Abstract

BackgroundThe extent and depth of BK polyomavirus (BKPyV) infection in renal allograft correlate with prognosis. This study was designed to evaluate the value of urinary sediment double-immunostaining for predicting BKPyV infection in proximal tubular epithelium.Materials and methodsA total of 76 urine sediment cell blocks, as well as the corresponding transplanted kidney tissues with BK polyomavirus associated-nephropathy (BKPyVAN), were evaluated by automatic double-immunostaining with anti-58-kDa Golgi protein (58K, a proximal renal tubular marker) + anti-SV40-T and anti-homogentisate 1, 2-dioxygenase (HGD, a renal tubular marker) + anti-SV40-T.ResultsImmunohistochemical staining demonstrated that 58K was expressed in proximal tubular epithelium but not in distal tubular epithelium or transitional epithelium. Of the 76 patients, 28 (36.8%) had urinary 58K(+)/SV40-T(+) cells and HGD(+)/SV40-T(+) cells, 41 (53.9%) had only HGD(+)/SV40-T(+) cells, one (1.3%) had only 58K(+)/SV40-T(+) cells, and six (7.9%) had only 58K(−)/HGD(−)/SV40-T(+) cells. The presence of urinary 58K(+)/SV40-T(+) cells was correlated with BKPyV infection in proximal tubular epithelium (P < 0.001, r = 0.806). The mean extent of SV40-T staining was significantly more extensive in patients with urinary 58K(+)/SV40-T(+) cells than those without urinary 58K(+)/SV40-T(+) cells (21.4 vs. 12.0%, P < 0.001). The positive predictive value, negative predictive value, sensitivity, and specificity of urinary 58K(+)/SV40-T(+) cells for predicting BKPyV infection in proximal tubular epithelium were 89.7% (95% CI: 71.5–97.3%), 91.5% (95% CI: 78.7–97.2%), 86.7% (95% CI: 68.4–95.6%), and 93.5% (95% CI: 81.1–98.3%), respectively.ConclusionUrinary sediment double-immunostaining with anti-58K and anti-SV40-T is valuable for predicting the extent and depth of BKPyV infection in renal allograft.

Highlights

  • BK polyomavirus-associated nephropathy (BKPyVAN) is one of the severe complications resulting in renal graft dysfunction and graft loss [1, 2]

  • The presence of urinary 58-kDa Golgi protein (58K)(+)/SV40-T(+) cells was correlated with BKPyV infection in proximal tubular epithelium (P < 0.001, r = 0.806)

  • Urinary sediment double-immunostaining with anti-58K and anti-SV40-T is valuable for predicting the extent and depth of BKPyV infection in renal allograft

Read more

Summary

Introduction

BK polyomavirus-associated nephropathy (BKPyVAN) is one of the severe complications resulting in renal graft dysfunction and graft loss [1, 2]. In some cases of severe infection, BKPyV can spread to the glomerular parietal epithelial cells [9,10,11]. Our previous study has demonstrated that BKPyV infection in glomerular parietal epithelial cells is a risk factor for accelerated renal graft failure, indicating the infection depth of BKPyV in allograft has an adverse effect on prognosis [9]. If the depth and extent of BKPyV infection in allograft could be determined non-invasively, it may provide some useful information for risk stratification and prognosis evaluation of BKPyVAN. The extent and depth of BK polyomavirus (BKPyV) infection in renal allograft correlate with prognosis. This study was designed to evaluate the value of urinary sediment double-immunostaining for predicting BKPyV infection in proximal tubular epithelium

Methods
Results
Conclusion
Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call