BK virus-associated hemophagocytic syndrome in a renal transplant recipient

Yaïch, S.; Charfeddine, K.; Hsairi, D; Zaghdane, S; Kammoun, K.; Makni, S.; Boudawara, Tahia; Hachicha, J.

doi:10.4103/1319-2442.132205

Cited by 13 publications

(11 citation statements)

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“…Emmenegger et al reported a 59% response with 1.6 g/kg IVIG for 3 days in patients with different Fever (> 38ºC for at least 7 days) Cytopenia affecting 2 or 3 cell types (hemoglobin < 9.0g/dL; neutrophils < 1.000/mm³; platelets < 100.000/mm³) underlying conditions (infection, malignancy, and systemic lupus erythematosus), confirming the effectiveness of this therapeutic strategy, especially with the infectious condition (78% versus 39%). 5,10,12,15,17 The main predictive factor of good clinical response was starting therapy within 2 days of serum ferritin peak. 5,15 Asci et al reported that of the 13 patients with post-KTx HLH analyzed in their study, 6 recovered and received IVIG therapy.…”

Section: Discussionmentioning

confidence: 99%

Secondary hemophagocytic syndrome after renal transplantation: two case-reports

et al. 2020

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Hemophagocytic syndrome or hemophagocytic lymphohistiocytosis (HLH) is an infrequent and underdiagnosed condition caused by an overactive immune response, resulting in blood cells phagocytosis. After kidney transplantation (KTx), HLH is usually secondary (or reactive) to infectious and neoplastic processes and has a high mortality rate. No effective treatment is available for this condition. Usual procedures include detecting and treating the pathology triggering the immune system dysregulation, other than administration of intravenous human immunoglobulin (IVIG) and high doses of steroids, and plasmapheresis. The best protocol for maintenance immunosuppressive therapy is also unknown. This article presents two cases of post-KTx reactive HLH that underwent adjuvant IVIG treatment and obtained good clinical results. Despite the high morbidity and mortality associated with reactive HLH after KTx, the early and precise diagnosis and the administration of IVIG therapy along with the treatment of the triggering disease, was an effective strategy to control HLH.

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Section: Discussionmentioning

confidence: 99%

Secondary hemophagocytic syndrome after renal transplantation: two case-reports

et al. 2020

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“…Pancytopenia or severe neutropenia associated with BKV infection have been found in kidney transplant recipients[ 284 - 286 ]. Hemophagocytic syndrome was diagnosed in one of these patients[ 286 ].…”

Section: Clinical Manifestations Of Bkv Infection Other Than Nephropamentioning

confidence: 99%

BK nephropathy in the native kidneys of patients with organ transplants: Clinical spectrum of BK infection

Vigil

Konstantinov

Barry

et al. 2016

WJT

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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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“…Secondary HPS was first described at 1979 in 19 patients interestingly, thirteen of of these patients were renal transplant recipients. In transplant recipients, HPS often triggers by an infection, mainly viral, including adenovirus, human herpes virus 8 (HHV-8), Epstein-Barr virus (EBV), cytomegalovirus (CMV) ( 12 , 13 ), HHV-6 ( 14 ), parvovirus B19 ( 15 , 16 ) and BK polyomavirus ( 17 ), herpes viruses account for 62% of viral cases of HPS, and EBV is known as the most prominent of them ( 2 ). Tuberculosis, toxoplasmosis, leishmaniosis, babesiosis, Rickettsia spp, and Staphylococcus spp and Escherichia coli have been reported as the causative infections triger for initiation and development of HPS ( 18 - 20 ) .…”

Section: Mechanisms and Diagnostic Criteriamentioning

confidence: 99%

An update on renal involvement in hemophagocytic syndrome (macrophage activation syndrome)

et al. 2015

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Context: Hemophagocytic syndrome (HPS) is mainly characterized by massive infiltration of bone marrow by activated macrophages and often presents with pancytopenia. Thrombotic microangiopathy (TMA) is also present with thrombocytopenia and renal involvement. Both conditions could coexist with each other and complicate the condition. Evidence Acquisition: Directory of Open Access Journals (DOAJ), EMBASE, Google Scholar, PubMed, EBSCO, and Web of Science with keywords relevant to; Hemophagocytic syndrome, macrophage activation syndrome, interferon-gamma and thrombotic microangiopathy, have been searched. Results: Viral infection, rheumatologic disease and malignancies are the main underlying causes for secondary HPS. calcineurin inhibitors and viral infections are also the main underlying causes of TMA in transplant recipients. In this review, we discussed a 39-year-old male who presented with pancytopenia and renal allograft dysfunction. With the diagnosis of HPS induced TMA his renal condition and pancytopenia improved after receiving intravenous immunoglobulin (IVIG) and plasmapheresis therapy. Conclusions: HPS is an increasingly recognized disorder in the realm of different medical specialties. Renal involvement complicates the clinical picture of the disease, and this condition even is more complex in renal transplant recipients. We should consider the possibility of HPS in any renal transplant recipient with pancytopenia and allograft dysfunction. The combination of HPS with TMA future increases the complexity of the situation.

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BK virus-associated hemophagocytic syndrome in a renal transplant recipient

Cited by 13 publications

References 0 publications

Secondary hemophagocytic syndrome after renal transplantation: two case-reports

Secondary hemophagocytic syndrome after renal transplantation: two case-reports

BK nephropathy in the native kidneys of patients with organ transplants: Clinical spectrum of BK infection

An update on renal involvement in hemophagocytic syndrome (macrophage activation syndrome)

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