal tissue [ 7 , 8 ]. In contrast, renal complications in immunocompetent adults are rare and are typically reported as transient or mild renal dysfunction rather than biopsy-evaluated cases. In the present case, the patient was previously healthy and immunocompetent, with no history of chronic illness or recent medication use. Notably, acute kidney injury developed in the absence of any prior antibiotic or nephrotoxic drug exposure, making drug-induced acute interstitial nephritis unlikely. Blood and urine cultures were negative, and an extensive respiratory viral panel excluded alternative viral pathogens, supporting adenovirus as the most probable infectious trigger. Histopathological evaluation demonstrated preserved glomerular architecture without immune-complex deposition or proliferative changes. Mild tubular alterations, including focal granular-hyaline casts, were observed, while no specific vascular pathology was identified. These findings argue against immune-complex–mediated glomerulonephritis and severe ischemic acute tubular necrosis. Instead, they suggest infection-associated tubular injury, likely mediated by systemic inflammation and cytokine activation during severe viral pneumonia. Although adenoviral PCR was not performed on renal tissue and direct viral invasion cannot be confirmed, the temporal association between severe adenovirus pneumonia and acute kidney injury supports infection-related renal involvement. Clinical improvement following supportive management and short-course corticosteroid therapy further suggests a potentially reversible inflammatory component. This case broadens the clinical spectrum of adenovirus-associated renal injury in immunocompetent adults and highlights the importance of considering infection-associated AKI in patients presenting with renal dysfunction during severe viral pneumonia. CONCLUSİON Although adenovirus was not demonstrated in renal tissue, the temporal association between severe adenovirus pneumonia and acute kidney injury, together with the exclusion of alternative causes, suggests infection-associated renal involvement potentially mediated by systemic inflammatory mechanisms. Severe adenovirus infection may be complicated by acute kidney injury even in immunocompetent adults. In the absence of immune-complex deposition or overt glomerular pathology, renal dysfunction may reflect infection-related tubular injury rather than classic immune-mediated interstitial nephritis. Early recognition and appropriate supportive management are essential to optimize renal outcomes. Declarations Ethical approval was not required for this retrospective single case report according to institutional policy. Consent for publication Written informed consent was obtained from the patient for publication of this case report and accompanying clinical information. Conflicts of Interest The authors declare no conflicts of interest. Funding No funding was received for this case report. Author Contribution N.N.O.S. conceived the study, collected the clinical data, and wrote the main manuscript text,Y.A. contributed to clinical interpretation, supervised the study, and critically revised the manuscript. Data Availability The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions. References Lynch JP 3rd, Kajon AE, Adenovirus. Epidemiology, Global Spread of Novel Types, and Approach to Treatment. Semin Respir Crit Care Med. 2021;42(6):800–21. Florescu DF, Schaenman JM, AST Infectious Diseases Community of Practice. Adenovirus in solid organ transplant recipients: Guidelines from the American Society of Transplantation Infectious Diseases Community of Practice. Clin Transpl. 2019;33(9):e13527. Kiran PVS, Gupta N, Prabhu AR, Sebastian A, Boodman C, Kumar TP. Adenovirus nephritis in adult kidney allograft recipients: a systematic review of literature. Infection. 2025;53(1):25–37. Praga M, González E. Acute interstitial nephritis. Kidney Int. 2010;77(11):956–61. Xu X, Zeng T, Chen S, Tian N, Zhang C, Chen Y, Deng S, Mao Z, Liao J, Zhang T, He Y, Wang W, Chen P, Song Y. Acute kidney injury: pathogenesis and therapeutic interventions. Mol Biomed. 2025;6(1):61. Raina R, Ale S, Chaturvedi T, Fraley L, Novak R, Tanphaichitr N. Infection associated acute interstitial nephritis; a case report. J Nephropathol. 2017;6(2):53–7. Florescu DF, Schaenman JM, AST Infectious Diseases Community of Practice. Adenovirus in solid organ transplant recipients: Guidelines from the American Society of Transplantation Infectious Diseases Community of Practice. Clin Transpl. 2019;33(9):e13527. Bruno B, Zager RA, Boeckh MJ, Gooley TA, Myerson DH, Huang ML, Hackman RC. Adenovirus nephritis in hematopoietic stem-cell transplantation. Transplantation. 2004;77(7):1049–57. Additional Declarations No competing interests reported. Supplementary Files CAREchecklistEnglish2013.pdf Cite Share Download PDF Status: Under Review Version 1 posted Editorial decision: Revision requested 27 Apr, 2026 Reviews received at journal 16 Apr, 2026 Reviews received at journal 12 Apr, 2026 Reviewers agreed at journal 08 Apr, 2026 Reviewers agreed at journal 05 Apr, 2026 Reviews received at journal 04 Apr, 2026 Reviewers agreed at journal 03 Apr, 2026 Reviewers agreed at journal 03 Apr, 2026 Reviews received at journal 03 Apr, 2026 Reviewers agreed at journal 03 Apr, 2026 Reviewers invited by journal 03 Apr, 2026 Editor assigned by journal 31 Mar, 2026 Editor invited by journal 11 Mar, 2026 Submission checks completed at journal 10 Mar, 2026 First submitted to journal 10 Mar, 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. 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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-9050096","acceptedTermsAndConditions":true,"allowDirectSubmit":false,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":619914125,"identity":"e88aa5ed-90a7-47d4-b284-d196fbbf48e4","order_by":0,"name":"Nazife Nur Özer Şensoy","email":"data:image/png;base64,iVBORw0KGgoAAAANSUhEUgAAAZAAAAAyAQMAAABI0h/eAAAABlBMVEX///8AAABVwtN+AAAACXBIWXMAAA7EAAAOxAGVKw4bAAAAy0lEQVRIiWNgGAWjYDADfgkwJSFDvBbJGQyMDUAtPMRrMbgB1sJAWIu5RO7Dhz8q7jEY324+/uhGjQUPA/vhoxvwabGckW5sIHGmmMHszrHE5pxjQIfxpKXdwO+eNDYJw7YEBrMbOYbNOWxALRI8ZoS1JP5LYDCeAdLyj1gtBxsSGAwkgFpy24jRcuYZs2HDsQQGiRtpibNz+yR42Aj65Xga48MfNQkM/DOSD3zO+VYnx89++BheLTBQ3wBjsRGjfBSMglEwCkYBfgAAlxxCciY/MB0AAAAASUVORK5CYII=","orcid":"","institution":"University of Health Sciences, Bursa City Training and Research Hospital","correspondingAuthor":true,"prefix":"","firstName":"Nazife","middleName":"Nur Özer","lastName":"Şensoy","suffix":""},{"id":619914126,"identity":"15ac7114-940f-4fbe-b3f6-8ccdfea956ca","order_by":1,"name":"Yavuz Ayar","email":"","orcid":"","institution":"University of Health Sciences, Bursa City Training and Research Hospital","correspondingAuthor":false,"prefix":"","firstName":"Yavuz","middleName":"","lastName":"Ayar","suffix":""}],"badges":[],"createdAt":"2026-03-06 11:39:25","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-9050096/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-9050096/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":106544512,"identity":"bfb1cd6b-15bb-412c-adbc-c634db7c7130","added_by":"auto","created_at":"2026-04-09 16:41:12","extension":"jpg","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":110428,"visible":true,"origin":"","legend":"\u003cp\u003eChest CT (Computer Tomography) and chest radiography demonstrating bilateral ground-glass opacities and consolidations consistent with severe viral pneumonia .\u003c/p\u003e","description":"","filename":"1.jpg","url":"https://assets-eu.researchsquare.com/files/rs-9050096/v1/df76980ffc7928d9a7bed75c.jpg"},{"id":106544630,"identity":"65321a99-e4c0-421e-a24f-8df0f8098a53","added_by":"auto","created_at":"2026-04-09 16:41:43","extension":"png","order_by":2,"title":"Figure 2","display":"","copyAsset":false,"role":"figure","size":577149,"visible":true,"origin":"","legend":"\u003cp\u003eKidney biopsy showing tubular epithelial injury and dilated tubules containing eosinophilic proteinaceous casts (hyaline casts) with mild interstitial inflammatory infiltration (H\u0026amp;E stain).\u003c/p\u003e","description":"","filename":"2.png","url":"https://assets-eu.researchsquare.com/files/rs-9050096/v1/c25d9de2f303777dc3a21c6e.png"},{"id":106544699,"identity":"9dce61de-ec86-4cf1-b553-03ec26f8cbc0","added_by":"auto","created_at":"2026-04-09 16:41:56","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":1102348,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-9050096/v1/1fc5da6d-f2cb-4a04-81c5-ee44f2ab6c99.pdf"},{"id":106544513,"identity":"76dc3813-e5a1-4fd2-bfbe-6e34d9b49d05","added_by":"auto","created_at":"2026-04-09 16:41:12","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"supplement","size":804562,"visible":true,"origin":"","legend":"","description":"","filename":"CAREchecklistEnglish2013.pdf","url":"https://assets-eu.researchsquare.com/files/rs-9050096/v1/efc9c8ee3cce08665cbac484.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"Severe Adenovirus Pneumonia Associated with Biopsy-Evaluated Acute Kidney Injury in an Immunocompetent Adult: A Case Report","fulltext":[{"header":"İNTRODUCTİON","content":"\u003cp\u003eAdenovirus infections are generally mild and self-limited in immunocompetent adults [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. Severe pulmonary involvement is uncommon and occurs more frequently in immunocompromised individuals and transplant recipients [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. Renal complications associated with adenovirus are rare and have been described predominantly in immunosuppressed populations [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eAcute kidney injury (AKI) during viral infections may result from multiple mechanisms, including systemic inflammatory response, hemodynamic alterations, or tubular injury. Immune-complex\u0026ndash;mediated glomerular disease is uncommon in adenovirus infection, particularly in immunocompetent adults. Reports describing biopsy-evaluated renal involvement in this population remain limited [\u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eHere, we describe a case of severe adenovirus pneumonia complicated by biopsy-evaluated acute kidney injury in a previously healthy woman.\u003c/p\u003e"},{"header":"CASE PRESENTATION","content":"\u003cp\u003eA previously healthy young woman with no history of chronic disease, immunodeficiency, or recent drug exposure was admitted with severe pneumonia. Chest computed tomography demonstrated bilateral ground-glass opacities and consolidations consistent with severe viral pneumonia (Fig.\u0026nbsp;\u003cspan refid=\"Fig2\" class=\"InternalRef\"\u003e1\u003c/span\u003e).\u003c/p\u003e \u003cp\u003eA comprehensive upper respiratory tract PCR panel was performed. SARS-CoV-2 (COVID-19), influenza A/B, respiratory syncytial virus, parainfluenza virus, and other common respiratory pathogens were negative; adenovirus was the only detected pathogen. Blood and urine cultures were also negative.\u003c/p\u003e \u003cp\u003eLaboratory evaluation revealed marked systemic inflammation (C-reactive protein 256 mg/L; procalcitonin 15 ng/mL). At admission, serum creatinine was elevated to 4,0 mg/dL from previously normal baseline levels. Notably, renal dysfunction developed prior to the initiation of antibiotic therapy. Urinalysis demonstrated leukocyturia (7 leukocytes per high-power field), microscopic hematuria (5 erythrocytes per high-power field), and subnephrotic proteinuria (860 mg/24 h), without clinical features suggestive of primary glomerular disease\u003c/p\u003e \u003cp\u003eDue to persistent renal dysfunction and absence of an alternative explanation, a percutaneous kidney biopsy was performed. Light microscopy demonstrated preserved glomerular architecture without proliferative or crescentic changes. Immunofluorescence staining was negative for IgG, IgA, IgM, C3, and C1q. Mild tubular alterations, including focal granular-hyaline casts, were observed. No granuloma formation, immune-complex deposition, or specific vascular pathology was identified. Overall, the findings were compatible with infection-associated acute kidney injury. (Fig.\u0026nbsp;\u003cspan refid=\"Fig1\" class=\"InternalRef\"\u003e2\u003c/span\u003e)\u003c/p\u003e \u003cp\u003eMini-pulse corticosteroid therapy was initiated in the setting of persistent renal dysfunction and systemic inflammation. Broad-spectrum antibiotics were administered empirically according to infectious disease recommendations. Renal function progressively improved during follow-up.\u003c/p\u003e"},{"header":"DISCUSSION","content":"\u003cp\u003eAcute kidney injury (AKI) during systemic infections may result from multiple mechanisms, including hemodynamic instability, systemic inflammatory response, cytokine-mediated tubular stress, or less commonly immune-mediated processes [\u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. Drug-induced acute interstitial nephritis represents a frequent cause of biopsy-proven AKI; however, infection-associated renal injury may occur even in the absence of drug exposure [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eAdenovirus-associated renal involvement has predominantly been described in immunocompromised individuals, particularly hematopoietic stem cell and solid organ transplant recipients, where direct viral cytopathic effects have been demonstrated in renal tissue [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e, \u003cspan citationid=\"CR8\" class=\"CitationRef\"\u003e8\u003c/span\u003e]. In contrast, renal complications in immunocompetent adults are rare and are typically reported as transient or mild renal dysfunction rather than biopsy-evaluated cases.\u003c/p\u003e \u003cp\u003eIn the present case, the patient was previously healthy and immunocompetent, with no history of chronic illness or recent medication use. Notably, acute kidney injury developed in the absence of any prior antibiotic or nephrotoxic drug exposure, making drug-induced acute interstitial nephritis unlikely. Blood and urine cultures were negative, and an extensive respiratory viral panel excluded alternative viral pathogens, supporting adenovirus as the most probable infectious trigger.\u003c/p\u003e \u003cp\u003eHistopathological evaluation demonstrated preserved glomerular architecture without immune-complex deposition or proliferative changes. Mild tubular alterations, including focal granular-hyaline casts, were observed, while no specific vascular pathology was identified. These findings argue against immune-complex\u0026ndash;mediated glomerulonephritis and severe ischemic acute tubular necrosis. Instead, they suggest infection-associated tubular injury, likely mediated by systemic inflammation and cytokine activation during severe viral pneumonia.\u003c/p\u003e \u003cp\u003eAlthough adenoviral PCR was not performed on renal tissue and direct viral invasion cannot be confirmed, the temporal association between severe adenovirus pneumonia and acute kidney injury supports infection-related renal involvement. Clinical improvement following supportive management and short-course corticosteroid therapy further suggests a potentially reversible inflammatory component.\u003c/p\u003e \u003cp\u003eThis case broadens the clinical spectrum of adenovirus-associated renal injury in immunocompetent adults and highlights the importance of considering infection-associated AKI in patients presenting with renal dysfunction during severe viral pneumonia.\u003c/p\u003e"},{"header":"CONCLUSİON","content":"\u003cp\u003eAlthough adenovirus was not demonstrated in renal tissue, the temporal association between severe adenovirus pneumonia and acute kidney injury, together with the exclusion of alternative causes, suggests infection-associated renal involvement potentially mediated by systemic inflammatory mechanisms.\u003c/p\u003e \u003cp\u003eSevere adenovirus infection may be complicated by acute kidney injury even in immunocompetent adults. In the absence of immune-complex deposition or overt glomerular pathology, renal dysfunction may reflect infection-related tubular injury rather than classic immune-mediated interstitial nephritis. Early recognition and appropriate supportive management are essential to optimize renal outcomes.\u003c/p\u003e "},{"header":"Declarations","content":"\u003cp\u003e \u003cstrong\u003eEthical approval\u003c/strong\u003e \u003cp\u003ewas not required for this retrospective single case report according to institutional policy.\u003c/p\u003e \u003c/p\u003e \u003cp\u003e \u003cstrong\u003eConsent for publication\u003c/strong\u003e \u003cp\u003eWritten informed consent was obtained from the patient for publication of this case report and accompanying clinical information.\u003c/p\u003e \u003c/p\u003e \u003cp\u003e \u003cstrong\u003eConflicts of Interest\u003c/strong\u003e \u003cp\u003eThe authors declare no conflicts of interest.\u003c/p\u003e \u003c/p\u003e\u003ch2\u003eFunding\u003c/h2\u003e \u003cp\u003eNo funding was received for this case report.\u003c/p\u003e\u003ch2\u003eAuthor Contribution\u003c/h2\u003e\u003cp\u003eN.N.O.S. conceived the study, collected the clinical data, and wrote the main manuscript text,Y.A. contributed to clinical interpretation, supervised the study, and critically revised the manuscript.\u003c/p\u003e\u003ch2\u003eData Availability\u003c/h2\u003e\u003cp\u003eThe data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\u003cli\u003e\u003cspan\u003eLynch JP 3rd, Kajon AE, Adenovirus. Epidemiology, Global Spread of Novel Types, and Approach to Treatment. Semin Respir Crit Care Med. 2021;42(6):800\u0026ndash;21.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFlorescu DF, Schaenman JM, AST Infectious Diseases Community of Practice. Adenovirus in solid organ transplant recipients: Guidelines from the American Society of Transplantation Infectious Diseases Community of Practice. Clin Transpl. 2019;33(9):e13527.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eKiran PVS, Gupta N, Prabhu AR, Sebastian A, Boodman C, Kumar TP. Adenovirus nephritis in adult kidney allograft recipients: a systematic review of literature. Infection. 2025;53(1):25\u0026ndash;37.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003ePraga M, Gonz\u0026aacute;lez E. Acute interstitial nephritis. Kidney Int. 2010;77(11):956\u0026ndash;61.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eXu X, Zeng T, Chen S, Tian N, Zhang C, Chen Y, Deng S, Mao Z, Liao J, Zhang T, He Y, Wang W, Chen P, Song Y. Acute kidney injury: pathogenesis and therapeutic interventions. Mol Biomed. 2025;6(1):61.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eRaina R, Ale S, Chaturvedi T, Fraley L, Novak R, Tanphaichitr N. Infection associated acute interstitial nephritis; a case report. J Nephropathol. 2017;6(2):53\u0026ndash;7.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eFlorescu DF, Schaenman JM, AST Infectious Diseases Community of Practice. Adenovirus in solid organ transplant recipients: Guidelines from the American Society of Transplantation Infectious Diseases Community of Practice. Clin Transpl. 2019;33(9):e13527.\u003c/span\u003e\u003c/li\u003e \u003cli\u003e\u003cspan\u003eBruno B, Zager RA, Boeckh MJ, Gooley TA, Myerson DH, Huang ML, Hackman RC. Adenovirus nephritis in hematopoietic stem-cell transplantation. Transplantation. 2004;77(7):1049\u0026ndash;57.\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":"Adenovirus, Acute kidney injury, Viral infection, Kidney biopsy, Immunocompetent patient, Case report","lastPublishedDoi":"10.21203/rs.3.rs-9050096/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-9050096/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003e\u003cstrong\u003eBackground\u003c/strong\u003e\u003cbr\u003e\nAdenovirus infection is typically self-limited in immunocompetent individuals. Severe pneumonia with renal involvement is uncommon and predominantly reported in immunocompromised hosts. Acute kidney injury (AKI) during viral infections may occur through inflammatory or tubular mechanisms even in the absence of immune-complex–mediated glomerular disease.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCase Presentation\u003c/strong\u003e\u003cbr\u003e\nA previously healthy young woman presented with severe pneumonia. Upper respiratory tract PCR was positive for adenovirus, while blood and urine cultures were negative. Laboratory findings showed marked systemic inflammation (CRP 256 mg/L; procalcitonin 15 ng/mL). Serum creatinine was elevated to 4.0 mg/dL prior to antibiotic therapy. Urinalysis revealed leukocyturia, microscopic hematuria, and subnephrotic proteinuria (860 mg/24 h).\u003c/p\u003e\n\u003cp\u003eDue to persistent renal dysfunction, a kidney biopsy was performed. Light microscopy demonstrated preserved glomerular architecture without proliferative or crescentic changes. Immunofluorescence staining was negative for IgG, IgA, IgM, C3, and C1q. Mild tubular alterations, including focal granular-hyaline casts, were observed, without specific vascular pathology. Overall findings were compatible with infection-associated acute kidney injury.\u003c/p\u003e\n\u003cp\u003eMini-pulse corticosteroid therapy and empirical broad-spectrum antibiotics were administered. Renal function subsequently improved.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eConclusion\u003c/strong\u003e\u003cbr\u003e\nSevere adenovirus infection may be associated with acute kidney injury even in immunocompetent adults. In the absence of immune-complex deposition or overt glomerular pathology, renal dysfunction may reflect infection-associated tubular injury or systemic inflammatory mechanisms.\u003c/p\u003e","manuscriptTitle":"Severe Adenovirus Pneumonia Associated with Biopsy-Evaluated Acute Kidney Injury in an Immunocompetent Adult: A Case Report","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2026-04-09 16:39:39","doi":"10.21203/rs.3.rs-9050096/v1","editorialEvents":[{"type":"communityComments","content":0},{"type":"decision","content":"Revision requested","date":"2026-04-27T16:21:05+00:00","index":"","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-04-16T18:52:58+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-04-12T17:11:43+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"221392748482772845579110123927419291857","date":"2026-04-08T15:38:25+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"301535292374488467955914558751999445417","date":"2026-04-05T09:07:51+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-04-04T06:11:24+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"329277299275479860347743981666068291022","date":"2026-04-04T01:44:36+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"252944716482764774398579089962030502910","date":"2026-04-03T20:28:17+00:00","index":"hide","fulltext":""},{"type":"editorInvitedReview","content":"","date":"2026-04-03T14:33:37+00:00","index":"hide","fulltext":""},{"type":"reviewerAgreed","content":"318851385505063816029273951127436539950","date":"2026-04-03T13:52:09+00:00","index":"hide","fulltext":""},{"type":"reviewersInvited","content":"","date":"2026-04-03T12:50:26+00:00","index":"","fulltext":""},{"type":"editorAssigned","content":"","date":"2026-03-31T08:46:26+00:00","index":"","fulltext":""},{"type":"editorInvited","content":"","date":"2026-03-11T04:20:01+00:00","index":"","fulltext":""},{"type":"checksComplete","content":"","date":"2026-03-11T00:16:49+00:00","index":"","fulltext":""},{"type":"submitted","content":"BMC Nephrology","date":"2026-03-10T17:54:08+00:00","index":"","fulltext":""}],"status":"published","journal":{"display":true,"email":"
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