BK virus nephropathy after kidney transplantation

被引:0
作者
Broecker, V. [1 ]
Schwarz, A. [2 ]
Becker, J. U. [1 ]
机构
[1] Hannover Med Sch, Inst Pathol, D-30625 Hannover, Germany
[2] Hannover Med Sch, Klin Nieren & Hochdruckerkrankungen, D-30625 Hannover, Germany
来源
PATHOLOGE | 2011年 / 32卷 / 05期
关键词
BK virus; Polyomavirus nephropathy; Kidney transplantation; Immunosuppression; Transplant loss; POLYOMAVIRUS-ASSOCIATED NEPHROPATHY; NATIVE KIDNEYS; RENAL-TRANSPLANTATION; JC VIRUS; INFECTION; RECIPIENT; IMMUNOSUPPRESSION; IMMUNODEFICIENCY; PAPOVAVIRUS; PREVALENCE;
D O I
10.1007/s00292-011-1450-2
中图分类号
R36 [病理学];
学科分类号
100104 ;
摘要
JC and BK viruses are strains of the polyomavirus group with pathogenic potential in humans. BK is the most frequent pathogenic agent of polyomavirus nephropathy (BKVN) in kidney transplant patients, which is only exceptionally caused by JC virus. Asymptomatic BK virus infection is often acquired in childhood and the virus persists in urothelium and kidneys of healthy individuals, where it can be reactivated under immunosuppression. Up to 10% of transplanted kidneys are affected by BKVN, while the risk of transplant failure due to BKVN exceeds 50% in some publications. In kidney biopsies BKVN leads to tubulointerstitial nephritis, which may be difficult to distinguish from acute cellular rejection without additional use of immunohistochemistry for a polyomavirus antigen. Typical hallmarks of BKVN include cytopathic effects caused by the virus with cell lysis, denudation of tubular basement membranes and nuclear inclusion bodies. An early diagnosis is essential for transplant survival, making screening of blood and urine for BK virus after kidney transplantation part of the standard care of renal transplant patients today. In the case of significant viremia or biopsy-proven BKVN immunosuppression is reduced to allow clearing of the virus.
引用
收藏
页码:399 / 405
页数:7
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