<scp>BK</scp> virus nephropathy in a pediatric patient after hematopoietic stem cell transplantation

Aksenova, Marina; Tsetlina, V.A.; Gutovskaya, Elena; Mitrofanova, Anna; Balashov, D.N.; Maschan, Alexey

doi:10.1111/petr.12411

Cited by 13 publications

(11 citation statements)

References 15 publications

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“…Our patient received non‐myeloablative conditioning and had no episodes of GVHD and that could explain the absence of hemorrhagic cystitis. Also, native kidney nephropathy sometimes leading to ESRD, with or without mortality, can occur in adult and pediatric HSCT and non‐renal SOT recipients 4,30‐37 . The nephropathy may occur with or without hemorrhagic cystitis.…”

Section: Discussionmentioning

confidence: 99%

BK virus encephalitis and end‐stage renal disease in a child with hematopoietic stem cell transplantation

Bush

Johns

Betty

et al. 2020

Pediatric Transplantation

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BK virus encephalitis after HSCT is uncommon. Several reports of native kidney BKVN in patients with HSCT, hematologic malignancies, human immunodeficiency virus infection, and non‐renal solid organ transplantation have been described. However, an uncommon combination of BK encephalitis and ESRD of native kidneys secondary to BK virus in a child with HSCT has not been described. We report a 10‐year‐old boy who presented with a gradually rising serum creatinine during treatment for severe autoimmune hemolytic anemia, which he developed 9 months after receiving an allogeneic HSCT for aplastic anemia. There was no proteinuria or hematuria present. Serum BK virus load was 5 × 106 copies/mL. A renal biopsy showed evidence of BKVN. He developed fever, seizures, and confusion, and the (CSF) showed significant presence of the BK virus (1 × 106 copies/mL) along with biochemical evidence of viral encephalitis. Cerebrospinal fluid cultures were negative. Despite significant clinical symptoms and presence of BK virus in CSF, the magnetic resonance brain imaging findings were minimal. With reduction of immunosuppression, there was resolution of BK encephalitis but BKVN remained resistant to multiple anti‐BK virus agents, including leflunomide and cidofovir. He eventually became dialysis‐dependent and, 6 years later, received a renal transplant from his mother. This case illustrates that BK virus in severely immunocompromised HSCT recipient may lead to BK encephalitis and BKVN of native kidneys, even without hemorrhagic cystitis, leading to ESRD. Knowledge of such is important for appropriate timely evaluation and management.

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Section: Discussionmentioning

confidence: 99%

BK virus encephalitis and end‐stage renal disease in a child with hematopoietic stem cell transplantation

Bush

Johns

Betty

et al. 2020

Pediatric Transplantation

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“…Studies have shown that children with a peak plasma BK virus load of 10,000 copies per milliliter or more during the first year after transplantation, regardless of the urinary viral load, have worse renal disease (with 70% requiring dialysis), more severe hemorrhagic cystitis leading to urologic complications requiring surgical interventions, and a lower rate of survival at 1 year than those with fewer than 10,000 copies per milliliter. 48,93 In patients with BK viremia or nephropathy, the first-line therapy is often the reduction of immunosuppression, when possible, before the initiation of treatment with cidofovir or other antiviral agents, including leflunomide. Cidofovir has been used to treat severe cases of hemorrhagic cystitis, with mixed results.…”

Section: Viral Infectionsmentioning

confidence: 99%

Renal Complications of Hematopoietic-Cell Transplantation

Hingorani¹

2016

N Engl J Med

170

177

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ach year, approximately 50,000 patients worldwide undergo hematopoietic-cell transplantation. This procedure, which is used to treat a wide range of malignant and nonmalignant diseases, may involve either a myeloablative or reduced-intensity conditioning regimen; the use of alternative allogeneic donors (i.e., haploidentical or mismatched donors); cells from bone marrow, cord blood, or peripheral-blood stem cells; and new immunomodulatory agents to prevent graft-versus-host disease (GVHD) 1 (Table 1). Despite the overall improvement in outcomes after hematopoietic-cell transplantation, kidney injury remains a frequent complication and contributes to the morbidity and mortality associated with the procedure. 2-11 The onset of acute kidney injury and chronic kidney disease, which affect from 10 to 70% of transplant recipients, 2,7,12,13 varies from days after transplantation to months or years afterward. Acute injury is generally indicated by elevated levels of serum creatinine up to 100 days after transplantation, and chronic injury by elevated levels at or after 100 days. Acute kidney injury that persists for 3 months or longer is usually reclassified as chronic kidney disease. The overall health of the patient at the time of transplantation is generally assessed with use of a hematopoietic-cell transplantation-specific comorbidity index that includes the serum creatinine level. 14 In this index, which includes 17 categories of organ dysfunction, scores for organ-specific coexisting conditions range from 0 to 3, with higher scores indicating a greater severity of the condition. The risk categories are not fixed and can vary according to conditioning regimens. Scores on the comorbidity index range from 0 to 12. Higher scores on the index (the weighted sum of all the scores for organ-specific conditions and other pretransplantation characteristics) indicate a greater risk of death that is not associated with relapse. In general, patients with a score of 0 are considered to be at low risk of death that is not associated with relapse, those with a score of 1 or 2 are considered to be at intermediate risk, and those with a score of 3 or greater are considered to be at high risk. A score of 1 or more is correlated with a risk of acute post-transplantation kidney injury. 3 Such kidney injury may be caused by conditioning chemotherapy, total-body irradiation, nephrotoxic agents, infections, the hepatic sinusoidal obstruction syndrome (previously called veno-occlusive disease of the liver), transplantation-associated thrombotic microangiopathy, and GVHD. 3-7,15-19 This article reviews the causes, diagnosis, and management of complications and disorders of the kidney after hematopoietic-cell transplantation. Definition a nd Epidemiol ogy of K idne y Injur y Acute kidney injury after transplantation was initially defined as a doubling of the baseline serum creatinine level within the first 100 days after transplantation.

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“…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) …”

Section: Introductionmentioning

confidence: 99%

Severe hemorrhagic cystitis caused by the BK polyomavirus is associated with decreased survival post‐allogeneic hematopoietic stem cell transplantation

Kerbauy

Bautzer

et al. 2019

Transplant Infectious Dis

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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

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BK virus nephropathy in a pediatric patient after hematopoietic stem cell transplantation

Cited by 13 publications

References 15 publications

BK virus encephalitis and end‐stage renal disease in a child with hematopoietic stem cell transplantation

BK virus encephalitis and end‐stage renal disease in a child with hematopoietic stem cell transplantation

Renal Complications of Hematopoietic-Cell Transplantation

Severe hemorrhagic cystitis caused by the BK polyomavirus is associated with decreased survival post‐allogeneic hematopoietic stem cell transplantation

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