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Copyright ©The Author(s) 2016. Published by Baishideng Publishing Group Inc. All rights reserved.
World J Transplant. Sep 24, 2016; 6(3): 472-504
Published online Sep 24, 2016. doi: 10.5500/wjt.v6.i3.472
BK nephropathy in the native kidneys of patients with organ transplants: Clinical spectrum of BK infection
Darlene Vigil, Nikifor K Konstantinov, Marc Barry, Antonia M Harford, Karen S Servilla, Young Ho Kim, Yijuan Sun, Kavitha Ganta, Antonios H Tzamaloukas
Darlene Vigil, Karen S Servilla, Yijuan Sun, Kavitha Ganta, Antonios H Tzamaloukas, Nephrology Section, Medicine Service, Raymond G. Murphy VA Medical Center and Department of Medicine, University of New Mexico School of Medicine, Albuquerque, NM 87108, United States
Nikifor K Konstantinov, Department of Medicine, University of Minnesota School of Medicine, Minneapolis, MN 55455, United States
Marc Barry, Department of Pathology, University of New Mexico School of Medicine, Albuquerque, NM 87131, United States
Antonia M Harford, Division of Nephrology, Department of Medicine, University of New Mexico School of Medicine, Albuquerque, NM 87131, United States
Young Ho Kim, Division of Nephrology, University of North Carolina School of Medicine, Chappel Hill, NC 27599, United States
Author contributions: Vigil D reviewed the literature and composed the first draft of this report; Konstantinov NK assisted in the bibliographic search and wrote part of the report; Barry M produced the histology pictures of this report and made critical changes in the report; Harford AM reviewed the literature and made critical changes in the report; Servilla KS made critical changes in the manuscript; Kim YH assisted in the search of the literature and made important changes in the report; Sun Y made important changes in this report; Ganta K made important changes in the manuscript; Tzamaloukas AH assisted in the search of the literature and wrote parts of the report.
Conflict-of-interest statement: Authors declare no conflicts of interest for this article.
Open-Access: This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
Correspondence to: Antonios H Tzamaloukas, MD, MACP, Nephrology Section, Medicine Service, Raymond G. Murphy VA Medical Center and Department of Medicine, University of New Mexico School of Medicine, 1501 San Pedro, SE, Albuquerque, NM 87108, United States. antonios.tzamaloukas@va.gov
Telephone: +1-505-2651711-4733 Fax: +1-505-2566441
Received: June 29, 2016
Peer-review started: July 1, 2016
First decision: August 5, 2016
Revised: August 26, 2016
Accepted: September 7, 2016
Article in press: September 8, 2016
Published online: September 24, 2016
Processing time: 86 Days and 6.8 Hours
Abstract

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.

Keywords: BK viral infection, BK nephropathy, Cardiac transplant, Bone marrow transplant, Liver transplant, Pancreatic transplant, Lung transplant

Core tip: BK virus (BKV) is a member of a family of viruses that cause various diseases in animals and humans. Severe disease in transplanted kidneys was the first recognized human disease caused by BKV. In more recent times, BKV was also recognized as a cause of disease in the native kidneys of patients who had received bone marrow, heart, lung, liver and pancreas transplants, as well as in the kidneys of patients with loss of resistance to infection, such as patients with acquired immune deficiency syndrome or patients treated for malignant tumors. In addition to disease of the kidneys, BKV has also caused severe disease of the urinary bladder, the brain, the lungs, the gut and the blood. The diagnosis and particularly the management of infection by BKV present difficulties. Research for new medications specific for treating this infection is imperative.