研究活動情報

• Renoprotective Effects of Goreisan via Modulation of RAAS Activity, Oxidative Stress, and AQP2 Trafficking in a Rat Model of Nephrotic Syndrome

  Mao Shimizu, Shunsuke Goto, Satoshi Yamatani, Kazuo Sakamoto, Keiji Kono, Hideki Fujii

  Background/Objectives: We evaluated Goreisan, a traditional Chinese medicine, for its effects on nephrotic syndrome in a rat model. Methods: Male Sprague–Dawley rats underwent right nephrectomy at 5 weeks of age, followed by adriamycin administration (5 mg/kg) at 6 and 8 weeks of age to induce nephrotic syndrome. At 10 weeks, rats were divided into three groups: vehicle (control), Goreisan 0.5 g/kg (GL), and Goreisan 1.0 g/kg (GH). Goreisan was administered daily for 4 weeks. At 14 weeks, blood, urine, mRNA expressions, and kidney histopathology were analyzed. Data were analyzed using one-way ANOVA followed by Tukey–Kramer post hoc testing. Results: Goreisan prevented worsening kidney function, with reduced glomerular and tubulointerstitial damage, lower systemic and intrarenal 8-hydroxy-2′-deoxyguanosine levels, and lower plasma aldosterone levels and expression of intrarenal renin–angiotensin–aldosterone system (RAAS)-related factors. Urine volume significantly increased in GL and GH groups compared with the control group. In the GH group, urine volume increased markedly (Δ urine volume: 10.0 ± 2.6 mL/day), whereas it tended to decrease in the Vehicle group (Δ urine volume: −1.3 ± 2.5 mL/day). Urine osmolality was lower in the GH group, with a larger decrease in Δ urine osmolality (−616.3 ± 132.8 mOsm/L). These changes occurred without an increase in urinary sodium excretion, suggesting an aquaretic effect independent of natriuresis. Creatinine clearance (CCr/kg) declined markedly in the Vehicle group but was significantly preserved in the GH group (Δ CCr/kg: −2.2 ± 0.19 vs. −0.7 ± 0.28), indicating renoprotective effects. No differences were found in serum arginine–vasopressin levels. Real-time PCR and immunohistochemical staining showed no significant differences in aquaporin (AQP) mRNA expression (AQP1, AQP2, AQP3, and AQP4), but AQP2 localization to the apical membrane in the collecting ducts was reduced with Goreisan treatment. Conclusions: Goreisan demonstrates kidney-protective and diuretic effects in nephrotic syndrome, potentially through reducing systemic oxidative stress, modulating RAAS activation, and altering AQP2 trafficking.

  MDPI AG, 2025年12月, Biomedicines, 14(1) (1), 8 - 8

  研究論文（学術雑誌）

  神戸大学リポジトリ（Kernel）へのリンク


• A novel glomerulopathy model demonstrates renal counterbalance via local angiotensin II regulation.

  Kazuo Sakamoto, Kunio Kawanishi, Jun-Dal Kim, Masahiro Koizumi, Shin-Ichi Muroi, Saori Tabara, Akiyoshi Fukamizu, Taiji Matsusaka, Michio Nagata

  Renal counterbalance, involving compensatory hypertrophy of the healthy kidney and atrophy of the injured one, remains incompletely understood, particularly at the glomerular level. In this study, we employed NEP25 mice, which selectively express human CD25 in podocytes, enabling precise induction of unilateral podocyte injury through the administration of LMB2, a CD25-targeted immunotoxin. Using a two-kidney, one-nephropathy (2K1N) model, we demonstrated that asymmetric changes in renal blood flow and proteinuria, with histological and transcriptomic analyses uncovering distinct pathological and molecular features between the injured and contralateral healthy kidneys. Notably, an imbalance in intrarenal angiotensin (Ang) II levels was observed, and angiotensin-converting enzyme inhibition ameliorated the glomerular damage and restored perfusion. These findings indicate that local Ang II dysregulation is a key factor in renal counterbalance. Our study provides the first glomerulopathy-based experimental platform to dissect asymmetric renal adaptation, offering fundamental insight into the homeostatic mechanisms of renal function in health and disease.

  2025年06月, Proceedings of the Japan Academy. Series B, Physical and biological sciences, 英語, 国内誌

  研究論文（学術雑誌）


• Association of abnormalities in electrocardiography and ultrasonic echocardiography with the occurrence of cardiovascular disease in patients with advanced chronic kidney disease.

  Ken Hirabayashi, Hideki Fujii, Keiji Kono, Satoshi Yamatani, Mao Shimizu, Kentaro Watanabe, Kazuo Sakamoto, Shunsuke Goto, Shinichi Nishi

  BACKGROUND: In patients with chronic kidney disease (CKD), the incidence of cardiovascular disease (CVD) increases with disease progression. CVD screening tests in those with CKD were researched to determine whether abnormalities observed in electrocardiography (ECG) and ultrasonic echocardiography (UCG) were risk factors associated with the development of CVD. METHODS: This study included 604 patients with CKD G4 and G5, for whom both ECG and UCG were performed. They were divided into four groups: those without ECG- and UCG-indicated abnormalities (group A, n = 333), with only ECG abnormalities (group B, n = 106), with only UCG abnormalities (group C, n = 75), and with both ECG and UCG abnormalities (group D, n = 90). Multivariate analysis using Cox regression analysis of the occurrence of CVD was performed during a follow-up period. RESULTS: During the observation period, 124 patients had clinical events. Among them, 45 patients (13.5%) were in Group A, 25 patients (23.6%) in Group B, 19 patients (25.3%) in Group C, and 35 patients (38.9%) in Group D, respectively. CVD event occurrence was highest in Group D. The results of the multivariate analysis also showed that the CVD event rates were significantly higher in Group C (HR: 2.96, P = < .001) and D (HR: 4.22, P < .001) than in Group A. CONCLUSION: In patients with advanced CKD, there was a significant correlation of ECG and UCG abnormalities with CVD events. Additionally, those having both types of abnormalities may have a higher risk of coronary artery disease than other groups.

  2024年04月, Clinical and experimental nephrology, 28(4) (4), 307 - 315, 英語, 国内誌

  研究論文（学術雑誌）


• Clinical Implication of Consistently Strict Phosphate Control for Coronary and Valvular Calcification in Incident Patients Undergoing Hemodialysis.

  Mao Shimizu, Hideki Fujii, Keiji Kono, Shunsuke Goto, Kentaro Watanabe, Kazuo Sakamoto, Shinichi Nishi

  AIMS: Serum phosphate control is crucial for the progression of vascular and valvular calcifications. Strict phosphate control is recently suggested; however, there is a lack of convincing evidence. Therefore, we explored the effects of strict phosphate control on vascular and valvular calcifications in incident patients undergoing hemodialysis. METHODS: A total of 64 patients undergoing hemodialysis from our previous randomized controlled trial were included in this study. Coronary artery calcification score (CACS) and cardiac valvular calcification score (CVCS) were evaluated using computed tomography and ultrasound cardiography at baseline and 18 months after the initiation of hemodialysis. The absolute changes in CACS (ΔCACS) and CVCS (ΔCVCS) and the percent change in CACS (%ΔCACS) and CVCS (%ΔCVCS) were calculated. Serum phosphate level was measured at 6, 12, and 18 months after the initiation of hemodialysis. Moreover, phosphate control status was evaluated using the area under the curve (AUC) by the amount of time spent with a serum phosphate level of ≥ 4.5 mg/dL and the extent to which this threshold exceeded over the observation period. RESULTS: ΔCACS, %ΔCACS, ΔCVCS, and %ΔCVCS were significantly lower in the low AUC group than in the high AUC group. ΔCACS and %ΔCACS were also significantly lower. ΔCVCS and %ΔCVCS tended to be lower in patients whose serum phosphate level never exceeded 4.5 mg/dL than in those whose serum phosphate level continuously exceeded 4.5 mg/dL. AUC significantly correlated with ΔCACS and ΔCVCS. CONCLUSION: Consistently strict phosphate control may slow the progression of coronary and valvular calcifications in incident patients undergoing hemodialysis.

  2023年11月, Journal of atherosclerosis and thrombosis, 30(11) (11), 1568 - 1579, 英語, 国内誌

  研究論文（学術雑誌）


• COVID-19感染を契機にネフローゼ症候群を発症し,膜性増殖性糸球体腎炎(MGPN)と診断された1例

  黒野 博義, 渡邉 健太郎, 坂本 和雄, 河野 圭志, 後藤 俊介, 兵頭 俊紀, 藤井 秀毅

  (一社)日本腎臓学会, 2023年09月, 日本腎臓学会誌, 65(6-W) (6-W), 771 - 771, 日本語


• Renal protective effects of astragalus root in rat models of chronic kidney disease.

  Shunsuke Goto, Hideki Fujii, Kentaro Watanabe, Mao Shimizu, Hidehisa Okamoto, Kazuo Sakamoto, Keiji Kono, Shinichi Nishi

  BACKGROUND: Astragalus root is a commonly used herb in traditional Chinese medicine. Although renoprotective effects have been reported in some clinical and experimental studies, the details remain unknown. METHODS: We used 5/6 nephrectomized rats as chronic kidney disease (CKD) models. At 10 weeks, they were divided into four groups, namely, CKD, low-dose astragalus (AR400), high-dose astragalus (AR800), and sham groups. At 14 weeks, they were sacrificed for the evaluation of blood, urine, mRNA expression in the kidney, and renal histopathology. RESULTS: Kidney dysfunction was significantly improved following astragalus administration (creatinine clearance: sham group; 3.8 ± 0.3 mL/min, CKD group; 1.5 ± 0.1 mL/min, AR400 group; 2.5 ± 0.3 mL/min, AR800 group; 2.7 ± 0.1 mL/min). Blood pressure, urinary albumin, and urinary NGAL levels were significantly lower in the astragalus-treated groups than those in the CKD group. Excretion of urinary 8-OHdG, an oxidative stress marker, and intrarenal oxidative stress were lower in the astragalus-treated groups than those in the CKD group. Furthermore, the mRNA expression of NADPH p22 phox, NADPH p47 phox, Nox4, renin, angiotensin II type 1 receptor, and angiotensinogen in the kidney was lower in the astragalus-treated groups compared with the CKD group. CONCLUSION: This study suggests that astragalus root slowed CKD progression, possibly through the suppression of oxidative stress and the renin-angiotensin system.

  2023年07月, Clinical and experimental nephrology, 27(7) (7), 593 - 602, 英語, 国内誌

  研究論文（学術雑誌）


• Glomerular filtrate affects the dynamics of podocyte detachment in a model of diffuse toxic podocytopathy.

  Nobuyuki Saga, Kazuo Sakamoto, Taiji Matsusaka, Michio Nagata

  Podocyte injury and subsequent detachment are hallmarks of progressive glomerulosclerosis. In addition to cell injury, unknown mechanical forces on the injured podocyte may promote detachment. To identify the nature of these mechanical forces, we studied the dynamics of podocyte detachment using sequential ultrastructural geometry analysis by transmission electron microscopy in NEP25, a mouse model of podocytopathy induced by anti-Tac(Fv)-PE38 (LMB2), a fusion protein attached to Pseudomonas exotoxin A, targeting CD25 on podocytes. After LMB2 injection, foot process effacement occurred on day three but detachment commenced on day eight and extended to day ten, reaching toward the urinary pole in clusters. Podocyte detachment was associated with foot process effacement covering over 60% of the glomerular basement membrane length. However, approximately 25% of glomeruli with diffuse (over 80%) foot process effacement showed no detachment. Blocking glomerular filtration via unilateral ureteral obstruction resulted in diffuse foot process effacement but no pseudocysts or detachment, whereas uninephrectomy increased pseudocysts and accelerated detachment, indicating that glomerular filtrate drives podocyte detachment via pseudocyst formation as a forerunner. Additionally, more detachment was observed in juxtamedullary glomeruli than in superficial glomeruli. Thus, glomerular filtrate drives the dynamics of podocyte detachment in this model of podocytopathy. Hence, foot process effacement may be a prerequisite allowing filtrate to generate local mechanical forces that expand the subpodocyte space forming pseudocysts, promote podocyte detachment and subsequent segmental sclerosis.

  2021年05月, Kidney international, 99(5) (5), 1149 - 1161, 英語, 国際誌

  研究論文（学術雑誌）


• 健常腎存在下での対側ネフローゼ腎の病態変化:One nephrotic two-kidney model

  坂本 和雄, 金 俊達, 小泉 賢洋, 川西 邦夫, 松阪 泰二, 深水 昭吉, 長田 道夫

  (一社)日本腎臓学会, 2020年07月, 日本腎臓学会誌, 62(4) (4), 255 - 255, 日本語


• Biphasic MIF and SDF1 expression during podocyte injury promote CD44-mediated glomerular parietal cell migration in focal segmental glomerulosclerosis.

  Naoko Ito, Kazuo Sakamoto, Chihiro Hikichi, Taiji Matsusaka, Michio Nagata

  Glomerular parietal epithelial cell (PEC) activation, as revealed by de novo expression of CD44 and cell migration toward the injured filtration barrier, is a hallmark of podocyte injury-driven focal segmental glomerulosclerosis (FSGS). However, the signaling pathway that mediates activation of PECs in response to podocyte injury is unknown. The present study focused on CD44 signaling, particularly the roles of two CD44-related chemokines, migration inhibitory factor (MIF) and stromal cell-derived factor 1 (SDF1), and their common receptor, chemokine (C-X-C motif) receptor 4 (CXCR4), in the NEP25/LMB2 mouse podocyte-toxin model of FSGS. In the early phase of the disease, CD44-positive PECs were locally evident on the opposite side of the intact glomerular tuft and subsequently increased in the vicinity of synechiae with podocyte loss. Expression of MIF and SDF1 was first increased in injured podocytes and subsequently transferred to activated PECs expressing CD44 and CXCR4. In an immortalized mouse PEC (mPEC) line, recombinant MIF and SDF1 (rMIF and rSDF1, respectively) individually increased CD44 and CXCR4 mRNA and protein levels. rMIF and rSDF1 stimulated endogenous MIF and SDF1 production. rMIF- and rSDF1-induced mPEC migration was suppressed by CD44 siRNA. However, MIF and SDF1 inhibitors failed to show any impact on proteinuria, podocyte number, and CD44 expression in NEP25/LMB2 mice. Our data suggest that injured podocytes upregulate MIF and SDF1 that stimulate CD44 expression and CD44-mediated migration, which is enhanced by endogenous MIF and SDF1 in PECs. This biphasic expression pattern of the chemokine-CD44 axis in podocytes and PECs may be a novel mechanism of "podocyte-PEC cross-talk" signaling underlying podocyte injury-driven FSGS.

  2020年03月, American journal of physiology. Renal physiology, 318(3) (3), F741-F753, 英語, 国際誌

  研究論文（学術雑誌）


• 糸球体濾過による力学的負荷は障害ポドサイトを剥離に進展させる

  佐賀 信之, 井藤 奈央子, 坂本 和雄, 川西 邦夫, 松阪 泰二, 長田 道夫

  (一社)日本腎臓学会, 2019年05月, 日本腎臓学会誌, 61(3) (3), 298 - 298, 日本語


• ポドサイト障害におけるボウマン嚢壁側上皮細胞の遊走メカニズム

  井藤 奈央子, 坂本 和雄, 佐賀 信之, 川西 邦夫, 長田 道夫

  (一社)日本腎臓学会, 2019年05月, 日本腎臓学会誌, 61(3) (3), 322 - 322, 日本語


• 腎生検病理診断に必要な臨床情報

  佐賀 信之, 井藤 奈央子, 坂本 和雄, 川西 邦夫, 長田 道夫

  (一社)日本腎臓学会, 2019年05月, 日本腎臓学会誌, 61(3) (3), 392 - 392, 日本語


• ポドサイト障害におけるボウマン嚢壁側上皮細胞の遊走メカニズム

  井藤 奈央子, 坂本 和雄, 佐賀 信之, 川西 邦夫, 長田 道夫

  (一社)日本小児腎臓病学会, 2019年05月, 日本小児腎臓病学会雑誌, 32(1Suppl.) (1Suppl.), 188 - 188, 日本語


• Podocyte injury-driven lipid peroxidation accelerates the infiltration of glomerular foam cells in focal segmental glomerulosclerosis.

  Satoshi Hara, Namiko Kobayashi, Kazuo Sakamoto, Toshiharu Ueno, Shun Manabe, Yasutoshi Takashima, Juri Hamada, Ira Pastan, Akiyoshi Fukamizu, Taiji Matsusaka, Michio Nagata

  Intracapillary foam cell infiltration with podocyte alterations is a characteristic pathology of focal segmental glomerulosclerosis (FSGS). We investigated the possible role of podocyte injury in glomerular macrophage and foam cell infiltration in a podocyte-selective injury model (NEP25 mice) and hypercholesterolemic model [low-density lipoprotein receptor deficiency (LDLR(-/-)) mice] with doxorubicin-induced nephropathy. Acute podocyte selective injury alone failed to induce glomerular macrophages in the NEP25 mice. However, in the doxorubicin-treated hypercholesterolemic LDLR(-/-) mice, glomerular macrophages/foam cells significantly increased and were accompanied by lipid deposition and the formation and ingestion of oxidized phospholipids (oxPLs). Glomerular macrophages significantly correlated with the amount of glomerular oxPL. The NEP25/LDLR(-/-) mice exhibited severe hypercholesterolemia, glomerular lipid deposition, and renal dysfunction. Imaging mass spectrometry revealed that a major component of oxidized low-density lipoprotein, lysophosphatidylcholine 16:0 and 18:0, was present only in the glomeruli of NEP25/LDLR(-/-) mice. Lysophosphatidylcholine 16:0 stimulated mesangial cells and macrophages, and lysophosphatidylcholine 18:0 stimulated glomerular endothelial cells to express adhesion molecules and chemokines, promoting macrophage adhesion and migration in vitro. In human FSGS, glomerular macrophage-derived foam cells contained oxPLs accompanied by the expression of chemokines in the tuft. In conclusion, glomerular lipid modification represents a novel pathology by podocyte injury, promoting FSGS. Podocyte injury-driven lysophosphatidylcholine de novo accelerated glomerular macrophage-derived foam cell infiltration via lysophosphatidylcholine-mediated expression of adhesion molecules and chemokines in glomerular resident cells.

  2015年08月, The American journal of pathology, 185(8) (8), 2118 - 31, 英語, 国際誌

  研究論文（学術雑誌）


• Podocyte injury-driven intracapillary plasminogen activator inhibitor type 1 accelerates podocyte loss via uPAR-mediated β1-integrin endocytosis.

  Namiko Kobayashi, Toshiharu Ueno, Kumi Ohashi, Hanako Yamashita, Yukina Takahashi, Kazuo Sakamoto, Shun Manabe, Satoshi Hara, Yasutoshi Takashima, Takashi Dan, Ira Pastan, Toshio Miyata, Hidetake Kurihara, Taiji Matsusaka, Jochen Reiser, Michio Nagata

  Podocyte-endothelial cell cross-talk is paramount for maintaining the filtration barrier. The present study investigated the endothelial response to podocyte injury and its subsequent role in glomerulosclerosis using the podocyte-specific injury model of NEP25/LMB2 mice. NEP25/LMB2 mice showed proteinuria and local podocyte loss accompanied by thrombotic microangiopathy on day 8. Mice showed an increase of glomerular plasminogen activator inhibitor type 1 (PAI-1) mRNA and aberrant endothelial PAI-1 protein already on day 1, before thrombosis and proteinuria. A PAI-1-specific inhibitor reduced proteinuria and thrombosis and preserved podocyte numbers in NEP25/LMB2 mice by stabilization of β1-integrin translocation. Heparin loading significantly reduced thrombotic formation, whereas proteinuria and podocyte numbers were unchanged. Immortalized podocytes treated with PAI-1 and the urokinase plasminogen activator (uPA) complex caused significant cell detachment, whereas podocytes treated with PAI-1 or uPA alone or with the PAI-1/uPA complex pretreated with an anti-uPA receptor (uPAR) antibody failed to cause detachment. Confocal microscopy and cell surface biotinylation experiments showed that internalized β1-integrin was found together with uPAR in endocytotic vesicles. The administration of PAI-1 inhibitor or uPAR-blocking antibody protected cultured podocytes from cell detachment. In conclusion, PAI-1/uPA complex-mediated uPAR-dependent podocyte β1-integrin endocytosis represents a novel mechanism of glomerular injury leading to progressive podocytopenia. This aberrant cross-talk between podocytes and endothelial cells represents a feedforward injury response driving podocyte loss and progressive glomerulosclerosis.

  2015年03月, American journal of physiology. Renal physiology, 308(6) (6), F614-26, 英語, 国際誌

  研究論文（学術雑誌）


• The direction and role of phenotypic transition between podocytes and parietal epithelial cells in focal segmental glomerulosclerosis.

  Kazuo Sakamoto, Toshiharu Ueno, Namiko Kobayashi, Satoshi Hara, Yasutoshi Takashima, Ira Pastan, Taiji Matsusaka, Michio Nagata

  Focal segmental glomerulosclerosis (FSGS) is a podocyte disease. Among the various histologies of FSGS, active epithelial changes, hyperplasia, as typically seen in the collapsing variant, indicates disease progression. Using a podocyte-specific injury model of FSGS carrying a genetic podocyte tag combined with double immunostaining by different sets of podocytes and parietal epithelial cell (PEC) markers [nestin/Pax8, Wilms' tumor-1 (WT1)/claudin1, and podocalyxin/Pax2], we investigated the direction of epithelial phenotypic transition and its role in FSGS. FSGS mice showed progressive proteinuria and renal dysfunction often accompanied by epithelial hyperplasia, wherein 5-bromo-4-chloro-3-indoyl β-d-galactoside (X-gal)-positive podocyte-tagged cells were markedly decreased. The average numbers of double-positive cells in all sets of markers were significantly increased in the FSGS mice compared with the controls. In addition, the average numbers of double-positive cells for X-gal/Pax8, nestin/Pax8 and podocalyxin/Pax2 staining in the FSGS mice were comparable, whereas those of WT1/claudin1 were significantly increased. When we divided glomeruli from FSGS mice into those with FSGS lesions and those without, double-positive cells tended to be more closely associated with glomeruli without FSGS lesions compared with those with FSGS lesions. Moreover, the majority of double-positive cells appeared to be isolated and very rarely associated with FSGS lesions (1/1,997 glomeruli). This study is the first to show the incidence and localization of epithelial cells with phenotypical changes in FSGS using a genetic tag. The results suggest that the major direction of epithelial phenotypic transition in cellular FSGS is from podocytes to PECs and that these cells were less represented in the active lesions of FSGS.

  2014年01月, American journal of physiology. Renal physiology, 306(1) (1), F98-F104, 英語, 国際誌

  研究論文（学術雑誌）


• PAI-1/uPA/uPAR複合体は細胞骨格変化を介してポドサイト剥離を起こす

  小林 凡子, 上野 智敏, 山下 春渚子, 原 怜史, 坂本 和雄, 高島 康利, 長田 道夫

  (一社)日本腎臓学会, 2013年04月, 日本腎臓学会誌, 55(3) (3), 320 - 320, 日本語

• 紫斑病性腎炎

  坂本和雄

  2025年12月, 今日の臨床サポート（第6版）


• 移植後拒絶を疑う腎機能低下から腎動脈狭窄が判明した一例

  黒野 博義, 河野 圭志, 兵頭 俊紀, 岡本 隼樹, 坂本 和雄, 後藤 俊介, 兵頭 洋二, 三宅 秀明, 藤井 秀毅

  (一社)日本移植学会, 2025年10月, 移植, 60(2) (2), 138 - 139, 日本語


• 腎性貧血

  坂本和雄

  2025年09月, 今日の臨床サポート（第12版）


• 腎生検病理診断コンサルテーション・アンド・レビュー (症例1)大動脈周囲の軟部影と高IgG4血症及び腎機能障害を認めた一例

  西庵 良哉, 坂本 和雄, 後藤 俊介, 兵頭 俊紀, 原 重雄, 藤井 秀毅

  (一社)日本腎臓学会, 2025年06月, 日本腎臓学会誌, 67(4) (4), 457 - 457, 日本語


• 片側性/両側性糸球体障害モデルに基づく腎カウンターバランスの再評価

  坂本 和雄, 川西 邦夫, 金 俊達, 深水 昭吉, 松阪 泰二, 長田 道夫

  (一社)日本腎臓学会, 2025年06月, 日本腎臓学会誌, 67(4) (4), 518 - 518, 日本語


• 抗ネフリン抗体の関与が疑われた巣状分節性糸球体硬化症の腎移植後再発の一例

  黒野 博義, 河野 圭志, 市川 裕太, 兵頭 俊紀, 岡本 隼樹, 坂本 和雄, 後藤 俊介, 兵頭 洋二, 野津 寛大, 藤井 秀毅

  (一社)日本移植学会, 2024年11月, 移植, 59(2) (2), 208 - 209, 日本語


• 大動脈周囲の軟部影と高IgG4血症及び腎機能障害を認めた1例

  西庵 良哉, 坂本 和雄, 中 智孝, 河野 圭志, 後藤 俊介, 兵頭 俊紀, 藤井 秀毅

  (一社)日本腎臓学会, 2024年09月, 日本腎臓学会誌, 66(6-W) (6-W), 1081 - 1081, 日本語


• 紅麹含有サプリメントを摂取した13例の臨床経過の検討

  坂口 岳彦, 坂本 和雄, 河野 圭志, 後藤 俊介, 米倉 由利子, 中西 昌平, 齊藤 慶, 渡邉 周平, 藤井 秀毅

  (一社)日本腎臓学会, 2024年09月, 日本腎臓学会誌, 66(6-W) (6-W), 1093 - 1093, 日本語


• 【腎臓リハビリテーション 理論と実際】(第3章)腎臓リハビリテーションの要素と実際 薬物療法 腎移植患者の薬物療法

  坂本 和雄

  (株)日本メディカルセンター, 2024年06月, 臨床透析, 40(7) (7), 864 - 869, 日本語


• カルシウム感知受容体(CaSR)作動薬による心肥大抑制とレニン-アンジオテンシン-アルドステロン系(RAAS)の変化

  岡本 英久, 能瀬 勇馬, 岡本 隼樹, 渡邉 健太郎, 坂本 和雄, 河野 圭志, 後藤 俊介, 藤井 秀毅

  (一社)日本腎臓学会, 2024年06月, 日本腎臓学会誌, 66(4) (4), 644 - 644, 日本語


• Fabry病における酵素補充療法前後の血中Lyso-Gb3の変化率に関する検討

  平井 俊行, 後藤 俊介, 岡本 隼樹, 坂本 和雄, 河野 圭志, 藤井 秀毅

  (一社)日本腎臓学会, 2024年06月, 日本腎臓学会誌, 66(4) (4), 675 - 675, 日本語


• 【病因・病態生理から読み解く腎・泌尿器疾患のすべて】腎移植関連 生活習慣病 睡眠時無呼吸症候群

  坂本 和雄, 西 慎一

  (株)東京医学社, 2023年12月, 腎と透析, 95(増刊) (増刊), 601 - 603, 日本語


• 【腎移植2023:最新の動向とトピックス】腎移植患者とHIF-PH阻害薬

  坂本 和雄

  (株)東京医学社, 2023年12月, 腎と透析, 95(6) (6), 805 - 807, 日本語


• 多発性嚢胞腎を原疾患とした生体腎移植後に巣状分節性糸球体硬化症を発症した一例

  川勝 拓也, 河野 圭志, 渡邉 健太郎, 坂本 和雄, 後藤 俊介, 藤井 秀毅

  (一社)日本移植学会, 2023年11月, 移植, 58(2) (2), 172 - 172, 日本語


• COVID-19感染を契機にネフローゼ症候群を発症し,膜性増殖性糸球体腎炎(MGPN)と診断された1例

  黒野 博義, 渡邉 健太郎, 坂本 和雄, 河野 圭志, 後藤 俊介, 兵頭 俊紀, 藤井 秀毅

  (一社)日本腎臓学会, 2023年09月, 日本腎臓学会誌, 65(6-W) (6-W), 771 - 771, 日本語


• 詳細な遺伝子解析により診断に至った常染色体優性尿細管間質性腎疾患(ADTKD)の1例

  錦 惠那, 清水 真央, 渡邉 健太郎, 坂本 和雄, 河野 圭志, 後藤 俊介, 藤井 秀毅, 岡田 里枝子, 野津 寛大

  (一社)日本腎臓学会, 2023年09月, 日本腎臓学会誌, 65(6-W) (6-W), 804 - 804, 日本語


• 慢性腎臓病+心肥大モデルラットにおけるカルシウム受容体作動薬の効果

  岡本 英久, 能瀬 勇馬, 藤井 秀毅, 岡本 隼樹, 渡邉 健太郎, 坂本 和雄, 河野 圭志, 後藤 俊介, 西 慎一

  (一社)日本腎臓学会, 2023年05月, 日本腎臓学会誌, 65(3) (3), 258 - 258, 日本語


• 慢性腎臓病に対する五苓散の臨床的な効果

  寺田 菜々子, 後藤 俊介, 藤井 秀毅, 清水 真央, 渡邉 健太郎, 坂本 和雄, 河野 圭志, 西 愼一

  (一社)日本腎臓学会, 2023年05月, 日本腎臓学会誌, 65(3) (3), 327 - 327, 日本語


• 【急性腎障害(AKI)】AKIの病態とその対応 腎移植とAKI

  坂本 和雄, 西 慎一

  (株)東京医学社, 2023年01月, 腎と透析, 94(1) (1), 101 - 104, 日本語


• HIF-PH阻害薬への期待と懸念 心肺保護薬としての期待と懸念

  坂本 和雄, 西 慎一

  (株)日本メディカルセンター, 2022年09月, 臨床透析, 38(10) (10), 1337 - 1341, 日本語


• ファブリー病患者における骨密度低下に関する検討

  能瀬 勇馬, 後藤 俊介, 藤井 秀毅, 渡邉 健太郎, 坂本 和雄, 河野 圭志, 西 慎一

  (一社)日本腎臓学会, 2022年05月, 日本腎臓学会誌, 64(3) (3), 269 - 269, 日本語


• ネフローゼモデルラットにおける五苓散の効果

  清水 真央, 藤井 秀毅, 山谷 哲史, 平林 顕, 河野 圭志, 坂本 和雄, 後藤 俊介, 西 慎一

  (一社)日本腎臓学会, 2022年05月, 日本腎臓学会誌, 64(3) (3), 293 - 293, 日本語


• 【腎と妊娠update】腎と妊娠を巡って 腎移植患者の妊娠管理

  坂本 和雄, 西 慎一

  (有)科学評論社, 2022年03月, 腎臓内科, 15(3) (3), 306 - 312, 日本語


• 症例による透析患者の画像診断 Mycobacterium goodiiによる出口部感染から腹膜炎に至った腹膜透析患者の1例

  岩崎 慧, 河野 圭志, 岡本 英久, 渡邉 健太郎, 坂本 和雄, 藤井 秀毅, 西 慎一

  (株)日本メディカルセンター, 2022年03月, 臨床透析, 38(3) (3), 317 - 322, 日本語


• 腎移植後のTMAについて病理・リスク因子・臨床像 移植前に考えるTMAのリスク、TMAの再発予防のためにできること

  坂本 和雄

  (一社)日本臨床腎移植学会, 2022年02月, 日本臨床腎移植学会プログラム・抄録集, 55回, 109 - 109, 日本語


• 【感染症と腎臓】感染関連腎炎 細菌・ウイルス感染に伴う間質性腎障害

  坂本 和雄, 西 慎一

  (有)科学評論社, 2021年12月, 腎臓内科, 14(6) (6), 706 - 711, 日本語


• IgA型膜性腎症の1例

  高木 泰尚, 坂本 和雄, 藤田 直志, 後藤 俊介, 藤井 秀毅, 原 重雄, 西 慎一

  (一社)日本腎臓学会, 2021年09月, 日本腎臓学会誌, 63(6-W) (6-W), 847 - 847, 日本語


• PLA2RとTHSD7A共陽性の特発性膜性腎症と巣状分節性糸球体硬化症の合併例

  井出 文枝, 坂本 和雄, 藤本 千恵, 渡邉 健太郎, 原 重雄, 藤井 秀毅, 西 慎一

  (一社)日本腎臓学会, 2020年09月, 日本腎臓学会誌, 62(6) (6), 672 - 672, 日本語


• 糸球体濾過はポドサイト剥離を促す内的因子である

  佐賀 信之, 坂本 和雄, 松阪 泰二, 長田 道夫

  (一社)日本腎臓学会, 2020年07月, 日本腎臓学会誌, 62(4) (4), 312 - 312, 日本語


• 5種類の内科連携-それぞれのメリットに迫る- 神戸大学の泌尿器科 腎臓内科併診のカタチ

  吉川 美喜子, 香川 友紀, 原 麻由美, 原 明子, 藤田 直志, 坂本 和雄, 石村 武志, 藤澤 正人, 西 慎一

  (一社)日本臨床腎移植学会, 2020年02月, 日本臨床腎移植学会プログラム・抄録集, 53回, 136 - 136, 日本語


• 移植後1時間生検でTMA所見が認められた献腎移植小児例

  坂本 和雄, 後藤 俊介, 吉川 美喜子, 西 慎一, 小川 悟史, 石村 武志, 藤澤 正人, 飯島 一誠, 原 重雄

  (一社)日本臨床腎移植学会, 2020年02月, 日本臨床腎移植学会プログラム・抄録集, 53回, 172 - 172, 日本語


• 可溶性VCAM-1産生はポドサイト内因性の障害適応機構である

  眞部 俊, 坂本 和雄, 井藤 奈央子, 佐賀 信行, 新田 孝作, 長田 道夫

  (一社)日本腎臓学会, 2018年04月, 日本腎臓学会誌, 60(3) (3), 352 - 352, 日本語


• 糸球体濾過の多様性とポドサイト剥離

  佐賀 信之, 井藤 奈央子, 坂本 和雄, 眞部 俊, 長田 道夫

  (一社)日本腎臓学会, 2018年04月, 日本腎臓学会誌, 60(3) (3), 352 - 352, 日本語


• 【ポドサイトupdate】基礎 ポドサイト障害と糸球体瘢痕

  上野 智敏, 坂本 和雄, 乳原 善文, 高市 憲明

  (株)東京医学社, 2015年03月, 腎と透析, 78(3) (3), 404 - 408, 日本語


• Basic nephrology 免疫・病理 FSGSにおける上皮細胞の変化

  坂本 和雄, 上野 智敏, 長田 道夫

  (株)中外医学社, 2015年01月, Annual Review腎臓, 2015, 51 - 57, 日本語


• ポドサイト障害は高脂血症下において糸球体脂質沈着と酸化を促す

  原怜史, 小林凡子, 眞部俊, 坂本和雄, 高島康利, 上野智敏, 濱田樹里, 松阪泰二, 長田道夫

  (一社)日本腎臓学会, 2014年05月25日, 日本腎臓学会誌, 56(3) (3), 303 - 303, 日本語


• 二次性副甲状腺機能亢進症による高Ca血症、意識障害に対しゾレドロネートを使用し、縦隔内手術を要した血液透析患者の一例

  坂本 和雄, 神 幸希, 豊永 次郎, 武田 一人

  (一社)日本透析医学会, 2014年05月, 日本透析医学会雑誌, 47(Suppl.1) (Suppl.1), 613 - 613, 日本語


• 成長因子シグナル伝達を制御する細胞外Sulfataseは糖尿病性腎症の進展を抑制する

  高島 康利, 屋代 紘, 大橋 久美, 山下 春緒子, 坂本 和雄, 眞部 俊, 原 怜史, 小林 凡子, 上野 智敏, 桝 正幸, 桝 和子, 長田 道夫

  (一社)日本腎臓学会, 2014年05月, 日本腎臓学会誌, 56(3) (3), 275 - 275, 日本語


• PODOCYTE INJURY PROMOTES GLOMERULAR LIPID DEPOSITION AND PEROXIDATION UNDER HYPERCHOLESTEROLEMIA

  Hara Satoshi, Kobayashi Namiko, Manabe Shun, Sakamoto Kazuo, Takashima Yasutoshi, Ueno Toshiharu, Hamada Juri, Matsusaka Taiji, Nagata Michio

  2014年05月, NEPHROLOGY, 19, 49 - 49, 英語

  研究発表ペーパー・要旨（国際会議）


• PRIMARY PODOCYTE INJURY-CAUSED IN SITU THROMBOTIC MICROANGIOPATHY PROMOTES EXTRA PODOCYTE DAMAGE BY PAI-1/uPA/uPAR COMPLEX MEDIATED BETA1-INTEGRIN ENDOCYTOSIS

  Kobayashi Namiko, Ueno Toshiharu, Ohashi Kumi, Hara Satoshi, Sakamoto Kazuo, Manabe Shun, Takashima Yasutoshi, Matsusaka Taiji, Miyata Toshio, Nagata Michio

  2014年05月, NEPHROLOGY, 19, 31 - 31, 英語

  研究発表ペーパー・要旨（国際会議）


• 超高齢のグッドパスチャー症候群にて血漿交換、免疫抑制剤治療を行い救命しえた1症例

  高江 啓太, 豊永 次郎, 坂本 和雄, 向井 秀幸, 原 由紀子, 中下 さつき, 三浦 修平, 武田 一人

  (一社)日本腎臓学会, 2013年08月, 日本腎臓学会誌, 55(6) (6), 1183 - 1183, 日本語


• 経過中に2回治療中止後、肺出血や中枢神経症状を合併し慢性透析へ移行したループス腎炎(4型DPLN)症例

  三浦 修平, 高江 啓太, 坂本 和雄, 原 由紀子, 向井 秀幸, 中下 さつき, 豊永 次郎, 武田 一人

  (一社)日本腎臓学会, 2013年08月, 日本腎臓学会誌, 55(6) (6), 1191 - 1191, 日本語


• Focal Segmental Glomerulosclerosis(FSGS)におけるポドサイトとParietal epithelial cell(PEC)の相互形質変換

  坂本和雄, 上野智敏, 小林凡子, 原怜史, 高島康利, 山下春渚子, 松阪泰二, 長田道夫

  (一社)日本腎臓学会, 2013年04月25日, 日本腎臓学会誌, 55(3) (3), 321 - 321, 日本語


• 当院における急速進行性糸球体腎炎(RPGN)の予後についての検討

  原 由紀子, 高江 啓太, 坂本 和雄, 向井 秀幸, 中下 さつき, 豊永 次郎, 三浦 修平, 武田 一人

  (一社)日本腎臓学会, 2013年04月, 日本腎臓学会誌, 55(3) (3), 330 - 330, 日本語


• 細胞外スルファターゼは糸球体内Growth factor signalingの調節因子である

  高島 康利, 山下 春渚子, 坂本 和雄, 原 怜史, 小林 凡子, 上野 智敏, 上杉 憲子, 桝 和子, 桝 正幸, 長田 道夫

  (一社)日本腎臓学会, 2013年04月, 日本腎臓学会誌, 55(3) (3), 297 - 297, 日本語


• 【腎アミロイドーシスの新展開】腎アミロイドーシスの病理組織所見と診断上の問題点

  坂本 和雄, 長田 道夫

  (株)メディカルレビュー社, 2013年03月, Nephrology Frontier, 12(1) (1), 30 - 36, 日本語


• 黄色ブドウ球菌による細菌性心外膜炎の1剖検例

  尾田 琢也, 坂本 和雄, 井村 洋

  (一社)日本集中治療医学会, 2013年01月, 日本集中治療医学会雑誌, 20(Suppl.) (Suppl.), 365 - 365, 日本語

• 腎臓栄養学

  加藤, 明彦 (内科学), 竹谷, 豊, 脇野, 修, 北島, 幸枝

  朝倉書店, 2024年04月, 日本語, ISBN: 9784254322682


• Annual review 腎臓

  越川, 昭三, 長沢, 俊彦, 伊藤, 克己, 御手洗, 哲也, 富野, 康日己, 柏原, 直樹, 成田, 一衛

  中外医学社, 1987年, 日本語

• 長期高齢腎移植モデルと老化細胞除去による移植腎の若返り戦略の確立

  坂本 和雄

  日本学術振興会, 科学研究費助成事業, 若手研究, 神戸大学, 2025年04月01日 - 2028年03月31日