The Experts below are selected from a list of 312 Experts worldwide ranked by ideXlab platform

Benjamin T Davis - One of the best experts on this subject based on the ideXlab platform.

  • BK Virus associated hemorrhagic cystitis in a human immunodeficiency Virus infected patient
    Clinical Infectious Diseases, 2002
    Co-Authors: Dan H Barouch, Igor J Koralnik, Gregory K. Robbins, William C Faquin, Yiping Chen, Benjamin T Davis
    Abstract:

    BK Virus-associated hemorrhagic cystitis is a common clinical problem in bone marrow transplant recipients but is considered rare in other immunosuppressed patient populations. We describe a human immunodeficiency Virus-infected patient with non-Hodgkin's lymphoma in whom BK Virus-associated hemorrhagic cystitis developed; viruria was quantitated in urine by immunocytochemistry, and the patient showed no response to cidofovir.

  • BK Virus–Associated Hemorrhagic Cystitis in a Human Immunodeficiency Virus–Infected Patient
    Clinical Infectious Diseases, 2002
    Co-Authors: Dan H Barouch, Igor J Koralnik, Gregory K. Robbins, William C Faquin, Yiping Chen, Benjamin T Davis
    Abstract:

    BK Virus-associated hemorrhagic cystitis is a common clinical problem in bone marrow transplant recipients but is considered rare in other immunosuppressed patient populations. We describe a human immunodeficiency Virus-infected patient with non-Hodgkin's lymphoma in whom BK Virus-associated hemorrhagic cystitis developed; viruria was quantitated in urine by immunocytochemistry, and the patient showed no response to cidofovir.

Christopher L Marsh - One of the best experts on this subject based on the ideXlab platform.

  • quantitation of BK Virus load in serum for the diagnosis of BK Virus associated nephropathy in renal transplant recipients
    The Journal of Infectious Diseases, 2001
    Co-Authors: Ajit P. Limaye, Lawrence Corey, Keith R. Jerome, Christian S Kuhr, James Ferrenberg, Meei Li Huang, Connie L Davis, Christopher L Marsh
    Abstract:

    BK Virus-associated nephropathy is an increasingly recognized cause of graft dysfunction among kidney transplant recipients, and definitive diagnosis requires renal biopsy. By using a newly developed, quantitative, real-time polymerase chain reaction (PCR) assay for BK Virus DNA, a retrospective analysis was done of sequential serum samples (n = 28) from 4 transplant recipients with histopathologically documented BK Virus nephropathy and from samples (n = 76) from 16 transplant recipient control patients. BK Virus DNA was detected in serum samples from all 4 case patients versus 0 of 16 control patients (P<.0001, Fisher's exact test) at a median of 32 weeks (range, 17-61 weeks) before the diagnosis of BK Virus nephropathy. BK Virus load decreased in 3 of 3 patients after the reduction of immunosuppression and/or nephrectomy. It is concluded that quantitative PCR for BK Virus DNA in serum is useful both for identifying transplant recipients at risk for BK Virus nephropathy and for monitoring the response to therapy.

  • Quantitation of BK Virus Load in Serum for the Diagnosis of BK Virus–Associated Nephropathy in Renal Transplant Recipients
    The Journal of infectious diseases, 2001
    Co-Authors: Ajit P. Limaye, Lawrence Corey, Keith R. Jerome, Christian S Kuhr, James Ferrenberg, Meei Li Huang, Connie L Davis, Christopher L Marsh
    Abstract:

    BK Virus-associated nephropathy is an increasingly recognized cause of graft dysfunction among kidney transplant recipients, and definitive diagnosis requires renal biopsy. By using a newly developed, quantitative, real-time polymerase chain reaction (PCR) assay for BK Virus DNA, a retrospective analysis was done of sequential serum samples (n = 28) from 4 transplant recipients with histopathologically documented BK Virus nephropathy and from samples (n = 76) from 16 transplant recipient control patients. BK Virus DNA was detected in serum samples from all 4 case patients versus 0 of 16 control patients (P

Dan H Barouch - One of the best experts on this subject based on the ideXlab platform.

  • BK Virus associated hemorrhagic cystitis in a human immunodeficiency Virus infected patient
    Clinical Infectious Diseases, 2002
    Co-Authors: Dan H Barouch, Igor J Koralnik, Gregory K. Robbins, William C Faquin, Yiping Chen, Benjamin T Davis
    Abstract:

    BK Virus-associated hemorrhagic cystitis is a common clinical problem in bone marrow transplant recipients but is considered rare in other immunosuppressed patient populations. We describe a human immunodeficiency Virus-infected patient with non-Hodgkin's lymphoma in whom BK Virus-associated hemorrhagic cystitis developed; viruria was quantitated in urine by immunocytochemistry, and the patient showed no response to cidofovir.

  • BK Virus–Associated Hemorrhagic Cystitis in a Human Immunodeficiency Virus–Infected Patient
    Clinical Infectious Diseases, 2002
    Co-Authors: Dan H Barouch, Igor J Koralnik, Gregory K. Robbins, William C Faquin, Yiping Chen, Benjamin T Davis
    Abstract:

    BK Virus-associated hemorrhagic cystitis is a common clinical problem in bone marrow transplant recipients but is considered rare in other immunosuppressed patient populations. We describe a human immunodeficiency Virus-infected patient with non-Hodgkin's lymphoma in whom BK Virus-associated hemorrhagic cystitis developed; viruria was quantitated in urine by immunocytochemistry, and the patient showed no response to cidofovir.

Ajit P. Limaye - One of the best experts on this subject based on the ideXlab platform.

  • Treatment of refractory BK Virus-associated nephropathy with cidofovir.
    American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons, 2003
    Co-Authors: Pradeep V. Kadambi, Michelle A. Josephson, James W. Williams, Lawrence Corey, Keith R. Jerome, Shane M. Meehan, Ajit P. Limaye
    Abstract:

    BK Virus-associated nephropathy (BKVN) has become recognized as an important cause of allograft dysfunction in renal transplant recipients and despite reduction in immunosuppression, 30–40% of recipients ultimately progress to allograft loss. Cidofovir is an antiviral agent that demonstrates in vitro activity against murine polyomaVirus and has been proposed for treatment of BKVN in renal allograft recipients. We describe the clinical course, renal function, serial renal histology and urine and blood viral load measurements in two consecutive patients with refractory BKVN who were treated with low-dose cidofovir (0.25 mg/kg IV). In each case, renal dysfunction and BK viral load progressed despite reduced immunosuppression, and persistent BK Virus infection was documented in serial renal allograft biopsy specimens. Administration of low-dose cidofovir was associated with clearance of BK Virus DNA from blood and allograft, and stabilization of renal function in both patients, without significant toxicity. These preliminary data suggest that low-dose cidofovir may be tolerated, even among renal transplant recipients with significant renal dysfunction due to BKVN. Prospective, controlled trials are warranted to further define the optimal dose, toxicity and potential role of cidofovir in renal transplant recipients with BK Virus nephropathy.

  • quantitation of BK Virus load in serum for the diagnosis of BK Virus associated nephropathy in renal transplant recipients
    The Journal of Infectious Diseases, 2001
    Co-Authors: Ajit P. Limaye, Lawrence Corey, Keith R. Jerome, Christian S Kuhr, James Ferrenberg, Meei Li Huang, Connie L Davis, Christopher L Marsh
    Abstract:

    BK Virus-associated nephropathy is an increasingly recognized cause of graft dysfunction among kidney transplant recipients, and definitive diagnosis requires renal biopsy. By using a newly developed, quantitative, real-time polymerase chain reaction (PCR) assay for BK Virus DNA, a retrospective analysis was done of sequential serum samples (n = 28) from 4 transplant recipients with histopathologically documented BK Virus nephropathy and from samples (n = 76) from 16 transplant recipient control patients. BK Virus DNA was detected in serum samples from all 4 case patients versus 0 of 16 control patients (P<.0001, Fisher's exact test) at a median of 32 weeks (range, 17-61 weeks) before the diagnosis of BK Virus nephropathy. BK Virus load decreased in 3 of 3 patients after the reduction of immunosuppression and/or nephrectomy. It is concluded that quantitative PCR for BK Virus DNA in serum is useful both for identifying transplant recipients at risk for BK Virus nephropathy and for monitoring the response to therapy.

  • Quantitation of BK Virus Load in Serum for the Diagnosis of BK Virus–Associated Nephropathy in Renal Transplant Recipients
    The Journal of infectious diseases, 2001
    Co-Authors: Ajit P. Limaye, Lawrence Corey, Keith R. Jerome, Christian S Kuhr, James Ferrenberg, Meei Li Huang, Connie L Davis, Christopher L Marsh
    Abstract:

    BK Virus-associated nephropathy is an increasingly recognized cause of graft dysfunction among kidney transplant recipients, and definitive diagnosis requires renal biopsy. By using a newly developed, quantitative, real-time polymerase chain reaction (PCR) assay for BK Virus DNA, a retrospective analysis was done of sequential serum samples (n = 28) from 4 transplant recipients with histopathologically documented BK Virus nephropathy and from samples (n = 76) from 16 transplant recipient control patients. BK Virus DNA was detected in serum samples from all 4 case patients versus 0 of 16 control patients (P

Sundaram Hariharan - One of the best experts on this subject based on the ideXlab platform.

  • BK Virus infection after renal transplantation
    Dialysis & Transplantation, 2011
    Co-Authors: Puneet Sood, Sundaram Hariharan
    Abstract:

    In this review, we will discuss updates in diagnosis, treatment, and primary prevention, as well as unresolved issues and future directions for BK Virus nephropathy in renal transplant patients.

  • BK Virus Nephritis after Renal Transplantation
    Clinical Journal of the American Society of Nephrology, 2008
    Co-Authors: Aaron Dall, Sundaram Hariharan
    Abstract:

    BK Virus nephritis is an increasing problem and is posing a threat to improving renal transplant graft survival. The pathogenesis of this condition remains to be investigated. Higher prevalence of BK Virus infection in recent years has been correlated with declining acute rejection rates and the use of potent immunosuppressive agents. Patients with this infection usually have asymptomatic viremia and/or nephritis with or without worsening of renal function. The diagnosis of this disease is based on detecting the Virus or its effects in urine, blood, and renal tissue. In the past, approximately 30 to 60% of patients with BK Virus nephritis developed graft failure. In recent years, the combination of early detection, prompt diagnosis, and therapies including preventive measures have resulted in better outcomes.

  • BK Virus infection after renal transplantation
    Current Opinion in Organ Transplantation, 2006
    Co-Authors: Syed A. Hussain, Sundaram Hariharan
    Abstract:

    Purpose of review Increasing prevalence of BK Virus nephritis after renal transplantation has prompted review of important publications on this topic. Recent findings Nephritis from the BK Virus occurs specifically in renal transplant recipients, but not after other solid organ transplantation. A mouse renal transplant model of polyoma nephritis unveils the role of alloimmune activity in the development of BK Virus nephritis. BK Virus nephritis occurs approximately 1 year after transplantation, as opposed to acute rejection, which occurs early after transplantation. No identifiable donor, recipient, or transplant variables correlate with this disease. Recipients who receive a kidney from a seropositive kidney donor and the lack of HLA C7 in either donor or recipient may play a role in BK Virus infection. Mycophenolate mofetil and tacrolimus combination therapy is associated with a slightly higher chance of infection. Recovery from BK Virus nephritis is associated with increase in BK Virus-specific humoral and cellular immunity, which suggests that they are relevant factors in the pathogenesis of this disease. Summary Nephritis from BK Virus infection occurs through seropositive donors. Lack of HLA C7 in donor and recipient and BK Virus-specific humoral and cellular immune deficiencies may precipitate infection.