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Aki Mafune, Yudo Tanno,
Hiroyasu Yamamoto,
Akimitsu Kobayashi,
Hajime Saigawa,
Takashi Yokoo,
Hiroshi Hayakawa,
Youichi Miyazaki,
Keitaro Yokoyama,
Yutaka Yamaguchi,
Tatsuo Hosoya
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ABSTRACT: The BK virus is a double-stranded DNA virus to which 90% of adults have been exposed. BK virus infections typically result in an oral or respiratory infection; however, BK virus reactivation is an infectious disease of concern in kidney transplant recipients. The prevalence of BK virus nephropathy (BKN) in kidney transplant recipients is approximately 5%, and most cases occur within one yr after kidney transplantation. Graft survival of BKN is reported to be 30-60%, and the standard treatment strategy for BKN is reducing immunosuppressive therapy and close monitoring for rejection. Viral infection is most common in the early post-transplantation phase, and BKN or acute rejection is one of the major factors involved in graft loss. However, in this report, we describe the successful management of BKN and cytomegalovirus infection concurrent with plasma cell-rich acute rejection.
Clinical Transplantation 07/2012; 26 Suppl 24:49-53. · 1.67 Impact Factor
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Kidney International 07/2012; 82(2):244-5. · 6.61 Impact Factor
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Tatsuhiro Yaginuma,
Izumi Yamamoto,
Hiroyasu Yamamoto,
Jun Mitome, Yudo Tanno,
Keitaro Yokoyama,
Takenori Hayashi,
Tetsuya Kobayashi,
Michiaki Watanabe,
Yutaka Yamaguchi,
Tatsuo Hosoya
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ABSTRACT: 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.♢ RESULTS: Angiogenic responses were more frequent in the compact zone than in regenerated layers. The number of capillaries positive for anti-CD34 and anti-podoplanin monoclonal antibodies per unit area of visceral peritoneal tissue was, respectively, 41.1 ± 29.3/mm(2) in EPS patients and 2.7 ± 4.4/mm(2) in controls (p ≤ 0.01) and 48.1±43.9/mm(2) in EPS patients and 4.1±5.4/mm(2) in controls (p ≤ 0.01). The percentage of capillaries positive for anti-Ki-67, CD34, and podoplanin was 4.6% in EPS patients (p ≤ 0.01) and 0.8% in controls (p = 0.09). The immunogold electron microscopy analysis revealed that podoplanin was localized to endothelial cells with anchoring filaments, a specific feature of lymphatic vessels. Furthermore, compared with parietal peritoneal membrane, visceral peritoneal membrane had a more prominent podoplanin-positive capillary profile, but not a prominent CD34-positive capillary profile. In addition, fibroblast-like cells double-positive for podoplanin and smooth muscle actin were markedly increased in the degenerated layer, as previously reported.♢ CONCLUSIONS: Our study demonstrated that lymphatic vessels are increased in the visceral peritoneum of patients with EPS.
Peritoneal dialysis international : journal of the International Society for Peritoneal Dialysis. 06/2012;
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Kidney International 04/2012; 81(8):800-1; author reply 801. · 6.61 Impact Factor
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Kidney International 03/2012; 81(6):595. · 6.61 Impact Factor
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Tatsuhiro Yaginuma,
Hiroyasu Yamamoto,
Jun Mitome,
Akimitsu Kobayashi,
Izumi Yamamoto, Yudo Tanno,
Hiroshi Hayakawa,
Youichi Miyazaki,
Keitaro Yokoyama,
Yasunori Utsunomiya,
Jun Miki,
Hiroki Yamada,
Nozomu Furuta,
Yutaka Yamaguchi,
Tatsuo Hosoya
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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.
Clinical Transplantation 07/2011; 25 Suppl 23:28-33. · 1.67 Impact Factor
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Nihon Naika Gakkai Zasshi 06/2011; 100(6):1648-50.
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Jun Mitome,
Hiroyasu Yamamoto,
Yukio Maruyama,
Akimitsu Kobayashi,
Tatsuhiro Yaginuma,
Nanae Matsuo, Yudo Tanno,
Hiroshi Hayakawa,
Youichi Miyazaki,
Keitaro Yokoyama,
Yasunori Utsunomiya,
Yutaka Yamaguchi,
Tatsuo Hosoya
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ABSTRACT: A 31-yr-old Japanese man with end-stage kidney disease caused by primary focal segmental glomerulosclerosis (FSGS) underwent living related kidney transplantation at the age of 26 yr. The allograft functioned well immediately after surgery, and we did not observe histological findings of rejection and recurrent FSGS in protocol biopsies at two months and one yr after transplantation. Four years after transplantation, the urine protein excretion reached 11 g/d, and the serum creatinine increased over 2.5 mg/dL. We diagnosed nephrotic syndrome due to recurrent FSGS with graft dysfunction and confirmed FSGS lesions with severe endothelial injury with an allograft biopsy, associated with calcineurin inhibitor (CNI) nephrotoxicity. Thereafter, we performed plasmapheresis and steroid therapy with subsequent low-density lipoprotein adsorption, combined with the reduction of tacrolimus. The nephrotic syndrome improved dramatically with the multiple therapeutic approaches. Primary FSGS recurs frequently in patients immediately after kidney transplantation. Post-transplant FSGS has various causes, such as recurrent primary disease, obesity, hyperfiltration, donor-related nephrosclerosis, and CNI-induced arteriolopathy. In the case of nephrotic syndrome after kidney transplantation, we should consider not only recurrent FSGS, but also CNI-induced nephrotoxicity to determine the optimal treatment.
Clinical Transplantation 07/2010; 24 Suppl 22:48-53. · 1.67 Impact Factor
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Nephrology Dialysis Transplantation 09/2009; 24(12):3900-1. · 3.40 Impact Factor
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Akimitsu Kobayashi,
Hiroyasu Yamamoto,
Kentaro Matsuoka,
Hideyuki Ito,
Izumi Yamamoto,
Yoshimi Kawamura, Yudo Tanno,
Tatsuhiro Yaginuma,
Jun Mitome,
Hiroshi Hayakawa,
Yoichi Miyazaki,
Yasunori Utsunomiya,
Yutaka Yamaguchi,
Tatsuo Hosoya
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ABSTRACT: Hypertension is a common complication after kidney transplantation and adversely affects graft and patient survival. Strategies for anti-hypertensive therapy in an allograft from a hypertensive donor with arteriolosclerosis and the target blood pressure have not been clearly defined. Here, we report the case of deteriorating transplanted kidney function after anti-hypertensive treatment. A 40-yr-old man had received a kidney transplant from a living relative donor (his 69-yr-old father), who was hypertensive and had severe arteriolosclerosis. The recipient showed good allograft function immediately (s-Cr 1.8 mg/dL); however, blood pressure and proteinuria increased markedly two wk after transplantation (blood pressure 180/90, urinary protein 3.4 g/d). We then started anti-hypertensive agents (a calcium channel blocker and an angiotensin II receptor blocker). Blood pressure and proteinuria were corrected to the normal range within two wk of starting the treatment (blood pressure 130/80, urinary protein 0.3 g/d). However, his kidney function continued to deteriorate (s-Cr 2.7 mg/dL). A biopsy, performed at that time, revealed glomerular collapse, advanced interstitial fibrosis and severe arteriolosclerosis, with no evidence of rejection. These findings could have been the result of renal allograft hypoperfusion. We then reduced the anti-hypertensive agents on day 45 after transplantation and observed improved allograft function within a week (s-Cr 1.6 mg/dL). This case suggests that renal hemodynamic responses may be impaired and renal perfusion may not be appropriately maintained in an allograft with severe arteriolosclerosis at a blood pressure level suitable for the recipient. Anti-hypertensive treatment should be performed carefully when the allograft is from an elderly hypertensive donor.
Clinical Transplantation 07/2008; 22(s19):68 - 71. · 1.67 Impact Factor
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Yudo Tanno,
Hiroyasu Yamamoto,
Izumi Yamamoto,
Tatsuhiro Yaginuma,
Jun Mitome,
Yoshimi Kawamura,
Yoichi Miyazaki,
Keitaro Yokoyama,
Yasunori Utsunomiya,
Yutaka Yamaguchi,
Tatsuo Hosoya
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ABSTRACT: 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.
Clinical Transplantation 06/2007; 21(s18):36 - 39. · 1.67 Impact Factor
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Nephrology Dialysis Transplantation 08/2006; 21(7):2041. · 3.40 Impact Factor
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ABSTRACT: Peripheral tolerance can be induced after the feeding of Ag, which is referred to as oral tolerance. We demonstrated in this study that the oral administration of OVA induced tolerance in an experimental model of asthma in mice, and investigated which cells function as the regulatory cells in the transfer of this oral tolerance. In OVA-fed mice, the percentage of eosinophils in bronchoalveolar lavage fluid, serum IgE levels, airway hyperresponsiveness, and mRNA levels of IL-13 and eotaxin were significantly lower than found in nonfed mice. Histological examination of lung tissue showed a suppression of the accumulation of inflammatory cells in the peribronchial area of OVA-fed mice. Feeding after the first immunization or between the first and the second immunization suppressed these findings, whereas feeding just before the airway Ag challenge did not. The suppression of disease in OVA-fed mice was successfully transferred by injection of whole spleen cells of OVA-fed mice. When CD11c+ dendritic cells (DCs) were removed from splenocytes, this transfer of suppression was completely abolished. The injection of splenic DCs purified from OVA-fed mice alone transferred the suppression, whereas the injection of splenic DCs from naive mice that were cocultured with OVA in vitro did not. These data suggest that not only CD4+ T cells, but also CD11c+ DCs induced by Ag feeding are important for the active transfer of oral tolerance in this murine experimental model of asthma.
The Journal of Immunology 03/2006; 176(3):1481-9. · 5.79 Impact Factor
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ABSTRACT: Although recurrent diabetic nephropathy is common in patients with type I diabetes after kidney transplantation, the development of focal segmental glomerulosclerosis (FGS) is rare, and its development generally takes several years. We report here a case of type I diabetes mellitus with secondary FGS accompanied by proteinuria 10 months following kidney transplantation. Episode biopsy showed secondary FGS, evidenced by glomerular capillary collapse and large epithelial cells with ballooning degeneration. Exudative dense deposition of IgM in a diffuse global mesangial pattern and enlarged glomerular diameters were observed, suggestive of glomerular hyperfiltration which can lead to secondary FGS. An imbalance in body size between donor and recipient and/or uncontrolled diabetes are potential causes of glomerular hyperfiltration. We administered angiotensin-converting enzyme inhibitor and angiotensin II receptor blocker to reduce hyperfiltration-induced renal damage; the combination therapy reduced proteinuria from 2346 to 258 mg/d. Secondary FGS should be a consideration after kidney transplantation in patients with type I diabetes mellitus.
Clinical Transplantation 02/2006; 20 Suppl 15:7-10. · 1.67 Impact Factor
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ABSTRACT: The common intact parathyroid hormone (i-PTH) assay detects not only PTH (1-84) but also the PTH (7-84) fragment. Recently, it was reported that the PTH (7-84) fragment is an antagonist to the biological action of PTH (1-84). It was also reported that the accumulation of the PTH (7-84) fragment plays a role in skeletal resistance in haemodialysis (HD) patients. However, the role of accumulation of the PTH (7-84) fragment in continuous ambulatory peritoneal dialysis (CAPD) patients, with a different clearance rate from that of HD patients, is still unclear. Therefore, we have measured only the active form of PTH (1-84) using a new method of whole PTH (w-PTH) assay in 20 CAPD patients (15 male and five female; mean age 51.0+/-13.0 years). The mean w-PTH value was 88.5 +/-14.2 pg/ml in CAPD patients, which was 42.1% of i-PTH (152.6+/-23.6 pg/ml). The approximate value of w-PTH was calculated using the following formula (w-PTH=0.58 x iPTH-0.4, R(2)=0.94). PTH (7-84) fragment was calculated by the formula i-PTH-w-PTH. The PTH (7-84) fragment/w-PTH ratio as an index of skeletal resistance, and serum alkaline phosphatase activity as an osteoblastic marker were negatively correlated (P=0.02). From these results, we concluded that the i-PTH level as calculated using the common assay method might lead to an overestimation of parathyroid function and bone turnover in CAPD patients similarly to HD patients. The w-PTH assay may be useful for more precise evaluation of PTH activity in end-stage renal disease patients.
Nephrology Dialysis Transplantation 07/2003; 18 Suppl 3:iii97-8. · 3.40 Impact Factor
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ABSTRACT: The common intact-PTH assay detects not only PTH (1-84) but also PTH (7-84) fragment. Recently, it is reported that PTH (7-84) fragment is the antagonist to PTH (1-84) biological action. Thus, conventional intact-PTH assay might mislead the overestimation of parathyroid function in uremic patients. Whole PTH assay, which detect only PTH (1-84) fragments may be useful for more precise evaluation of PTH activity in uremic patient.
Clinical calcium 04/2003; 13(3):317-20.
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ABSTRACT: The administration of angiotensin II receptor antagonist(AIIA) to patients with advanced chronic renal failure(CRF) is not actively recommended. This study was performed to verify the appropriateness of this situation and to determine if there are any substantial differences between patients with a serum creatinine(SCr) level higher than 3 mg/dl and those with a lower SCr level in terms of the clinical effects such as renal function, serum potassium level and systemic blood pressure(BP) after the administration of AIIA. Sixteen patients with advanced CRF who were admitted to the out-patient clinic in Jikei University Hospital(1998/1-1999/12) were enrolled(average age: 65 years, underlying renal disease: diabetic nephropathy 6, CGN 5, and other 1). They had never been administered AIIA before. The patients were classified into two groups in accordance with their level of SCr: group A(SCr lower than 3.0 mg/dl; n = 11), and Group B(SCr higher than 3.0 mg/dl; n = 5). Losartan(50 mg/day) administration was started in order to examine parameters such as the SCr, potassium, BP at the out-patient clinic, and urinary protein excretion at the 0, 1, 3, 6, 9, and 12 month time points. Although the 1/SCr values provided negative slopes with time in both groups, no significant difference was found between the two slopes. There were no changes in the serum potassium levels or urinary protein excretion during the study period in either group, and no statistical difference was found between the two groups. Although the serum potassium level exceeded 5.5 mEq/l in two patients each in both groups, the level was controlled by diet therapy with restricted potassium. BP was reduced significantly in both groups during the study period, and no statistical difference in BP reduction was observed between the two groups. In conclusion, the results indicate there were no differences in the effect on renal function, serum potassium levels or systemic BP between the patients with a SCr level higher than 3.0 mg/dl and those with a lower level. The results also support the notion that patients with advanced renal dysfunction are not precluded from AIIA administration.
Nippon Jinzo Gakkai shi 11/2002; 44(7):530-6.
