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An Association between BK Virus Replication in Bone Marrow and Cytopenia in Kidney-Transplant Recipients

DOI: 10.1155/2014/252914

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Abstract:

The human polyomavirus BK (BKV) is associated with severe complications, such as ureteric stenosis and polyomavirus-associated nephropathy (PVAN), which often occur in kidney-transplant patients. However, it is unknown if BKV can replicate within bone marrow. The aim of this study was to search for BKV replication within the bone marrow of kidney-transplant patients presenting with a hematological disorder. Seventy-two kidney-transplant patients underwent bone-marrow aspiration for cytopenia. At least one virus was detected in the bone marrow of 25/72 patients (35%), that is, parvovirus B19 alone (n = 8), parvovirus plus Epstein-Barr virus (EBV) (n = 3), cytomegalovirus (n = 4), EBV (n = 2), BKV alone (n = 7), and BKV plus EBV (n = 1). Three of the eight patients who had BKV replication within the bone marrow had no detectable BKV replication in the blood. Neutropenia was observed in all patients with BKV replication in the bone marrow, and blockade of granulocyte maturation was observed. Hematological disorders disappeared in all patients after doses of immunosuppressants were reduced. In conclusion, an association between BKV replication in bone marrow and hematological disorders, especially neutropenia, was observed. Further studies are needed to confirm these findings. 1. Introduction Hematological abnormalities, that is, anemia, leucopenia, and thrombocytopenia, are commonly observed in kidney-transplant patients [1, 2]. Apart from anemia caused by impaired kidney function, most cases of cytopenia are related to viral infections or to bone-marrow toxicity caused by drugs used at posttransplantation [1–3]. In cases of cytopenia, viral infection is usually ruled out by searching for the viral genome in blood or in blood-marrow aspirates. Parvovirus B19 infection is a classic cause of anemia [4], and cytomegalovirus (CMV) is well known to suppress bone-marrow function [5]. Patients who present with severe cytopenia, and in whom bacterial, viral, and fungal infections have been ruled out, should be assessed for possible toxic causes for these hematology abnormalities. Indeed, several drugs that are frequently used after transplantation can suppress bone-marrow activity; these include the mycophenolates, azathioprine, the mammalian target of rapamycin inhibitors, (val) ganciclovir, and cotrimoxazole [1–3]. This toxicity can lead to immunosuppressants being discontinued and, thus, an increased risk of acute rejection [6], or the withdrawal of prophylactic drugs, which increases the risk of infections [3]. The human polyomavirus, BKV, is associated with

References

[1]  Y. Vanrenterghem, “Anemia after kidney transplantation,” Transplantation, vol. 87, no. 9, pp. 1265–1267, 2009.
[2]  J.-P. Rerolle, J.-C. Szelag, and Y. Le Meur, “Unexpected rate of severe leucopenia with the association of mycophenolate mofetil and valganciclovir in kidney transplant recipients,” Nephrology Dialysis Transplantation, vol. 22, no. 2, pp. 671–672, 2007.
[3]  L. Zafrani, L. Truffaut, H. Kreis et al., “Incidence, risk factors and clinical consequences of neutropenia following kidney transplantation: A Retrospective Study,” American Journal of Transplantation, vol. 9, no. 8, pp. 1816–1825, 2009.
[4]  M. Waldman and J. B. Kopp, “Parvovirus B19 and the kidney,” Clinical Journal of the American Society of Nephrology, vol. 2, no. 1, pp. S47–S56, 2007.
[5]  G. D. Almeida-Porada and J. L. Ascensao, “Cytomegalovirus as a cause of pancytopenia,” Leukemia and Lymphoma, vol. 21, no. 3-4, pp. 217–223, 1996.
[6]  G. A. Knoll, I. Macdonald, A. Khan, and C. Van Walraven, “Mycophenolate mofetil dose reduction and the risk of acute rejection after renal transplantation,” Journal of the American Society of Nephrology, vol. 14, no. 9, pp. 2381–2386, 2003.
[7]  H. H. Hirsch and J. Steiger, “Polyomavirus BK,” Lancet Infectious Diseases, vol. 3, no. 10, pp. 611–623, 2003.
[8]  H. H. Hirsch and P. Randhawa, “BK polyomavirus in solid organ transplantation,” American Journal of Transplantation, vol. 13, supplement 4, pp. 179–188, 2013.
[9]  T. Petrogiannis-Haliotis, G. Sakoulas, J. Kirby et al., “BK-related polyomavirus vasculopathy in a renal-transplant recipient,” The New England Journal of Medicine, vol. 345, no. 17, pp. 1250–1255, 2001.
[10]  L. Esposito, H. Hirsch, G. Basse, G. Fillola, N. Kamar, and L. Rostaing, “BK virus-related hemophagocytic syndrome in a renal transplant patient,” Transplantation, vol. 83, no. 3, p. 365, 2007.
[11]  S. H. M. Gardeniers, D. Mekahli, E. Levtchenko, E. Lerut, M. Renard, and R. Van Damme-Lombaerts, “Bone marrow aplasia and graft loss in a pediatric renal transplant patient with polyomavirus nephropathy,” Pediatric Nephrology, vol. 25, no. 10, pp. 2191–2192, 2010.
[12]  C. Mengelle, K. Sandres-Sauné, C. Pasquier et al., “Automated extraction and quantification of human cytomegalovirus DNA in whole blood by real-time PCR assay,” Journal of Clinical Microbiology, vol. 41, no. 8, pp. 3840–3845, 2003.
[13]  A. P. Limaye, K. R. Jerome, C. S. Kuhr et al., “Quantitation of BK virus load in serum for the diagnosis of BK virus—associated nephropathy in renal transplant recipients,” Journal of Infectious Diseases, vol. 183, no. 11, pp. 1669–1672, 2001.
[14]  L. ?hrmalm, M. Wong, C. Aust et al., “Viral findings in adult hematological patients with neutropenia,” PLoS ONE, vol. 7, no. 5, article e36543, 2012.

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