S- and u-suPAR after therapy may serve as clinical markers to judge the treatment response of untreated NS and differentiate MCNS from FSGS, but not in pretreatment patients. S-, but not u-suPAR may predict the severity of and crescent formation in ANCA-GN.

Atsumi H, Asaka M, Kimura S, Imura J, Fujimoto K, Chikazawa Y, Nakagawa M, Okuyama H, Yamaya H, Moriyama M, Tanaka T, Suzuki K, Yokoyama H. A case of second renal transplantation with acute antibody‐mediated rejection complicated with BK virus nephropathy.
Clin Transplant 2010: 24 (Suppl. 22): 35–38. © 2010 John Wiley & Sons A/S. Abstract:  We reported a 40‐year‐old female case of second renal transplantation with antibody‐mediated rejection (AMR) complicated by BK virus nephropathy. She started hemodialysis (HD) at the age of 17 because of IgA nephropathy. At the age of 18, she underwent living‐donor kidney transplantation from her father, but two and a half years after transplantation, she developed chronic rejection. This time, she received cadaveric renal transplantation under the negative cross‐match (AHG‐LCT), and HLA‐AB 1 mismatch and ‐DR 1 mismatch. Immunosuppressive therapy was initiated using the following four immunosuppressants: methylprednisolone, mycophenolate mofetil, cyclosporine, and basiliximab. However, renal graft showed delayed function, the biopsy showed glomerulitis (g2), endarteritis (v1), and cellular infiltration (ptc3) consisting mainly of mononuclear cells in the peritubular capillary with diffusely positive C4d and anti‐SV 40 large T‐antigen‐positive renal tubular epithelial cells on post‐operative day 19. The donor‐specific antibody for HLA‐B46 was proven by the LAB screen method. We performed plasma exchange three times and administered immunoglobulin (15 g in total). Then, methylprednisolone pulse therapy was added, and the serum creatinine (SCr) levels gradually decreased. On post‐operative day 44, the patient was removed from HD and was discharged with SCr level of 3.3 mg/dL.

A 94-year-old female patient presented with anorexia and left axillar lymphadenopathy on admission. Her past history was angina pectoris at 83 years of age and total gastrectomy due to gastric cancer at 87 years. The family history revealed that her son had had a malignant lymphoma, the histopathological diagnosis of which was diffuse large B-cell lymphoma. A physical examination showed both cervical, axillar, and inguinal lymphadenopathy without tenderness. She had elevated lactate dehydrogenase, ferritin, and soluble interleukin-2 receptor (sIL-2R). Whole-body computed tomography confirmed the cervical, axillary, and inguinal lymphadenopathy. Gallium-68 imaging revealed positive accumulation in these superficial lymph nodes. A right inguinal lymph node biopsy showed features of Epstein-Barr virus-associated lymphoproliferative disorder. Immunohistological studies on this lymph node biopsy showed CD20-positive large cells, CD3-positive small cells, and CD30-partly-positive large cells. In situ hybridization showed Epstein-Barr virus-positive, LMP-partly-positive, and EBNA2-negative cells. She refused chemotherapy as her son had died from hematemesis during chemotherapy. She received intravenous hyperalimentation for 1 month after admission. No palpable lymph nodes were identified by physical examination or computed tomography 3 months after admission, and regression of lactate dehydrogenase, ferritin, and sIL-2R was observed. She recovered from anorexia and was discharged. She died from pneumonia 10 months later after initial symptoms of anorexia. The autopsy showed no superficial lymphadenopathy.

Background: Interstitial fibrosis in chronic allograft injury has been suggested as a major cause of the loss of allograft. Methods: To clarify the involvement of circulating fibrocytes (CF) and α-smooth muscle actin (SMA)-positive cells in renal allograft injury, we investigated 36 renal transplanted cases at 0 h, 1 h, 2–4 weeks, 4–8 weeks, and 1 year, and 5 normal controls. Double immunofluorescence analysis for both COL1 and CD45 indicating CF (/mm²), and the positive area (%) of α-SMA and Masson trichrome (MT) stain were detected by an image analyzing system. Results: The mean number of CF was 0 in controls and 4.0 in total transplanted specimens (p < 0.05). CF correlated with the α-SMA-positive area in the graft (R² = 0.39, p < 0.01), but not with Banff 2005 scores. The number of CF increased in 2–4 weeks; however, decreased 1 year after transplantation. α-SMA-positive area gradually increased at 1 year concomitant with the increase of MT-positive area. A similar phenomenon was observed in a case of primary nonfunction kidney from 0 h to 6 weeks after transplantation. The electron microscopy score of fibrosis around peritubularcapillaries was correlated positively with COL1-positive area (R² = 0.72, p < 0.01), but negatively with infiltrated CF (R² = 0.25, p < 0.05). Conclusion: CF were transiently induced, probably due to ischemia-reperfusion injury, but fibrosis only slightly progressed in this process. The α-SMA-positive myofibroblasts may accelerate the expansion of fibrosis around peritubular capillaries in chronic allograft injury.

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