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Prevalence of polyoma BK virus infection among living‐donor renal transplant recipients
Author(s) -
El Ansary M.,
Abd Elhamid S.,
Saadi G.,
Ismail W.,
Ibrahim N.,
Bahaa ElDin N.,
Alhsyek S.
Publication year - 2016
Publication title -
transplant infectious disease
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.69
H-Index - 67
eISSN - 1399-3062
pISSN - 1398-2273
DOI - 10.1111/tid.12557
Subject(s) - medicine , bk virus , urine , polyomavirus infections , viremia , kidney , nephropathy , kidney transplantation , renal transplant , immunohistochemistry , jc virus , cytology , staining , virus , biopsy , pathology , virology , endocrinology , diabetes mellitus , progressive multifocal leukoencephalopathy
Abstract Background Polyomavirus nephropathy ( PVN ) mainly caused by BK polyomavirus ( BKP yV) remains the most common productive viral infection of the kidney in immunosuppressed patients. The diagnosis of PVN is based on the detection of BK viruria and BK viremia in conjunction with histological findings in the graft biopsy. Methods Our study was aimed to estimate the prevalence of productive BKP yV infection among renal transplant patients within the first year post‐transplant and identify those at risk of developing PVN . Our cross‐sectional study was conducted on 134 kidney transplant patients. Evidence of BKP yV replication was assessed by viral quantification of blood and urine samples of studied patients using a quantitative real‐time polymerase chain reaction (Q‐PCR) PCR ), detection of decoy cells in urine cytology smears, histological examination of graft biopsies from Q‐PCR BKPyV‐positive patients, and immunohistochemical staining by simian virus 40 ( SV 40) antibody. Results Significant BKP yV infection was prevalent in 8% ( n = 11) of our patients, with a peak of BKP yV infection about 8 months post transplant. BKP yV viral load by Q‐ PCR assay in these patients varied from 1350 to 20,000,000 (1.35 × 10 3 to 2 × 10 7 ) copies/mL for urine samples and 935 to 18,920 (9.35 × 10 2 to 1.89 × 10 4 ) copies/mL for blood samples. All the 11 patients were positive for decoy cells but only 3 developed PVN based on histology and positive SV 40 staining. BKP yV infection was more prevalent in older patients. All patients responded to reduction in their immunosuppressive regimens, apart from 2 patients who required replacement of calcineurin inhibitors‐based regimen with mammalian target of ramapycin inhibitors with an overall good response. Conclusion Protocol screening programs based on detection of viral replication by viruria, viremia, and decoy cells in urine are necessary to shed light on patients with high virus replication and hence increased risk of developing PVN , and to allow early diagnosis and intervention.