A 31-year-old man underwent living-related kidney transplantation in 2004 as a consequence of primary focal segmental glomerulosclerosis (FSGS). Four years after the transplantation, we confirmed nephrotic syndrome caused by recurrent FSGS. We performed plasmapheresis and low-density lipoprotein adsorption. We also combined steroid therapy with a reduction in the dose of tacrolimus and an increased dose of mycophenolate mofetil. The nephrotic syndrome improved dramatically with this combined therapeutic approach. However, 10 months after these treatments, he revisited our hospital because of altered consciousness. We detected multiple tumor masses in his brain that were ring enhanced on contrast magnetic resonance imaging. Consequently, we suspected primary central nervous system post-transplantation lymphoproliferative disorder (CNS-PTLD). We performed a craniotomy to biopsy the brain tumors. The biopsy specimen showed Epstein-Barr virus-associated diffuse large B-cell lymphoma. There is no definitive treatment for CNS-PTLD. Therefore, we treated the primary CNS-PTLD successfully with whole-brain radiation and discontinuation of immunosuppression therapy.

♦ Background: The angiogenic response is partly involved in the progression of encapsulating peritoneal sclerosis (EPS). However, the details of the angiogenic response, especially for lymphatic vessels in patients with EPS, remain unclear. In addition, because of technical limitations, morphology studies reported to date have examined only the parietal peritoneum. The morphologies of parietal and visceral lymphatic vessels in patients with EPS both need to be analyzed. ♦ Methods: We examined peritoneal samples from 18 patients with EPS who underwent enterolysis of the visceral peritoneum and compared them with samples from 17 autopsy cases (controls). To examine the angiogenic response, we performed immunohistochemistry for the endothelial markers CD34 (blood vessels) and podoplanin (lymphatic vessels) and for the cell proliferation marker Ki-67. Immunogold electron microscopy analysis for podoplanin was also performed. In 7 of 18 cases, we compared differences in the angiogenic response of the parietal and visceral peritoneal membranes.

Yaginuma T, Yamamoto H, Mitome J, Kobayashi A, Yamamoto I, Tanno Y, Hayakawa H, Miyazaki Y, Yokoyama K, Utsunomiya Y, Miki J, Yamada H, Furuta N, Yamaguchi Y, Hosoya T. Successful treatment of nephrotic syndrome caused by recurrent IgA nephropathy with chronic active antibody‐mediated rejection three years after kidney transplantation.
Clin Transplant 2011: 25 (Suppl. 23): 28–33.
© 2011 John Wiley & Sons A/S. Abstract:  Here, we report the successful treatment of a 38‐yr‐old Japanese man diagnosed with recurrent immunoglobulin A nephropathy (IgAN) with chronic active antibody‐mediated rejection (CAAMR), three yr after undergoing living‐related donor kidney transplantation. Immediately after transplantation, the allograft function was well maintained with a serum creatinine (S‐Cr) level of <1.8 mg/dL. About three yr after transplantation, urine protein excretion had reached 4.59 g/d, and the S‐Cr level had increased to more than 2.0 mg/dL. Based on the allograft biopsy, we diagnosed nephrotic syndrome because of recurrence of IgAN with CAAMR. Subsequently, we performed a tonsillectomy, administered three sessions of steroid pulse therapy, and added losartan for the recurrence of IgAN. We also changed his immunosuppressant from mizoribine to mycophenolate mofetil to treat the CAAMR. The nephrotic syndrome improved with the multiple therapeutic approaches; however, the S‐Cr level did not decrease below 2.0 mg/dL. We possibly could have performed additional treatments such as rituximab and intravenous immunoglobulin for the CAAMR, but therapeutic strategies for CAAMR have not yet been established.

Henoch–Schönlein purpura nephritis (HSPN) frequently recurs in patients following kidney transplantation, and pregnancy has been reported to be an exacerbating factor. However, little is known about the recurrence of HSPN during pregnancy in patients with superimposed pre‐eclampsia having excellent graft function who had experienced kidney transplantation. Here, we report a case of recurrent HSPN complicating severe pre‐eclampsia six yr after transplantation. A 31‐yr‐old woman who had received a living‐related kidney transplant at age 25 became pregnant. The cause of her end‐stage renal disease was biopsy‐proven HSPN. She had an excellent clinical course after transplantation, with good allograft function (serum creatinine <0.9 mg/dL, no proteinuria or hematuria, no episode of rejection), and normal blood pressure. We discontinued the angiotensin II receptor blocker that had been prescribed to prevent glomerular hyperfiltration. After week 17 of pregnancy, proteinuria and blood pressure increased markedly, and then her kidney function deteriorated progressively with intermittent mild microhematuria. At week 28 of pregnancy, umbilical blood flow and fetal growth were impaired, prompting preterm cesarean delivery. Subsequently, her blood pressure and serum creatinine normalized immediately, although the urinary protein excretion decreased insufficiently from 6.0 to 1.0 g/d at six months postpartum. In general, hematuria has a predictive value for the recurrence of HSPN. Clinically, we considered this case to be superimposed pre‐eclampsia, not recurrent HSPN. However, a biopsy conducted seven months postpartum suggested recurrent HSPN on her renal allograft. In addition, focal segmental membranous nephropathy with C1q deposition was observed. It was difficult to determine when the HSPN and membranous lesions occurred. This case suggests that a pathological evaluation is important in HSPN patients after transplantation to reduce adverse risks during and after pregnancy.

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