case_images: PMC5259612_01
case_images: Clinical course. CsA: cyclosporine; MMF: mycophenolate mofetil; mPSL: methylprednisolone; MZ: mizoribine; CMV: cytomegalovirus; KTx: kidney transplantation; Bx: kidney biopsy.
case_images: CRIT2017-1347052.001.jpg
case_images: PMC5259612_01_CRIT2017-1347052.001.jpg
case_images: fig1
case_images: The clinical course of the patient is shown in Figure 1.
case_images: Light microscopic findings for a 3-month protocol biopsy specimen. (a) Mononuclear inflammatory cell infiltration was seen in the interstitial lesions, with plasma cells accounting for approximately 20%. Moderately developed tubulitis was noted in the middle of the field (PAS, x200). (b-d) Negative staining of SV40 (b), EBER (c), and IgG4 (d) in allograft specimen (x200). (e) CD138-positive interstitial inflammatory cells (x200). (f, g) Infiltrating plasma cells positive for both kappa (f) and lambda (g) light chains, indicating that they are polyclonal (x200).
case_images: CRIT2017-1347052.002.jpg
case_images: PMC5259612_01_CRIT2017-1347052.002.jpg
case_images: fig2
case_images: A first protocol allograft biopsy, performed three months after kidney transplantation, incidentally showed focal aggressive interstitial mononuclear cell infiltration, with mild interstitial fibrosis and tubular atrophy and moderate tubulitis (Figure 2(a)). These examinations showed maturing polyclonal plasma cells positive for CD138 and both light chains (Figures 2(e), 2(f) (kappa), and 2(g) (lambda)). Negative staining for SV40 and IgG4 in these infiltrates excluded BK virus-related nephropathy and IgG4-related kidney disease, respectively (Figures 2(b) (SV40) and 2(d) (IgG4)). Moreover, negative staining for EBV-encoded small RNA by in situ hybridization excluded posttransplant lymphoproliferative disorder (PTLD) (Figure 2(c)).
case_images: Light microscopic findings in a second biopsy at 3 months after the first antirejection therapy. (a) Transplant glomerulitis, mild (PAS, x100), (b, c) mild infiltration of inflammatory cells including plasma cells; and mildly developed tubulitis was noted (HE, x400 (b), x200 (c)). (d) Peritubular capillaritis was moderately developed (Masson's Trichrome, x400).
case_images: CRIT2017-1347052.003.jpg
case_images: PMC5259612_01_CRIT2017-1347052.003.jpg
case_images: fig3
case_images: Pathological analysis revealed not only the presence of focal aggressive interstitial mononuclear cell infiltration (Figures 3(b) and 3(c)) but also de novo mild transplant glomerulitis (Figure 3(a)) and focal and moderate peritubular capillaritis (Figure 3(d)), which are characteristics of ABMR.
case_images: Time-dependent histopathological changes in tubulointerstitial lesions at 3 (a), 6 (b), and 12 months (c) after transplantation ((a-c) Masson's Trichrome, x100). Light microscopic findings revealed marked regression of plasma cell infiltration at 12 months, compared with at 3 or 6 months after transplantation.
case_images: CRIT2017-1347052.004.jpg
case_images: PMC5259612_01_CRIT2017-1347052.004.jpg
case_images: fig4
case_images: Figures 4(a)-4(c) demonstrate the gradual improvement of interstitial inflammation of PCAR ((a) first protocol biopsy, (b) second biopsy, and (c) third biopsy).