BK virus infections, IVIG, nephropathy – pro
BK viremia can be seen in patients with a wide variety of immunodeficiencies, but appears most frequently in renal and bone marrow transplant (BMT) patients. Immunosuppression leads to BKV reactivation and replication. When BKV replication is low the patient remains asymptomatic; however, higher levels of replication can cause significant uroepithelial cell lysis that results in hematuria. BK virus was observed to be associated with the development of hemorrhagic cystitis during BMT in early studies. Today, hemorrhagic cystitis is an important cause of morbidity and occasionally mortality in patients undergoing BMT. The clinical manifestations vary from microscopic hematuria to severe hemorrhage of the bladder leading to renal failure. Usually, the BKV induced hemorrhagic cystitis is managed conservatively. However several anti-viral agents have been shown to be effective against BKV and other polyoma viruses in-vitro and two agents, i.e. vidarabine and cidofovir have been used in clinical situations successfully. A recent study successfully treated renal transplant recipients with BKV interstitial nephritis with a reduced dose of cidofovir (10-20% of the recommended dose)5 The study suggests that cidofovir may be useful in treating a subgroup of patients.
K viremia can be seen in patients with a wide variety of immunodeficiencies, but appears most frequently in renal and bone marrow transplant (BMT) patients. Immunosuppression leads to BKV reactivation and replication. When BKV replication is low the patient remains asymptomatic; however, higher levels of replication can cause significant uroepithelial cell lysis that results in hematuria. Usually, the BKV induced hemorrhagic cystitis is managed conservatively. However several anti-viral agents have been shown to be effective against BKV and other polyoma viruses in-vitro and two agents, i.e. vidarabine and cidofovir have been used in clinical situations successfully.
The role of IVIG to prophylax viremia with BK virus is not defined and is under study in the clinical trial: “IVIg to Treat BK Viremia in Kidney Transplant Recipients”.
Kwak EJ, Vilchez RA, Randhawa, P,et al. Pathogenesis And Management of Polyomavirus Infection inTransplant Recipients. Clinical Infectious Diseases. 2002; 35:1081-1087.
Devi D Morrison, Samith Thomas Kochuparambil, David Deremer, Ethan Speir, Kristen Sterling, Meghan Sterrett, Vamsi Kota, Anand P. Jillella and Farrukh T Awan, Defining Treatment Paradigms for BK Virus-Induced Hemorrhagic Cystitis in the Post-Allogeneic Hematopoietic Stem Cell Transplant Setting, Blood 2011 118:4468;
Nienke M.G.Rorije et al, BK Virus Disease after Allogeneic Stem Cell Transplantation: A Cohort Analysis. Biology of Blood and Marrow Transplantation
Volume 20, Issue 4, April 2014, Pages 564-570
D. Vu et al, Efficacy of Intravenous Immunoglobulin in the Treatment of Persistent BK Viremia and BK Virus Nephropathy in Renal Transplant Recipients. Transplantation Proceedings 47(2):394-398, 2016
Kwak EJ, Vilchez RA, Randhawa, P,et al. Pathogenesis And Management of Polyomavirus Infection inTransplant Recipients. Clinical Infectious Diseases. 2002; 35:1081-1087. .
Vats A, Shapiro R, Randhawa PS, Scantlebury V, Tuzuner A et al. Role of Quantitative Viral Load and Cidofovir Therapy in The Management of BK Virus Nephropathy. Transplantation. 2003;75:105-112