BK virus (BKV)-related haemorrhagic cystitis (HC) is an important cause of morbidity following allogeneic haematopoietic stem cell transplantation (HSCT). The various risk factors include high-level BKV viruria and/or viremia, myeloablative conditioning, acute graft host disease (GVHD), cytomegalovirus viremia, and unrelated or HLA-mismatched donor. The presence of high plasma BK viral load and cytopenias have been implicated as important predictors for protracted disease course. These patients frequently require hospitalisation which may extend for several weeks. Supportive measures in the form of analgesics, intravenous hydration, bladder irrigation, and transfusion support remain the mainstay of management. Various drugs have been used with limited success in this setting. These include antiviral drugs, fluoroquinolones, leflunomide, growth factors, clotting factors, estrogens, and prostaglandins. The role of adoptive cellular immunotherapy has also been explored but lacks clinical validation. The strategies aimed at expediting urothelial repair like hyperbaric oxygen therapy (HBOT), intravesical fibrin glue and platelet-rich plasma (PRP) are emerging. Some patients with severe disease do require surgical intervention to relieve urinary obstruction. The frequent co-occurrence of acute GVHD and CMV disease further complicates the management in such patients. There is an unmet need for effective and evidence-based options for the prevention and management of this disease. Due to lack of robust data supported by randomised trials, the acceptability of the available guidelines to simplify the treatment is expected to be low. Despite the availability of various treatment options, the management of BKV-related HC in day-to-day practice continues to be a challenge. The aim of this article is to put forward an up-to-date review of the preventive and therapeutic strategies for BKV-related HC.
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http://dx.doi.org/10.1177/2049936121991377 | DOI Listing |
Sci Rep
January 2025
Department of Clinical Laboratory, Zhengzhou No. 7 People's Hospital, 17 Jingnan 5th Road, Jingkai District, Zhengzhou, Henan, China.
BK virus is implicated in polyomavirus-associated nephropathy (PVAN) and hemorrhagic cystitis, particularly in kidney transplant recipients, affecting the functionality of the transplanted kidney and posing a risk of graft loss. Despite these challenges, specific antiviral drugs targeting BK virus remain elusive. Agnoprotein, a small, positively charged protein encoded by the BK virus late gene, functions in the assembly, maturation, and release of the virus.
View Article and Find Full Text PDFIJID Reg
March 2025
Virology Department, Hôpital Paul Brousse, INSERM U1193, AP-HP, Université Paris Saclay, Paris, France.
Objectives: BK virus (BKV) is highly seroprevalent in humans. After primary infection, it remains latent in the urinary tract and can reactivate in immunocompromised individuals, leading to interstitial nephropathy or hemorrhagic cystitis. The BKV viral load (VL) in plasma correlates with the occurrence of nephropathy and can be monitored in kidney graft recipients; the early detection of BKV viremia can enable an early reduction of immunosuppressant drug doses and the prevention of BKV-associated nephropathy.
View Article and Find Full Text PDFBMC Vet Res
January 2025
Faculty of Veterinary Sciences, University of Buenos Aires, Buenos Aires, Argentina.
Background: Lower urinary tract disease is a common clinical condition in dogs, usually presenting with dysuria, pollakiuria and haematuria. Diabetes mellitus is a predisposing factor for urinary tract infection in both humans and dogs and does not necessarily present with clinical signs. In this case report, we describe for the first time a case of cystitis glandularis in a dog with diabetes mellitus, associated with Escherichia coli urinary tract infection.
View Article and Find Full Text PDFCureus
December 2024
Internal Medicine/Nephrology, Riverside Health System, Yonkers, USA.
We conducted a large-scale disproportionality analysis of the urotoxicity of cyclophosphamide (CYC) and the related drug ifosfamide (IFO) using the US Food and Drug Administration Adverse Event Reporting System (FAERS) database, with data ranging from Q4 2012 to Q2 2024. We compared the reporting odds ratio (ROR) of various urotoxicity manifestations of CYC and IFO across patient populations being treated for antineoplastic, immunosuppressive, and transplantation indications. When a wide range of urotoxicity manifestations was aggregated, we found that transplant patients had an increased relative susceptibility to CYC urotoxicity.
View Article and Find Full Text PDFBK polyomavirus (BKV) causes polyomavirus-associated nephropathy (PyVAN) and polyomavirus-associated hemorrhagic cystitis (PyVHC) following kidney transplantation and allogeneic hematopoietic stem cell transplantation (HST). BKV strains fall into four distinct genotypes (BKV-I, -II, -III, and -IV) with more than 80% of individuals are seropositive against BKV-I genotype, while the seroprevalence of the other four genotypes is lower. PyVAN and PyVHC occurs in immunosuppressed (e.
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