“…In 90% of the population, it remains in a latent state, mostly in tubular epithelial cells in the kidney and urothelial cells in the down‐stream urinary tract and asymptomatic shedding in the urine is seen . BKPyV reactivation may occur after the start of immunosuppressive therapy following allogeneic hematopoietic stem cell transplantation (allo‐HSCT) and could result in nephropathy, ureteral stenosis, or, more commonly, hemorrhagic cystitis (HC) …”
Background: BK polyomavirus reactivation can occur following allogeneic hematopoietic stem cell transplantation (allo-HSCT) and may lead to hemorrhagic cystitis (BKPyV-HC). We hypothesized that development of BKPyV-HC is associated with increased mortality post allo-HSCT.
Methods: We retrospectively reviewed data on 133 adult patients (≥18 years old) who underwent allo-HSCT from 2007 until 2014 at Hospital Israelita Albert Einstein in São Paulo, Brazil. Results: Thirty-six patients presented with BKPyV-HC after a median time of 42 days, with a 1-year cumulative incidence probability of 28.9% (95% CI 21.5%-36.7%). In a multivariate Cox model, risk factors for development of BKPyV-HC included younger age, male sex, development of grade 2-4 acute graft-versus-host disease and recipients of umbilical cord blood grafts. Development of grade 3-4 BKPyV-HC (but not grade 1-2) was associated with a decreased overall survival (OS) in a multivariate Cox model (hazard ratio [HR] 7.51, P < 0.0001) and an increased risk of TRM (HR 3.66, P < 0.0001). Grade 3-4 BKPyV-HC was also associated with an increased risk of relapse that did not reach statistical significance (HR 3.01, P = 0.07). Median overall survival (OS) post-BKPyV-HC was 4.7 months, and cidofovir had no impact on survival.Conclusion: Development of BKPyV-HC appears to be associated with decreased survival following allo-HSCT.
K E Y W O R D Sallogeneic stem cell transplantation, BK virus reactivation, hemorrhagic cystitis, mortality
“…In 90% of the population, it remains in a latent state, mostly in tubular epithelial cells in the kidney and urothelial cells in the down‐stream urinary tract and asymptomatic shedding in the urine is seen . BKPyV reactivation may occur after the start of immunosuppressive therapy following allogeneic hematopoietic stem cell transplantation (allo‐HSCT) and could result in nephropathy, ureteral stenosis, or, more commonly, hemorrhagic cystitis (HC) …”
Background: BK polyomavirus reactivation can occur following allogeneic hematopoietic stem cell transplantation (allo-HSCT) and may lead to hemorrhagic cystitis (BKPyV-HC). We hypothesized that development of BKPyV-HC is associated with increased mortality post allo-HSCT.
Methods: We retrospectively reviewed data on 133 adult patients (≥18 years old) who underwent allo-HSCT from 2007 until 2014 at Hospital Israelita Albert Einstein in São Paulo, Brazil. Results: Thirty-six patients presented with BKPyV-HC after a median time of 42 days, with a 1-year cumulative incidence probability of 28.9% (95% CI 21.5%-36.7%). In a multivariate Cox model, risk factors for development of BKPyV-HC included younger age, male sex, development of grade 2-4 acute graft-versus-host disease and recipients of umbilical cord blood grafts. Development of grade 3-4 BKPyV-HC (but not grade 1-2) was associated with a decreased overall survival (OS) in a multivariate Cox model (hazard ratio [HR] 7.51, P < 0.0001) and an increased risk of TRM (HR 3.66, P < 0.0001). Grade 3-4 BKPyV-HC was also associated with an increased risk of relapse that did not reach statistical significance (HR 3.01, P = 0.07). Median overall survival (OS) post-BKPyV-HC was 4.7 months, and cidofovir had no impact on survival.Conclusion: Development of BKPyV-HC appears to be associated with decreased survival following allo-HSCT.
K E Y W O R D Sallogeneic stem cell transplantation, BK virus reactivation, hemorrhagic cystitis, mortality
“…We report a first case, to our knowledge, of acute unilateral pan‐ureteritis caused by BKPyV in an allo‐SCT patient. Nine cases of bilateral ureteral obstruction related to hemorrhagic cystitis from BKPyV were reported in SCT patients . The cause of obstruction was likely blood clots and required nephrostomy tube placement .…”
Several cases of ureteral obstruction have been reported in stem cell transplant (SCT) patients; however, they were bilateral and concomitant with or preceded by hemorrhagic cystitis. We describe, to our knowledge, a first case of acute unilateral pan-ureteritis caused by BK polyomavirus (BKPyV) in an SCT patient. This case may represent an early phase of BKPyV reactivation. BKPyV infection should be considered as a potential cause of acute unilateral ureteritis even among SCT recipients.
“…In addition to the kidneys and urinary bladder, BKV was detected at autopsy in the epithelial cells of the ureters of a patient with non-Hodgkin’s lymphoma[ 15 ]. Ureteral involvement by BKV with various degrees of urinary obstruction was reported in patients with bone marrow or hematopoietic stem cell transplants[ 78 , 81 , 252 , 255 ] and renal transplants[ 251 , 253 , 254 ]. Fatal BK pneumonia was reported in three patients with hematopoietic stem cell transplants[ 257 , 259 , 260 ] and two patients under treatment for chronic lymphocytic leukemia[ 258 , 261 ].…”
Section: Clinical Manifestations Of Bkv Infection Other Than Nephropamentioning
Nephropathy secondary to BK virus, a member of the Papoviridae family of viruses, has been recognized for some time as an important cause of allograft dysfunction in renal transplant recipients. In recent times, BK nephropathy (BKN) of the native kidneys has being increasingly recognized as a cause of chronic kidney disease in patients with solid organ transplants, bone marrow transplants and in patients with other clinical entities associated with immunosuppression. In such patients renal dysfunction is often attributed to other factors including nephrotoxicity of medications used to prevent rejection of the transplanted organs. Renal biopsy is required for the diagnosis of BKN. Quantitation of the BK viral load in blood and urine are surrogate diagnostic methods. The treatment of BKN is based on reduction of the immunosuppressive medications. Several compounds have shown antiviral activity, but have not consistently shown to have beneficial effects in BKN. In addition to BKN, BK viral infection can cause severe urinary bladder cystitis, ureteritis and urinary tract obstruction as well as manifestations in other organ systems including the central nervous system, the respiratory system, the gastrointestinal system and the hematopoietic system. BK viral infection has also been implicated in tumorigenesis. The spectrum of clinical manifestations from BK infection and infection from other members of the Papoviridae family is widening. Prevention and treatment of BK infection and infections from other Papovaviruses are subjects of intense research.
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