Pediatr Nephrol DOI 10.1007/s00467-013-2438-3
BRIEF REPORT
Native kidney BK virus nephropathy associated with acute lymphocytic leukemia Guido Filler & Christoph Licht & Aaron Haig
Received: 14 December 2012 / Revised: 30 January 2013 / Accepted: 7 February 2013 # IPNA 2013
Abstract Background Polyoma BK virus nephropathy is a common complication after renal transplantation and is rarely seen in non-renal transplant recipients. There are only a couple of case reports of BK virus nephropathy in native kidneys in non-transplant patients, including a recent report of a 73year-old patient with chronic lymphatic leukemia. A variety of treatment options, including leflunomide and cidofovir, were reported in these patients. Case diagnosis/treatment Here we report the case of a 10year-old boy with acute lymphatic leukemia who presented with non-oliguric hypertensive acute kidney injury at the 12th maintenance cycle of his chemotherapy. The workup supported the clear diagnosis of BK virus nephropathy with tubulointerstitial changes, and the patient responded favorably to intravenous immunoglobulin therapy. Conclusions Pediatric nephrologists need to consider BK virus nephropathy as a differential diagnosis of acute kidney injury in immunocompromised non-transplant patients. Keywords Polyomavirus BK virus . Nephropathy . Renal transplantation . Acute lymphocytic leukemia G. Filler : A. Haig Department of Pathology & Laboratory Medicine, London Health Science Centre—University of Western Ontario, London, ON, Canada G. Filler (*) Department of Pediatrics, Division of Nephrology, Children’s Hospital, London Health Science Centre—University of Western Ontario, 800 Commissioners Road East, London, ON, Canada N6A 5W9 e-mail:
[email protected] C. Licht Division of Nephrology, Department of Pediatrics, The Hospital for Sick Children, 555 University Avenue, Toronto, ON M5G 1X8, Canada
Introduction Polyomavirus BK virus nephropathy is a well-recognized complication after renal transplantation, especially with the recent introduction of more potent immunosuppression [1]. Seroepidemiological studies suggest that the virus is normally acquired during early childhood and persists throughout adult life [2]. Most patients are asymptomatic carriers of the virus and have no related illness, but immunosuppression may cause reactivation of the virus. The highest prevalence is among renal transplant recipients, where it may cause premature kidney transplant failure [3]. The incidence after transplantation may be as high as 35 % [4]. In native kidneys, BK nephropathy has been described at a much lower rate after other solid organ or bone marrow transplantation [3, 5, 6]. The authors are aware of only one manuscript describing BK nephropathy in a 73-year-old Caucasian man diagnosed with chronic lymphocytic leukemia (CLL) [7]. Here, we describe BK nephropathy in a child with acute lymphocytic leukemia (ALL).
Case report A 10-year-old boy was diagnosed with normal risk ALL in 2009 and was on the 12th maintenance cycle of the therapy according to the COG AALL03311 protocol 3 years post initial diagnosis when the nephrology service was consulted to assess 1 Phase III Randomized Study of Different Combination Chemotherapy Regimens in Pediatric Patients With Newly Diagnosed Standard-Risk BPrecursor Acute Lymphoblastic Leukemia. All patients receive cytarabine intrathecally (IT) on day 1; vincristine intravenously (IV) on days 1, 8, 15, and 22; dexamethasone IVor orally twice daily on days 1– 28; pegaspargase intramuscularly (IM) (may give IVover 1–2 h) on day 4, 5, or 6; methotrexate IT on days 8 and 29 (and days 15 and 22 for patients with CNS3 disease.
Pediatr Nephrol
for hypertension, impaired kidney function, as well as nycturia, polyuria and polydipsia. Review of medical history records revealed multiple nephrotoxic medications 3 years earlier, including acyclovir, aminoglycosides, and vincristine, but more recently the only nephrotoxic drug the patient received was co-trimoxazole 3 days per week for pneumocystis prophylaxis. The patient had a viral illness 3 months earlier, after which the increased thirst was noted. The clinical assessment was unremarkable, and the patient was well hydrated and in good physical health. There was no organomegaly. Ophthalmology examination ruled out a uveitis, and there were no hypertensive fundus changes. The workup revealed moderate tubular proteinuria [372 mg/day (predominantly beta-2 microglobulin), with a beta-2 microglobulin/creatinine ratio of 114 and 95 g/mol (normal
