BK Virus Nephropathy in a Native Kidney of a Lung Transplant Patient | 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 BK Virus Nephropathy in a Native Kidney of a Lung Transplant Patient Mercedes Galloway, John Sousou, Xu Zeng, Alaa Awad, Charles Heilig This is a preprint; it has not been peer reviewed by a journal. https://doi.org/ 10.21203/rs.3.rs-5014825/v1 This work is licensed under a CC BY 4.0 License Status: Posted Version 1 posted You are reading this latest preprint version Abstract Background: BK virus nephropathy (BKVN) in native kidneys following lung transplantation is an exceptionally rare occurrence. This case report highlights a unique instance where BKVN developed in a patient’s native kidney post-lung transplantation, emphasizing its rarity and the importance of considering BKVN in differential diagnoses for patients presenting with acute kidney injury (AKI) after such transplants. Case Presentation: A patient who had undergone bilateral lung transplantation three years prior presented with worsening creatinine levels following an angiogram. The patient’s history included no exposure to toxic medications, contrast, or other known triggers for kidney disease. The worsening renal function was initially investigated through an angiogram, which was followed by the onset of hematuria and a progressive rise in creatinine levels. To determine the cause of the acute kidney injury, a kidney biopsy was performed. The biopsy of the left kidney revealed polyoma nephropathy. Confirmatory tests, including positive staining for Simian virus 40 (SV40), confirmed the diagnosis of BK virus nephropathy in the patient’s native kidney. Conclusion: The occurrence of BK virus nephropathy in the native kidney following lung transplantation is a rare phenomenon. This case underscores the necessity of considering BK virus nephropathy in the differential diagnosis of acute kidney injury in patients with a history of lung transplantation. Early recognition and diagnosis are crucial for appropriate management and potential modification of immunosuppressive therapy to prevent further kidney damage. BK Virus Nephropathy Lung Transplantation Acute Kidney Injury Polyoma Nephropathy Simian Virus 40 Native Kidney Renal Biopsy Figures Figure 1 Background The BK virus is a member of the Polyomaviridae family and henceforth possesses a circular, double-stranded DNA genome [ 1 ]. Its association with urethral stricture is widely recognized after the virus was first confirmed through biopsy in 1993 [ 1 ]. The BK virus typically remains in a latent phase within the genitourinary lining tract of the host, and is usually inactive under normal conditions. Initially detectable in urine, it may progress to viremia, and subsequently establish infection within the transplanted kidney, leading to injury. However in patients with immunocompromised states, such as post-transplant immunosuppression, the virus can become reactivated [ 2 ]. The mechanism of persistent BK virus infection involves its T antigens interacting with cell cycle regulatory proteins such as p53 and Rb. Following viremia, the virus can remain dormant in uroepithelial cells, potentially reactivating under conditions conducive to immunosuppression. The epidemiology of BK virus shows a seroprevalence peak of 91% in children aged 5–9 years, and overall seropositivity rate of 81%, with antibody titers declining with age. Although the mode of transmission is uncertain, some studies indicate that respiratory spread is suspected to be part of the transmission process [ 3 , 4 , 5 ]. In a study conducted by Tetsuya Kaneko et al, BK viruria was detected in 13.5% of normal individuals, with a much higher prevalence of 33.3% among patients with renal disease. BK viruria is even more pronounced in patients with renal disease undergoing steroid treatment, where it was observed in 55.6% of cases [ 3 ]. Most cases of BK virus nephropathy have been described in patients with transplanted kidneys and rarely described in native kidneys. Here, we present a case of a patient who underwent bilateral lung transplantation and subsequently developed biopsy-proven BK nephropathy in his native kidney. Case presentation A 67-year-old male with a medical history of chronic kidney disease (CKD), hypertension, steroid-induced type 2 diabetes mellitus, and a bilateral lung transplant three years ago for end-stage chronic obstructive pulmonary disease presented to the hospital with acute blood loss anemia. This condition was secondary to a renal hemorrhage that occurred 20 days after a renal biopsy, which had been performed to investigate the cause of his acute kidney injury. The patient had been following a pulmonologist for 3 years and had been stable on his long-term immunosuppression regimen of tacrolimus, mycophenolate mofetil, prednisone, and basiliximab. On admission, the patient was hemodynamically stable and in no apparent distress. Laboratory testing was notable for a hemoglobin of 6.6 g/dL, with his baseline being around 11 g/dL, and a creatinine of 3.39. His hemoglobin improved following red blood cell transfusion and angiography with embolization of a renal arteriovenous fistula by interventional radiology the same day. Seven months prior, labs indicated worsening creatinine despite 17 months of everolimus therapy. Renal function had worsened while the patient was on mTOR inhibitors (everolimus), leading to the discontinuation of the medication seven months prior. Despite stopping everolimus, there was no significant improvement in renal function. Two years prior, his baseline serum creatinine was approximately 1.3 mg/dL, but in the past month, it had increased to a range of 2-2.5 mg/dL. Proteinuria was detected with a microalbumin-to-creatinine ratio of 368 mg/gm. The patient had no recent history of antibiotics, nonsteroidal anti-inflammatory drugs, over-the-counter medications, herbal supplements, or intravenous contrast use in the past five years, prompting further investigation into the etiology of his kidney disease. Extensive viral testing is detailed in Table 1 . Table 1 Comprehensive viral testing demonstrating the presence of BK virus, with all other viral tests returning unremarkable results. Test Result Influenza A Virus NAA Not Detected CMV DNA, QN Not Detected CMV Quant PCR Log Not Detected Coronavirus (COVID-19) NAA Not Detected EBV Quant Not Detected Respiratory Syncytial Virus Not Detected SARS-CoV-2 (COVID-19) Not Detected BK Virus Quant PCR Detected BK Virus Quant PCR Detected CMV Quant < 59 CMV Quant PCR < 1.77 Hepatitis C RNA-PCR (Quantitative) Equivocal Hepatitis C RNA-PCR (Quantitative) Equivocal CMV DNA Not Detected CMV DNA < 200 CMV Quant PCR Not Detected CMV Quant PCR Not Detected CMV Quant PCR < 2.30 CMV Quant PCR < 2.30 The BK Virus DNA Quantitative PCR was initially diagnosed at 845,871 copies/mL, with a log value of 5.93 log cps/mL. The BK Virus DNA Quantitative Real-Time PCR performed on plasma yielded a result of "Detected." Similarly, the BK Virus DNA Qualitative Real-Time PCR performed on urine also returned a "detected" result. Both urine and plasma PCR tests were conducted on three separate occasions and consistently detected the BK virus in the patient's system. This information was surprising and suggested that the potential cause of the patient's AKI might be BKVN. However, the gold standard for confirming this diagnosis remained kidney biopsy which was subsequently performed on the patient. A computed tomography (CT) scan of the abdomen and pelvis without intravenous contrast revealed crescentic hyperdense collections surrounding the left kidney, consistent with renal hemorrhage, likely secondary to his recent renal biopsy. The CT scan also displayed large volumes of hyperdense debris within the bladder extending into the left ureter. Due to unexplained progressive worsening of his CKD over the past year, the patient subsequently underwent a real-time ultrasound-guided biopsy of the left native kidney. The biopsy results revealed foci of mild interstitial inflammation, consisting primarily of lymphocytes and mononuclear cells, along with a small number of neutrophils and a few eosinophils, accompanied by mild lymphocytic tubulitis (Fig. 1 ). Atypical nuclei with occasional nuclear inclusions were observed in the tubular epithelium. The glomeruli displayed normal mesangial cellularity and appeared unremarkable, with no significant immune complexes detected. Additionally, no active arteritis was noted in the current biopsy. Daily monitoring and recording of home spirometry were emphasized, with a requirement to report any decrease exceeding 10% from baseline over a 3-day period. Around the time of the BKVN diagnosis, the patient’s immunoglobulin G (IgG) level was 1030 mg/dL (635–1,616 mg/dl). Intravenous immunoglobulin (IVIg) treatment was initiated at 200 mg/kg every 2 weeks for a total of 5 doses to manage BKVN. During this treatment period, intravenous fluid hydration was avoided. Initially, the patient was receiving tacrolimus and basiliximab, but upon diagnosis of BKVN, adjustments to the immunosuppressive regimen were necessary following consultations with the pulmonary transplant team and nephrology. The revised immunosuppression plan included the continuation of everolimus and tacrolimus, with a target concentration range of 6 to 8 ng/mL. The plan also involved initiating a low dose of prednisone while discontinuing mycophenolate mofetil and basiliximab. Despite the BK infection, the patient's bilateral lung graft function remained stable, with quarterly pulmonary function tests planned. Home spirometry readings consistently ranged from 1.51 to 1.61 liters, indicating stable lung function. During adjustments to the immunosuppressive regimen, close monitoring of the patient's BK virus load and viral DNA levels, as shown in Table 2 , was crucial. The modifications to the patient's immunosuppression regimen led to a significant reduction in the viral load, as indicated by the decreasing number of copies over time. Table 2 Comparison of BK viral load at initial diagnosis and one month post-diagnosis during immunosuppressive therapy. Component Ref Range & Units A Month After Diagnosis First Diagnosis BK Virus DNA Quant PCR Copies/mL 593,848 High 845,871 High BK Virus DNA Log ops/mL Log ops/mL 5.77 High 5.93 High Discussion and Conclusions BKVN is a disease entity that has been mainly identified in recipients of kidney transplants and rarely found in nonsolid, non-renal solid organ transplant (NRSOT) patients [ 2 ]. The extent of immunosuppression is a well-established risk factor for the replication of the virus [ 6 ]. Although many NRSOT patients are subject to significant immunosuppression, native kidney BKVN remains relatively rare [ 2 ]. In most cases of NRSOT, heart transplant patients are the second most common group known to develop BKVN. The case presented highlights the critical importance of vigilance in monitoring renal function post-transplantation of any solid organ (including lungs), particularly in the context of immunosuppressive therapy, where opportunistic infections such as BK virus can manifest unexpectedly. This case is particularly noteworthy due to the initial lack of suspicion for BK virus infection; the patient was first assessed for acute kidney injury (AKI) attributed to other factors, such as his immunosuppressive therapy. The definitive diagnosis of BKVN emerged from the findings of the kidney biopsy. This outcome was unexpected, as BKVN is predominantly associated with renal solid organ transplants, with heart transplants being the second most common organ affected in NRSOTs. This case represents the first documented instance of a lung transplant recipient presenting with BKVN in a native kidney that was not transplanted. This case raises intriguing considerations regarding the differential diagnosis between BK virus and JC virus infections and highlights the importance of diagnostic accuracy. Although anti-SV40 antibodies cover both JC virus and BK virus, the definitive diagnosis was supported by the consistent detection of BK virus PCR in both serum and urine. This result was replicated on three separate occasions, each time yielding consistent findings. This clinical scenario is unique, as the infection is in a native kidney while the lungs are transplanted, leading to distinct management implications. Lung transplantation is significantly more complex and less flexible than kidney transplantation, where patients have the option of returning to dialysis if BKVN results in graft loss. Consequently, the management strategies for kidney versus lung transplant-related nephropathy are markedly different. The most well-established risk factor for BKVN is the extent of immunosuppression. Although other contributing factors have been explored, none have demonstrated as strong an association with BKVN as the degree of immunosuppression [ 7 ]. Managing BKVN requires a delicate balance in immunosuppressive therapy. While reducing immunosuppression is essential to control the virus, excessive reduction can compromise lung graft function and risk graft loss. On the other hand, insufficient reduction may allow the virus to persist and become more difficult to eradicate. Therefore, treatment involves careful adjustment of immunosuppression to effectively manage the infection while preserving graft viability [ 7 ]. With the rising incidence of BK virus-related complications, there is an urgent need for enhanced screening protocols, especially as the use of immunosuppressive therapies continues to grow in transplant medicine. Early detection of BK virus is crucial in transplant care to prevent the deterioration of kidney function. Abbreviations - AKI: Acute Kidney Injury - BKVN: BK Virus Nephropathy - CT: Computed Tomography - CKD: Chronic Kidney Disease - CMV: Cytomegalovirus - EBV: Epstein-Barr Virus - IgG: Immunoglobulin G - IVIg: Intravenous Immunoglobulin - mTOR: Mammalian Target of Rapamycin - NAA: Nucleic Acid Amplification - NRSOT: Non-Renal Solid Organ Transplant - PCR: Polymerase Chain Reaction - SV40: Simian Virus 40 Declarations Ethics approval and consent to participate : - A Consent to Participate declaration has been provided and obtained, confirming that all human participants have provided their consent. Clinical trial number: not applicable Human Ethics and Consent to Participate declarations: Human Ethics and Consent to Participate declarations: Consent for publication was obtained from the patient involved in this case report. This consent can be requested from the corresponding author. Availability of data and materials : The datasets generated and/or analyzed during the current study are included in the published article and its supplementary information files. Additional data related to this study are not publicly available but can be requested from the corresponding author. Competing interests : The authors declare that they have no competing interests. Funding : No funding was received for the conduct of this study or the preparation of this manuscript. Authors' contributions : - CWH, MM, JS, and XJ analyzed and interpreted the patient data regarding the kidney biopsy and BKVN diagnosis. - JS was a major contributor to writing the manuscript. - AA and CWH reviewed and provided critical revisions to the manuscript. - All authors read and approved the final manuscript. Acknowledgements : We acknowledge the assistance of the medical and laboratory staff at University of Florida for their support in the management and analysis of the patient's condition. References Kant S, Dasgupta A, Bagnasco S, Brennan DC. BK Virus Nephropathy in Kidney Transplantation: A State-of-the-Art Review. Viruses. 2022 Jul 25;14(8):1616. doi: 10.3390/v14081616. PMID: 35893681; PMCID: PMC9330039. Velliyur V, Yost SE, Kaplan B. The prevalence and implications of BK virus replication in non-renal solid organ transplant recipients: A systematic review. Transplantation Reviews. 2015;29(3):175-180. doi:10.1016/j.trre.2015.02.004. Kaneko T, Shinohara M, Tanaka M, et al. Prevalence of human polyoma virus (BK virus and JC virus) infection in patients with chronic renal disease. Clin Exp Nephrol. 2005 Jun;9(2):132-7. Knowles WA, Pipkin PA, Andrews N, et al. Population-based study of antibody to the human polyomaviruses BKV and JCV and the simian polyomavirus SV40. J Med Virol. 2003 Sep;71(1):115-23. Reploeg MD, Hota B, Schuster R, et al. BK Virus: A Clinical Review. Clin Infect Dis. 2001 Jul 15;33(2):191-202. Yooprasert P, Rotjanapan P. BK virus–associated nephropathy: Current situation in a resource-limited country. Transplantation Proceedings. 2018;50(1):130-136. https://doi.org/10.1016/j.transproceed.2017.11.007 Maung Myint T, Chong CH, Huben A, Attia J, Webster AC, Blosser CD, Craig JC, Teixeira-Pinto A, Wong G. Serum and urine nucleic acid screening tests for polyomavirus‐associated nephropathy in kidney and kidney‐pancreas transplant recipients. The Cochrane Database of Systematic Reviews. 2022;2022(6):CD014839. https://doi.org/10.1002/14651858.CD014839 Additional Declarations No competing interests reported. Cite Share Download PDF Status: Posted Version 1 posted 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. 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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-5014825","acceptedTermsAndConditions":true,"allowDirectSubmit":true,"archivedVersions":[],"articleType":"Case Report","associatedPublications":[],"authors":[{"id":355628303,"identity":"8d0cb3cd-24af-49c6-9c5a-acc6653c5939","order_by":0,"name":"Mercedes Galloway","email":"data:image/png;base64,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","orcid":"","institution":"University of Florida","correspondingAuthor":true,"prefix":"","firstName":"Mercedes","middleName":"","lastName":"Galloway","suffix":""},{"id":355628304,"identity":"18e926f5-1e72-4759-8f10-768bb189715b","order_by":1,"name":"John Sousou","email":"","orcid":"","institution":"University of Florida","correspondingAuthor":false,"prefix":"","firstName":"John","middleName":"","lastName":"Sousou","suffix":""},{"id":355628305,"identity":"68ec18b9-ec66-451d-8902-d5189803767f","order_by":2,"name":"Xu Zeng","email":"","orcid":"","institution":"University of Florida","correspondingAuthor":false,"prefix":"","firstName":"Xu","middleName":"","lastName":"Zeng","suffix":""},{"id":355628306,"identity":"84b24acc-d25e-49db-b3dc-db888d45c633","order_by":3,"name":"Alaa Awad","email":"","orcid":"","institution":"University of Florida","correspondingAuthor":false,"prefix":"","firstName":"Alaa","middleName":"","lastName":"Awad","suffix":""},{"id":355628307,"identity":"76730d27-bd9c-48b5-81aa-5239642c29e0","order_by":4,"name":"Charles Heilig","email":"","orcid":"","institution":"University of Florida","correspondingAuthor":false,"prefix":"","firstName":"Charles","middleName":"","lastName":"Heilig","suffix":""}],"badges":[],"createdAt":"2024-09-02 02:08:20","currentVersionCode":1,"declarations":"","doi":"10.21203/rs.3.rs-5014825/v1","doiUrl":"https://doi.org/10.21203/rs.3.rs-5014825/v1","draftVersion":[],"editorialEvents":[],"editorialNote":"","failedWorkflow":false,"files":[{"id":66528962,"identity":"55966413-9d03-48fe-be24-ca76c64aa87e","added_by":"auto","created_at":"2024-10-14 05:31:39","extension":"png","order_by":1,"title":"Figure 1","display":"","copyAsset":false,"role":"figure","size":477323,"visible":true,"origin":"","legend":"\u003cp\u003eA: The renal interstitium shows mild inflammation with tubulitis (10x40). The nuclear tubular epithelium are pleomorphic, some have nuclear inclusions. 1B: Stain for SV40\u003c/p\u003e\n\u003cp\u003eshows positive nuclear staining along tubular epithelium.\u003c/p\u003e","description":"","filename":"1.png","url":"https://assets-eu.researchsquare.com/files/rs-5014825/v1/765d1254021d513ad83e0210.png"},{"id":66530157,"identity":"26c7f2e6-9e0b-4e04-af32-783e2fd5d3d7","added_by":"auto","created_at":"2024-10-14 05:55:43","extension":"pdf","order_by":0,"title":"","display":"","copyAsset":false,"role":"manuscript-pdf","size":866266,"visible":true,"origin":"","legend":"","description":"","filename":"manuscript.pdf","url":"https://assets-eu.researchsquare.com/files/rs-5014825/v1/3fa5e9c9-1e37-475c-8532-7896a5e3710f.pdf"}],"financialInterests":"No competing interests reported.","formattedTitle":"BK Virus Nephropathy in a Native Kidney of a Lung Transplant Patient","fulltext":[{"header":"Background","content":"\u003cp\u003eThe BK virus is a member of the Polyomaviridae family and henceforth possesses a circular, double-stranded DNA genome [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. Its association with urethral stricture is widely recognized after the virus was first confirmed through biopsy in 1993 [\u003cspan citationid=\"CR1\" class=\"CitationRef\"\u003e1\u003c/span\u003e]. The BK virus typically remains in a latent phase within the genitourinary lining tract of the host, and is usually inactive under normal conditions. Initially detectable in urine, it may progress to viremia, and subsequently establish infection within the transplanted kidney, leading to injury. However in patients with immunocompromised states, such as post-transplant immunosuppression, the virus can become reactivated [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. The mechanism of persistent BK virus infection involves its T antigens interacting with cell cycle regulatory proteins such as p53 and Rb. Following viremia, the virus can remain dormant in uroepithelial cells, potentially reactivating under conditions conducive to immunosuppression.\u003c/p\u003e \u003cp\u003eThe epidemiology of BK virus shows a seroprevalence peak of 91% in children aged 5\u0026ndash;9 years, and overall seropositivity rate of 81%, with antibody titers declining with age. Although the mode of transmission is uncertain, some studies indicate that respiratory spread is suspected to be part of the transmission process [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e, \u003cspan citationid=\"CR4\" class=\"CitationRef\"\u003e4\u003c/span\u003e, \u003cspan citationid=\"CR5\" class=\"CitationRef\"\u003e5\u003c/span\u003e]. In a study conducted by Tetsuya Kaneko et al, BK viruria was detected in 13.5% of normal individuals, with a much higher prevalence of 33.3% among patients with renal disease. BK viruria is even more pronounced in patients with renal disease undergoing steroid treatment, where it was observed in 55.6% of cases [\u003cspan citationid=\"CR3\" class=\"CitationRef\"\u003e3\u003c/span\u003e]. Most cases of BK virus nephropathy have been described in patients with transplanted kidneys and rarely described in native kidneys.\u003c/p\u003e \u003cp\u003eHere, we present a case of a patient who underwent bilateral lung transplantation and subsequently developed biopsy-proven BK nephropathy in his native kidney.\u003c/p\u003e"},{"header":"Case presentation","content":"\u003cp\u003eA 67-year-old male with a medical history of chronic kidney disease (CKD), hypertension, steroid-induced type 2 diabetes mellitus, and a bilateral lung transplant three years ago for end-stage chronic obstructive pulmonary disease presented to the hospital with acute blood loss anemia. This condition was secondary to a renal hemorrhage that occurred 20 days after a renal biopsy, which had been performed to investigate the cause of his acute kidney injury. The patient had been following a pulmonologist for 3 years and had been stable on his long-term immunosuppression regimen of tacrolimus, mycophenolate mofetil, prednisone, and basiliximab.\u003c/p\u003e\n\u003cp\u003eOn admission, the patient was hemodynamically stable and in no apparent distress. Laboratory testing was notable for a hemoglobin of 6.6 g/dL, with his baseline being around 11 g/dL, and a creatinine of 3.39. His hemoglobin improved following red blood cell transfusion and angiography with embolization of a renal arteriovenous fistula by interventional radiology the same day. Seven months prior, labs indicated worsening creatinine despite 17 months of everolimus therapy. Renal function had worsened while the patient was on mTOR inhibitors (everolimus), leading to the discontinuation of the medication seven months prior. Despite stopping everolimus, there was no significant improvement in renal function.\u003c/p\u003e\n\u003cp\u003eTwo years prior, his baseline serum creatinine was approximately 1.3 mg/dL, but in the past month, it had increased to a range of 2-2.5 mg/dL. Proteinuria was detected with a microalbumin-to-creatinine ratio of 368 mg/gm. The patient had no recent history of antibiotics, nonsteroidal anti-inflammatory drugs, over-the-counter medications, herbal supplements, or intravenous contrast use in the past five years, prompting further investigation into the etiology of his kidney disease. Extensive viral testing is detailed in Table\u0026nbsp;\u003cspan class=\"InternalRef\"\u003e1\u003c/span\u003e.\u003c/p\u003e\n\u003cdiv class=\"gridtable\"\u003e\u0026nbsp;\u003ctable id=\"Tab1\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 1\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003eComprehensive viral testing demonstrating the presence of BK virus, with all other viral tests returning unremarkable results.\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003ccolgroup cols=\"2\"\u003e\u003c/colgroup\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eTest\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eResult\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eInfluenza A Virus NAA\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNot Detected\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eCMV DNA, QN\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNot Detected\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eCMV Quant PCR Log\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNot Detected\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eCoronavirus (COVID-19) NAA\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNot Detected\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eEBV Quant\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNot Detected\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eRespiratory Syncytial Virus\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNot Detected\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eSARS-CoV-2 (COVID-19)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNot Detected\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eBK Virus Quant PCR\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDetected\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eBK Virus Quant PCR\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eDetected\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eCMV Quant\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u0026lt;\u0026thinsp;59\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eCMV Quant PCR\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u0026lt;\u0026thinsp;1.77\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eHepatitis C RNA-PCR (Quantitative)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eEquivocal\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eHepatitis C RNA-PCR (Quantitative)\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eEquivocal\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eCMV DNA\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNot Detected\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eCMV DNA\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u0026lt;\u0026thinsp;200\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eCMV Quant PCR\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNot Detected\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eCMV Quant PCR\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eNot Detected\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eCMV Quant PCR\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u0026lt;\u0026thinsp;2.30\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u003cstrong\u003eCMV Quant PCR\u003c/strong\u003e\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e\u0026lt;\u0026thinsp;2.30\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n\u003c/div\u003e\n\u003cp\u003eThe BK Virus DNA Quantitative PCR was initially diagnosed at 845,871 copies/mL, with a log value of 5.93 log cps/mL. The BK Virus DNA Quantitative Real-Time PCR performed on plasma yielded a result of \u0026quot;Detected.\u0026quot; Similarly, the BK Virus DNA Qualitative Real-Time PCR performed on urine also returned a \u0026quot;detected\u0026quot; result. Both urine and plasma PCR tests were conducted on three separate occasions and consistently detected the BK virus in the patient\u0026apos;s system. This information was surprising and suggested that the potential cause of the patient\u0026apos;s AKI might be BKVN. However, the gold standard for confirming this diagnosis remained kidney biopsy which was subsequently performed on the patient.\u003c/p\u003e\n\u003cp\u003eA computed tomography (CT) scan of the abdomen and pelvis without intravenous contrast revealed crescentic hyperdense collections surrounding the left kidney, consistent with renal hemorrhage, likely secondary to his recent renal biopsy. The CT scan also displayed large volumes of hyperdense debris within the bladder extending into the left ureter.\u003c/p\u003e\n\u003cp\u003eDue to unexplained progressive worsening of his CKD over the past year, the patient subsequently underwent a real-time ultrasound-guided biopsy of the left native kidney. The biopsy results revealed foci of mild interstitial inflammation, consisting primarily of lymphocytes and mononuclear cells, along with a small number of neutrophils and a few eosinophils, accompanied by mild lymphocytic tubulitis (Fig. \u003cspan class=\"InternalRef\"\u003e1\u003c/span\u003e). Atypical nuclei with occasional nuclear inclusions were observed in the tubular epithelium. The glomeruli displayed normal mesangial cellularity and appeared unremarkable, with no significant immune complexes detected. Additionally, no active arteritis was noted in the current biopsy.\u003c/p\u003e\n\u003cp\u003eDaily monitoring and recording of home spirometry were emphasized, with a requirement to report any decrease exceeding 10% from baseline over a 3-day period. Around the time of the BKVN diagnosis, the patient\u0026rsquo;s immunoglobulin G (IgG) level was 1030 mg/dL (635\u0026ndash;1,616 mg/dl). Intravenous immunoglobulin (IVIg) treatment was initiated at 200 mg/kg every 2 weeks for a total of 5 doses to manage BKVN. During this treatment period, intravenous fluid hydration was avoided. Initially, the patient was receiving tacrolimus and basiliximab, but upon diagnosis of BKVN, adjustments to the immunosuppressive regimen were necessary following consultations with the pulmonary transplant team and nephrology. The revised immunosuppression plan included the continuation of everolimus and tacrolimus, with a target concentration range of 6 to 8 ng/mL. The plan also involved initiating a low dose of prednisone while discontinuing mycophenolate mofetil and basiliximab.\u003c/p\u003e\n\u003cp\u003eDespite the BK infection, the patient\u0026apos;s bilateral lung graft function remained stable, with quarterly pulmonary function tests planned. Home spirometry readings consistently ranged from 1.51 to 1.61 liters, indicating stable lung function. During adjustments to the immunosuppressive regimen, close monitoring of the patient\u0026apos;s BK virus load and viral DNA levels, as shown in Table \u003cspan class=\"InternalRef\"\u003e2\u003c/span\u003e, was crucial. The modifications to the patient\u0026apos;s immunosuppression regimen led to a significant reduction in the viral load, as indicated by the decreasing number of copies over time.\u003c/p\u003e\n\u003cdiv class=\"gridtable\"\u003e\u0026nbsp;\u003ctable id=\"Tab2\" border=\"1\"\u003e\n \u003ccaption language=\"En\"\u003e\n \u003cdiv class=\"CaptionNumber\"\u003eTable 2\u003c/div\u003e\n \u003cdiv class=\"CaptionContent\"\u003e\n \u003cp\u003eComparison of BK viral load at initial diagnosis and one month post-diagnosis during immunosuppressive therapy.\u003c/p\u003e\n \u003c/div\u003e\n \u003c/caption\u003e\n \u003ccolgroup cols=\"4\"\u003e\u003c/colgroup\u003e\n \u003cthead\u003e\n \u003ctr\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eComponent\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eRef Range \u0026amp; Units\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eA Month After Diagnosis\u003c/p\u003e\n \u003c/th\u003e\n \u003cth align=\"left\"\u003e\n \u003cp\u003eFirst Diagnosis\u003c/p\u003e\n \u003c/th\u003e\n \u003c/tr\u003e\n \u003c/thead\u003e\n \u003ctbody\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eBK Virus DNA Quant PCR\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eCopies/mL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e593,848 High\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e845,871 High\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003ctr\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eBK Virus DNA Log ops/mL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003eLog ops/mL\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5.77 High\u003c/p\u003e\n \u003c/td\u003e\n \u003ctd align=\"left\"\u003e\n \u003cp\u003e5.93 High\u003c/p\u003e\n \u003c/td\u003e\n \u003c/tr\u003e\n \u003c/tbody\u003e\n \u003c/table\u003e\n\u003c/div\u003e"},{"header":"Discussion and Conclusions","content":"\u003cp\u003eBKVN is a disease entity that has been mainly identified in recipients of kidney transplants and rarely found in nonsolid, non-renal solid organ transplant (NRSOT) patients [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. The extent of immunosuppression is a well-established risk factor for the replication of the virus [\u003cspan citationid=\"CR6\" class=\"CitationRef\"\u003e6\u003c/span\u003e]. Although many NRSOT patients are subject to significant immunosuppression, native kidney BKVN remains relatively rare [\u003cspan citationid=\"CR2\" class=\"CitationRef\"\u003e2\u003c/span\u003e]. In most cases of NRSOT, heart transplant patients are the second most common group known to develop BKVN. The case presented highlights the critical importance of vigilance in monitoring renal function post-transplantation of any solid organ (including lungs), particularly in the context of immunosuppressive therapy, where opportunistic infections such as BK virus can manifest unexpectedly.\u003c/p\u003e \u003cp\u003eThis case is particularly noteworthy due to the initial lack of suspicion for BK virus infection; the patient was first assessed for acute kidney injury (AKI) attributed to other factors, such as his immunosuppressive therapy. The definitive diagnosis of BKVN emerged from the findings of the kidney biopsy. This outcome was unexpected, as BKVN is predominantly associated with renal solid organ transplants, with heart transplants being the second most common organ affected in NRSOTs. This case represents the first documented instance of a lung transplant recipient presenting with BKVN in a native kidney that was not transplanted.\u003c/p\u003e \u003cp\u003eThis case raises intriguing considerations regarding the differential diagnosis between BK virus and JC virus infections and highlights the importance of diagnostic accuracy. Although anti-SV40 antibodies cover both JC virus and BK virus, the definitive diagnosis was supported by the consistent detection of BK virus PCR in both serum and urine. This result was replicated on three separate occasions, each time yielding consistent findings. This clinical scenario is unique, as the infection is in a native kidney while the lungs are transplanted, leading to distinct management implications. Lung transplantation is significantly more complex and less flexible than kidney transplantation, where patients have the option of returning to dialysis if BKVN results in graft loss. Consequently, the management strategies for kidney versus lung transplant-related nephropathy are markedly different. The most well-established risk factor for BKVN is the extent of immunosuppression. Although other contributing factors have been explored, none have demonstrated as strong an association with BKVN as the degree of immunosuppression [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eManaging BKVN requires a delicate balance in immunosuppressive therapy. While reducing immunosuppression is essential to control the virus, excessive reduction can compromise lung graft function and risk graft loss. On the other hand, insufficient reduction may allow the virus to persist and become more difficult to eradicate. Therefore, treatment involves careful adjustment of immunosuppression to effectively manage the infection while preserving graft viability [\u003cspan citationid=\"CR7\" class=\"CitationRef\"\u003e7\u003c/span\u003e].\u003c/p\u003e \u003cp\u003eWith the rising incidence of BK virus-related complications, there is an urgent need for enhanced screening protocols, especially as the use of immunosuppressive therapies continues to grow in transplant medicine. Early detection of BK virus is crucial in transplant care to prevent the deterioration of kidney function.\u003c/p\u003e"},{"header":"Abbreviations","content":"\u003cp\u003e- AKI: Acute Kidney Injury\u003c/p\u003e\n\u003cp\u003e- BKVN: BK Virus Nephropathy\u003c/p\u003e\n\u003cp\u003e- CT: Computed Tomography\u003c/p\u003e\n\u003cp\u003e- CKD: Chronic Kidney Disease\u003c/p\u003e\n\u003cp\u003e- CMV: Cytomegalovirus\u003c/p\u003e\n\u003cp\u003e- EBV: Epstein-Barr Virus\u003c/p\u003e\n\u003cp\u003e- IgG: Immunoglobulin G\u003c/p\u003e\n\u003cp\u003e- IVIg: Intravenous Immunoglobulin\u003c/p\u003e\n\u003cp\u003e- mTOR: Mammalian Target of Rapamycin\u003c/p\u003e\n\u003cp\u003e- NAA: Nucleic Acid Amplification\u003c/p\u003e\n\u003cp\u003e- NRSOT: Non-Renal Solid Organ Transplant\u003c/p\u003e\n\u003cp\u003e- PCR: Polymerase Chain Reaction\u003c/p\u003e\n\u003cp\u003e- SV40: Simian Virus 40\u003c/p\u003e"},{"header":"Declarations","content":"\u003cp\u003e\u003cstrong\u003eEthics approval and consent to participate\u003c/strong\u003e:\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e- A Consent to Participate declaration has been provided and obtained, confirming that all human participants have provided their consent.\u003c/p\u003e\n\u003cp\u003eClinical trial number: not applicable\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eHuman Ethics and Consent to Participate declarations:\u0026nbsp;\u003c/strong\u003e Human Ethics and Consent to Participate declarations: Consent for publication was obtained from the patient involved in this case report. This consent can be requested from the corresponding author.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAvailability of data and materials\u003c/strong\u003e:\u003c/p\u003e\n\u003cp\u003eThe datasets generated and/or analyzed during the current study are included in the published article and its supplementary information files. Additional data related to this study are not publicly available but can be requested from the corresponding author.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eCompeting interests\u003c/strong\u003e: The authors declare that they have no competing interests.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eFunding\u003c/strong\u003e: No funding was received for the conduct of this study or the preparation of this manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAuthors' contributions\u003c/strong\u003e:\u0026nbsp;\u003c/p\u003e\n\u003cp\u003e- CWH, MM, JS, and XJ analyzed and interpreted the patient data regarding the kidney biopsy and BKVN diagnosis. \u0026nbsp;\u003c/p\u003e\n\u003cp\u003e- JS was a major contributor to writing the manuscript. \u0026nbsp;\u003c/p\u003e\n\u003cp\u003e- AA and CWH reviewed and provided critical revisions to the manuscript. \u0026nbsp;\u003c/p\u003e\n\u003cp\u003e- All authors read and approved the final manuscript.\u003c/p\u003e\n\u003cp\u003e\u003cstrong\u003eAcknowledgements\u003c/strong\u003e:\u003c/p\u003e\n\u003cp\u003eWe acknowledge the assistance of the medical and laboratory staff at University of Florida for their support in the management and analysis of the patient's condition.\u0026nbsp;\u003c/p\u003e"},{"header":"References","content":"\u003col\u003e\n\u003cli\u003eKant S, Dasgupta A, Bagnasco S, Brennan DC. BK Virus Nephropathy in Kidney Transplantation: A State-of-the-Art Review. Viruses. 2022 Jul 25;14(8):1616. doi: 10.3390/v14081616. PMID: 35893681; PMCID: PMC9330039.\u003c/li\u003e\n\u003cli\u003eVelliyur V, Yost SE, Kaplan B. The prevalence and implications of BK virus replication in non-renal solid organ transplant recipients: A systematic review. Transplantation Reviews. 2015;29(3):175-180. doi:10.1016/j.trre.2015.02.004.\u003c/li\u003e\n\u003cli\u003eKaneko T, Shinohara M, Tanaka M, et al. Prevalence of human polyoma virus (BK virus and JC virus) infection in patients with chronic renal disease. Clin Exp Nephrol. 2005 Jun;9(2):132-7.\u003c/li\u003e\n\u003cli\u003eKnowles WA, Pipkin PA, Andrews N, et al. Population-based study of antibody to the human polyomaviruses BKV and JCV and the simian polyomavirus SV40. J Med Virol. 2003 Sep;71(1):115-23.\u003c/li\u003e\n\u003cli\u003eReploeg MD, Hota B, Schuster R, et al. BK Virus: A Clinical Review. Clin Infect Dis. 2001 Jul 15;33(2):191-202.\u003c/li\u003e\n\u003cli\u003eYooprasert P, Rotjanapan P. BK virus\u0026ndash;associated nephropathy: Current situation in a resource-limited country. Transplantation Proceedings. 2018;50(1):130-136. https://doi.org/10.1016/j.transproceed.2017.11.007\u003c/li\u003e\n\u003cli\u003eMaung Myint T, Chong CH, Huben A, Attia J, Webster AC, Blosser CD, Craig JC, Teixeira-Pinto A, Wong G. Serum and urine nucleic acid screening tests for polyomavirus‐associated nephropathy in kidney and kidney‐pancreas transplant recipients. The Cochrane Database of Systematic Reviews. 2022;2022(6):CD014839. https://doi.org/10.1002/14651858.CD014839\u003c/li\u003e\n\u003c/ol\u003e"}],"fulltextSource":"","fullText":"","funders":[],"hasAdminPriorityOnWorkflow":false,"hasManuscriptDocX":true,"hasOptedInToPreprint":true,"hasPassedJournalQc":"","hasAnyPriority":true,"hideJournal":true,"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":"researchsquare","isNatureJournal":false,"hasQc":true,"allowDirectSubmit":true,"externalIdentity":"","sideBox":"","snPcode":"","submissionUrl":"/submission","title":"Research Square","twitterHandle":"researchsquare","acdcEnabled":true,"dfaEnabled":false,"editorialSystem":"","reportingPortfolio":"","inReviewEnabled":false,"inReviewRevisionsEnabled":true},"keywords":"BK Virus, Nephropathy, Lung Transplantation, Acute Kidney Injury, Polyoma Nephropathy, Simian Virus 40, Native Kidney, Renal Biopsy","lastPublishedDoi":"10.21203/rs.3.rs-5014825/v1","lastPublishedDoiUrl":"https://doi.org/10.21203/rs.3.rs-5014825/v1","license":{"name":"CC BY 4.0","url":"https://creativecommons.org/licenses/by/4.0/"},"manuscriptAbstract":"\u003cp\u003eBackground: BK virus nephropathy (BKVN) in native kidneys following lung transplantation is an exceptionally rare occurrence. This case report highlights a unique instance where BKVN developed in a patient’s native kidney post-lung transplantation, emphasizing its rarity and the importance of considering BKVN in differential diagnoses for patients presenting with acute kidney injury (AKI) after such transplants.\u003c/p\u003e\n\u003cp\u003eCase Presentation: A patient who had undergone bilateral lung transplantation three years prior presented with worsening creatinine levels following an angiogram. The patient’s history included no exposure to toxic medications, contrast, or other known triggers for kidney disease. The worsening renal function was initially investigated through an angiogram, which was followed by the onset of hematuria and a progressive rise in creatinine levels. To determine the cause of the acute kidney injury, a kidney biopsy was performed. The biopsy of the left kidney revealed polyoma nephropathy. Confirmatory tests, including positive staining for Simian virus 40 (SV40), confirmed the diagnosis of BK virus nephropathy in the patient’s native kidney.\u003c/p\u003e\n\u003cp\u003eConclusion: The occurrence of BK virus nephropathy in the native kidney following lung transplantation is a rare phenomenon. This case underscores the necessity of considering BK virus nephropathy in the differential diagnosis of acute kidney injury in patients with a history of lung transplantation. Early recognition and diagnosis are crucial for appropriate management and potential modification of immunosuppressive therapy to prevent further kidney damage.\u003c/p\u003e","manuscriptTitle":"BK Virus Nephropathy in a Native Kidney of a Lung Transplant Patient","msid":"","msnumber":"","nonDraftVersions":[{"code":1,"date":"2024-10-14 05:31:34","doi":"10.21203/rs.3.rs-5014825/v1","editorialEvents":[{"type":"communityComments","content":0}],"status":"published","journal":{"display":true,"email":"
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