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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

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