岩見 大基

＜文献概要＞ポイント ・移植腎尿路結石の発生頻度は1%以下である.・5mm以上の上部尿路結石が治療適応である.・逆行性の内視鏡操作は尿路再建術の影響を受けやすく,容易ではない.・腎杯穿刺は腹膜損傷に注意が必要で,自己腎と比べて穿刺範囲が限定される.

今回、原発性胆汁性胆管炎による肝腎不全に対し脳死肝腎同時移植を施行したので報告する。症例は46歳女性。35歳頃、原発性胆汁性胆管炎と診断。43歳時に黄疸発症し、非代償性肝硬変(T-bil 7.4mg/dl、Child Turcotte Pugh(CTP)B9点、Model for End-stage Liver Disease(MELD)score 7点)で当院紹介。2年後に肝不全進行し(T-bil 15.9、CTP C12、MELD22)、脳死登録された。3ヵ月後、T-bil 21.1、CTP C12、MELD27と増悪し、肝腎症候群から透析導入となった。透析導入8週後に腎移植も脳死移植登録した。待機期間246日で脳死ドナー発生、肝腎同時移植を実施した。術後膵炎を認めたが、肝機能は良好に推移し、術後12日目で透析離脱、術後57日目で退院した。術後11ヵ月の時点で、経過良好で外来フォロー中である。今後、肝腎不全に陥った症例に対しても肝腎同時移植を施行することで長期予後改善の可能性が期待される。(著者抄録)

下部尿路機能障害の管理は腎移植患者には必要である。しかしながら、下部尿路症状(lower urinary tract symptoms:LUTS)を評価するための体系的なプロトコルは確立されていない。本稿では、そのLUTSに関連した最近の論文と日本発の質問票である主要下部尿路症状質問票(Core Lower urinary tract Symptom Score:CLSS)を紹介する。CLSSは医療スタッフがLUTSを評価する上で検証されている有用でシンプルなアンケートである。(著者抄録)

Chronic allograft rejection is the most common cause of long-term allograft failure. One reason is that current diagnostics and therapeutics for chronic allograft rejection are very limited. We here show that enhanced NFκB signaling in kidney grafts contributes to chronic active antibody-mediated rejection (CAAMR), which is a major pathology of chronic kidney allograft rejections. Moreover, we found that urinary orosomucoid 1 (ORM1) is a candidate marker molecule and therapeutic target for CAAMR. Indeed, urinary ORM1 concentration was significantly higher in kidney transplant recipients pathologically diagnosed with CAAMR than in kidney transplant recipients with normal histology, calcineurin inhibitor toxicity, or interstitial fibrosis and tubular atrophy. Additionally, we found that kidney biopsy samples with CAAMR expressed more ORM1 and had higher NFκB and STAT3 activation in tubular cells than samples from non-CAAMR samples. Consistently, ORM1 production was induced after cytokine-mediated NFκB and STAT3 activation in primary kidney tubular cells. The loss- and gain-of-function of ORM1 suppressed and promoted NFκB activation, respectively. Finally, ORM1 enhanced NFκB-mediated inflammation development in vivo. These results suggest that an enhanced NFκB-dependent pathway following NFκB and STAT3 activation in the grafts is involved in the development of chronic allograft rejection after kidney transplantation and that ORM1 is a non-invasive candidate biomarker and possible therapeutic target for chronic kidney allograft rejection.

BACKGROUND: Rituximab (RIT) is effective as a part of the desensitization therapy before ABO-incompatible kidney transplantation (ABOi-KTx), and a single dose of RIT at 375 mg/m2 or less is recommended. However, adequate RIT dose recommendations have not yet been established for individual recipients. Therefore, we evaluated the relationship between the proportion of B cells in peripheral blood and acute antibody-mediated rejection (AAMR). METHODS: Forty-four consecutive ABOi-KTx recipients were enrolled in this retrospective study. Before transplantation, subjects were treated with RIT at various doses, ranging from 65 to 400 mg/body (46-263 mg/m2), followed by plasmapheresis and intravenous immunoglobulin as a desensitization therapy. The percentage of CD19+ cells in the total peripheral blood lymphocytes population (%CD19) was determined the day before transplantation. Transplant recipients were divided into 2 groups according to pretransplant %CD19, as follows: low %CD19 group, ≤ 1.2% (n = 35) and high %CD19 group, > 1.2% (n = 9). The relationship between %CD19 and incidence of AAMR was evaluated, and the predicting factors for AAMR incidence were determined by univariate and multivariate analyses. RESULTS: The incidence of AAMR was significantly higher in the high %CD19 group than in the low %CD19 group (44.4% vs 5.7%, P = .006). Furthermore, multivariate analysis showed that %CD19 > 1.2% was the only independent factor to predict AAMR, with an odds ratio of 14.31 (P = .038). CONCLUSION: High %CD19 values after rituximab administration in ABOi-KTx recipients implies insufficient depletion of B cells, which can lead to AAMR.

BACKGROUND: Multiple renal arteries are found in approximately 20% of living donor kidneys. We have been using an accessory artery cutoff diameter of 2 mm on preoperative computed tomography angiography to determine whether to sacrifice or reconstruct the artery. In this study, we assessed the validity and feasibility of this cutoff value. METHODS: Living related kidney recipients from 2005 to 2013 were enrolled in this retrospective study. The diameter of the accessory artery and adverse events were evaluated. The lost parenchymal volume (%) due to vascular obstruction or branch ligation was calculated by computed tomography volumetry. RESULTS: Among 128 kidney transplants, 30 donor kidneys had multiple arteries. Accessory arteries were reconstructed in 18 cases and intentionally ligated in 12 cases (mean diameter of accessory arteries, 3.10 [SD, 0.75] mm and 1.81 [SD, 0.28] mm, respectively). The mean estimated glomerular filtration rate at 1 or 12 months after transplant was not significantly different between the groups. Among reconstructed cases, 14 cases (77.8%) had good patency in the reconstructed arteries whereas the other 4 had vascular complications. The percentage of lost parenchymal volume due to ligation or occlusion of the reconstructed artery (calculated in 16 cases) was predictable with the following formula: lost volume (%) = 9.09 × diameter (mm) - 10.5 (P= .03, rs= 0.533 by Spearman rank correlation coefficient). This formula indicated that ligation of a 2-mm accessory artery leads to 7.68% loss of the renal parenchyma. CONCLUSIONS: Reconstruction using a cutoff diameter of 2 mm is worth attempting in terms of the success rate and graft function. Sacrifice of a 2-mm accessory artery leads to parenchymal loss of <8%.