Ott U, Steiner T, Busch M, Gerth J, Wolf G
Department of Internal Medicine III, Friedrich Schiller University, Jena, Germany.
Clin Nephrol. 2008 Apr;69(4):244-50. doi: 10.5414/cnp69244.
BK virus nephropathy has an increasing role in renal transplant dysfunction, since new, highly potent immunosuppressive drugs have been introduced into therapy following renal transplantation. Diagnosis of acute impairment of renal transplant function is complicated by difficulty in differentiating BK virus nephropathy from acute rejection.
We retrospectively described the findings and therapeutic approaches of 6 consecutive patients with BK virus nephropathy in our transplantation center (75 - 80 transplantations/ year). BK virus nephropathy was classified according to Drachenberg et al. [2004].
We observed an incidence rate of < 1% for BK nephropathy in our center. Four patients had a pattern B whereas 2 patients revealed a pattern C of BK virus nephropathy. Focal C4d-positive staining of peritubular capillaries were found in 2 of the 6 cases. For earlier detection of BK nephropathy, a diagnostic algorithm for each patient after renal transplantation was established. Urine was continuously monitored by cytology for decoy cells and PCR for BK virus DNA. If PCR was also positive for the BK virus in plasma, biopsy of the renal allograft was performed. Thereby diagnosis could be confirmed sooner. For treatment of BK nephropathy in our center, we reduced immunosuppressive agents and initiated a virustatic treatment with cidofovir in the first 3 cases. However, results were not satisfactory and two allografts were lost. We then reconsidered our therapeutic approach and switched the immunosuppressive treatment to leflunomide with consistent low dose steroids. We use therapeutic drug monitoring for leflunomide and aim at a target level of 40 - 100 microg/ml. We lost no allograft with BK nephropathy since using this therapeutic approach.
In our center, leflunomide therapy, but not cidofovir, was effective in patients with BK virus nephropathy of the renal allograft.
自从新型强效免疫抑制药物被引入肾移植术后治疗以来，BK病毒肾病在肾移植功能障碍中所起的作用日益增加。肾移植功能急性损害的诊断因难以区分BK病毒肾病和急性排斥反应而变得复杂。
我们回顾性描述了我们移植中心（每年进行75 - 80例移植手术）连续6例BK病毒肾病患者的检查结果及治疗方法。BK病毒肾病根据Drachenberg等人[2004年]的方法进行分类。
我们中心BK肾病的发病率低于1%。4例为B型，2例为C型BK病毒肾病。6例中有2例在肾小管周围毛细血管发现局灶性C4d阳性染色。为了更早检测BK肾病，我们为每位肾移植术后患者建立了诊断算法。通过细胞学持续监测尿液中的诱饵细胞，并通过PCR检测BK病毒DNA。如果血浆中BK病毒的PCR检测也呈阳性，则对移植肾进行活检，从而能更快确诊。对于我们中心BK肾病的治疗，前3例患者我们减少了免疫抑制剂，并开始用西多福韦进行抗病毒治疗。然而，结果并不理想，2个移植肾失功。然后我们重新考虑治疗方法，将免疫抑制治疗改为来氟米特，并持续使用低剂量类固醇。我们对来氟米特进行治疗药物监测，目标水平为40 - 100微克/毫升。自从采用这种治疗方法以来，我们没有因BK肾病而导致移植肾失功。
在我们中心，来氟米特治疗而非西多福韦治疗对肾移植BK病毒肾病患者有效。
