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3. Urinary Epidermal Growth Factor Level as a Noninvasive Indicator of Tubular Repair in Patients with Acute Kidney Injury.

Author

Ono, Kazutoshi, Maeshima, Akito, Nagayama, Izumi, Kubo, Taro, Yagisawa, Takashi, and Nagata, Daisuke

Subjects
*EPIDERMAL growth factor, *ACUTE kidney failure, *KIDNEY tubules, *KIDNEY transplantation
Abstract

Epidermal growth factor (EGF), an essential factor for the proliferation and survival of renal tubular cells, is expressed by distal tubules and normally excreted via urine. Previous studies in rats demonstrated that acute tubular injury reduces urinary EGF levels. However, it is unclear whether urinary EGF is a suitable monitoring marker of tubular repair status after acute kidney injury (AKI) in humans. To address this question, we measured serum and urinary EGF in patients with AKI (n = 99) using ELISA and investigated whether urinary EGF levels were associated with the severity of tubular injury and renal prognosis. Urinary EGF was abundant in healthy controls but showed a significant decrease in AKI patients (14,522 ± 2190 pg/mL vs. 3201 ± 459.7 pg/mL, p < 0.05). The urinary EGF level in patients with renal AKI was notably lower than that in patients with pre-renal AKI. Furthermore, the urinary EGF level in patients with AKI stage 3 was significantly lower than that in patients with AKI stage 1. Urinary EGF levels were negatively correlated with urinary β-2MG and serum creatinine levels but positively correlated with hemoglobin levels and eGFR. Urinary EGF was not significantly correlated with urinary NAG, α-1MG, L-FABP, NGAL, KIM-1, or urinary protein concentrations. No significant correlation was observed between serum and urinary EGF levels, suggesting that urinary EGF is derived from the renal tubules rather than the blood. In living renal transplantation donors, the urinary EGF/Cr ratio was approximately half the preoperative urinary EGF/Cr ratio after unilateral nephrectomy. Collectively, these data suggest that urinary EGF is a suitable noninvasive indicator of not only the volume of functional normal renal tubules but also the status of tubular repair after AKI. [ABSTRACT FROM AUTHOR]

Published
2024
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5. A Case of Castleman's Disease with a Marked Infiltration of IgG4-Positive Cells in the Renal Interstitium.

Author

Sawada, Erika, Shioda, Yuya, Ogawa, Kohki, Iwashita, Takatsugu, Ono, Yuko, Hasegawa, Hajime, and Maeshima, Akito

Subjects
CASTLEMAN'S disease, PLASMA cells, VASCULAR endothelial growth factors, LYMPH nodes, PROGNOSIS, CEREBRAL amyloid angiopathy
Abstract

Multicentric Castleman's disease (MCD) is a benign lymphoproliferative disorder with heterogenous clinical symptoms, and involves systemic organs in addition to lymph nodes. Herein, we present the case of a 55-year-old man with MCD characterized by an extensive infiltration of IgG4+ plasma cells in the kidneys. The patient presented to our hospital with a high fever and diarrhea. On admission, laboratory analysis revealed anemia, renal dysfunction (eGFR 30 mL/min/1.73 m2), polyclonal gammopathy (IgG 7130 mg/dL), elevated serum IgG4 level (2130 mg/dL), and increased C-reactive protein (8.0 mg/dL). An enlargement of lymph nodes in the axillary, mediastinal, para-aortic, and inguinal regions was observed on abdominal computed tomography. Axillary lymph node biopsy revealed interfollicular expansion due to dense plasma cell infiltration. Renal biopsy demonstrated significant plasma cell infiltration into the tubulointerstitium. Immunohistochemical analysis showed a 40% IgG4-positive/IgG-positive plasma cell ratio, meeting the diagnostic criteria for an IgG4-related disease. Amyloid A deposition was observed along vessel walls, and immunofluorescence analysis indicated granular positivity of IgG and C3 along the glomerular capillary wall. Elevated levels of interleukin-6 (21 pg/mL) and vascular endothelial growth factor (VEGF; 1210 pg/mL) were noted. Based on these findings, and the histological finding of the lymph node biopsy, idiopathic MCD was diagnosed. Corticosteroid monotherapy was only partially effective. Subsequently, tocilizumab administration was initiated, leading to sustained remission, even after discontinuation of prednisolone. Due to the diverse responses to steroid therapy and the varying prognoses observed in MCD and IgG4-related disease, it is essential to carefully diagnose MCD by thoroughly assessing the organ distribution of the disease, its response to steroid therapy, and any additional pathological findings. [ABSTRACT FROM AUTHOR]

Published
2024
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12. Activin A is an endogenous inhibitor of ureteric bud outgrowth from the Wolffian duct

Author

Maeshima, Akito, Vaughn, Duke A., Choi, Yohan, and Nigam, Sanjay K.

Subjects
Transforming growth factors, Bone morphogenetic proteins, Biological sciences
Abstract

To link to full-text access for this article, visit this link: http://dx.doi.org/10.1016/j.ydbio.2006.03.011 Byline: Akito Maeshima, Duke A. Vaughn, Yohan Choi, Sanjay K. Nigam Keywords: Wolffian duct; Activin; Ureteric bud outgrowth; Smad; BMP4; Mesonephros; Ectopic bud; Nephrogenesis; Autocrine Abstract: Development of metanephric kidney begins with ureteric bud outgrowth from the Wolffian duct (WD). GDNF is believed to be a crucial positive signal in the budding process, but the negative regulation of this process remains unclear. Here, we examined the role of activin A, a member of TGF-[beta] family, in bud formation using an in vitro WD culture system. When cultured with the surrounding mesonephros, WDs formed many ectopic buds in response to GDNF. While the activin signaling pathway is normally active along the non-budding WD (as measured by expression of activin A and phospho-Smad2/3), activin A was absent and phospho-Smad2/3 was undetectable in the ectopic buds induced by GDNF. To examine the role of activin A in bud formation, we attempted to inactivate activin action. Interestingly, the addition of neutralizing anti-activin A antibody potentiated GDNF action. To further clarify the role of activin A, we also tested the effect of activin blockade on the WD cultured in the absence of mesonephros. WDs without mesonephros did not form ectopic buds even in the presence of GDNF. In contrast, blockade of activin action with a variety of agents acting through different mechanisms (natural antagonist, neutralizing antibodies, siRNA) enabled GDNF to induce ectopic buds. Inhibition of GDNF-induced bud formation by activin A was accompanied by inhibition of cell proliferation, reduced expression of Pax-2, and decreased phosphorylation of PI3-kinase and MAP kinase in the WD. Our data suggest that activin A is an endogenous inhibitor of bud formation and that cancellation of activin A autocrine action may be critical for the initiation of this process. Author Affiliation: Departments of Pediatrics, Medicine, and Cellular and Molecular Medicine, University of California, San Diego, 9500 Gilman Drive, La Jolla, CA 92093-0693, USA Article History: Received 8 November 2005; Revised 7 March 2006; Accepted 10 March 2006

Published
2006

15. Clinical outcomes in donors and recipients of kidney transplantations involving medically complex living donors – a retrospective study

Author

Kinoshita, Yoshitaka, primary, Yagisawa, Takashi, additional, Sugihara, Toru, additional, Hara, Konan, additional, Takeshima, Saki, additional, Kubo, Taro, additional, Shinzato, Takahiro, additional, Shimizu, Toshihiro, additional, Suzuki, Michiko, additional, Maeshima, Akito, additional, Kamei, Jun, additional, Fujisaki, Akira, additional, Ando, Satoshi, additional, Suzuki, Motofumi, additional, Kume, Haruki, additional, and Fujimura, Tetsuya, additional

Published
2020
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16. Importance of methodology in the evaluation of renal mononuclear phagocytes and analysis of a model of experimental nephritis with Shp1 conditional knockout mice

Author

Watanabe, Mitsuharu, primary, Kaneko, Yoriaki, additional, Ohishi, Yuko, additional, Kinoshita, Masato, additional, Sakairi, Toru, additional, Ikeuchi, Hidekazu, additional, Maeshima, Akito, additional, Saito, Yasuyuki, additional, Ohnishi, Hiroshi, additional, Nojima, Yoshihisa, additional, Matozaki, Takashi, additional, and Hiromura, Keiju, additional

Published
2020
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25. Different Effects on Fluid Distribution between Tolvaptan and Furosemide in a Liver Cirrhosis Patient with Chronic Kidney Disease

Author

Nagayama, Izumi, primary, Masuda, Takahiro, additional, Nakagawa, Saki, additional, Murakami, Takuya, additional, Ohara, Ken, additional, Matsuoka, Ryo, additional, Kobayashi, Takahisa, additional, Maeshima, Akito, additional, Akimoto, Tetsu, additional, Saito, Osamu, additional, Muto, Shigeaki, additional, and Nagata, Daisuke, additional

Published
2019
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28. The Analysis of Renal Infiltrating Cells in Acute Tubulointerstitial Nephritis Induced by Anti-PD-1 Antibodies: A Case Report and Review of the Literature

Author

Tabei, Akifumi, primary, Watanabe, Mitsuharu, additional, Ikeuchi, Hidekazu, additional, Nakasatomi, Masao, additional, Sakairi, Toru, additional, Kaneko, Yoriaki, additional, Maeshima, Akito, additional, Kaira, Kyoichi, additional, Hirato, Junko, additional, Nojima, Yoshihisa, additional, and Hiromura, Keiju, additional

Published
2018
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29. Hepatitis E during Tocilizumab Therapy in a Patient with Rheumatoid Arthritis: Case Report and Literature Review

Author

Ikeuchi, Hidekazu, primary, Koinuma, Kana, additional, Nakasatomi, Masao, additional, Sakairi, Toru, additional, Kaneko, Yoriaki, additional, Maeshima, Akito, additional, Yamazaki, Yuichi, additional, Okamoto, Hiroaki, additional, Mimura, Toshihide, additional, Mochida, Satoshi, additional, Nojima, Yoshihisa, additional, and Hiromura, Keiju, additional

Published
2018
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33. Diverse Cell Populations Involved in Regeneration of Renal Tubular Epithelium following Acute Kidney Injury

Author

Maeshima, Akito, Takahashi, Shunsuke, Nakasatomi, Masao, and Nojima, Yoshihisa

Subjects
Article Subject, urogenital system
Abstract

Renal tubular epithelium has the capacity to regenerate, repair, and reepithelialize in response to a variety of insults. Previous studies with several kidney injury models demonstrated that various growth factors, transcription factors, and extracellular matrices are involved in this process. Surviving tubular cells actively proliferate, migrate, and differentiate in the kidney regeneration process after injury, and some cells express putative stem cell markers or possess stem cell properties. Using fate mapping techniques, bone marrow-derived cells and endothelial progenitor cells have been shown to transdifferentiate into tubular components in vivo or ex vivo. Similarly, it has been demonstrated that, during tubular cell regeneration, several inflammatory cell populations migrate, assemble around tubular cells, and interact with tubular cells during the repair of tubular epithelium. In this review, we describe recent advances in understanding the regeneration mechanisms of renal tubules, particularly the characteristics of various cell populations contributing to tubular regeneration, and highlight the targets for the development of regenerative medicine for treating kidney diseases in humans.

Published
2015
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34. Regenerative Medicine for the Kidney: Renotropic Factors, Renal Stem/Progenitor Cells, and Stem Cell Therapy

Author

Maeshima, Akito, Nakasatomi, Masao, and Nojima, Yoshihisa

Subjects
Article Subject, urogenital system
Abstract

The kidney has the capacity for regeneration and repair after a variety of insults. Over the past few decades, factors that promote repair of the injured kidney have been extensively investigated. By using kidney injury animal models, the role of intrinsic and extrinsic growth factors, transcription factors, and extracellular matrix in this process has been examined. The identification of renal stem cells in the adult kidney as well as in the embryonic kidney is an active area of research. Cell populations expressing putative stem cell markers or possessing stem cell properties have been found in the tubules, interstitium, and glomeruli of the normal kidney. Cell therapies with bone marrow-derived hematopoietic stem cells, mesenchymal stem cells, endothelial progenitor cells, and amniotic fluid-derived stem cells have been highly effective for the treatment of acute or chronic renal failure in animals. Embryonic stem cells and induced pluripotent stem cells are also utilized for the construction of artificial kidneys or renal components. In this review, we highlight the advances in regenerative medicine for the kidney from the perspective of renotropic factors, renal stem/progenitor cells, and stem cell therapies and discuss the issues to be solved to realize regenerative therapy for kidney diseases in humans.

Published
2014
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44. Follistatin, an Activin Antagonist, Ameliorates Renal Interstitial Fibrosis in a Rat Model of Unilateral Ureteral Obstruction

Author

Maeshima, Akito, primary, Mishima, Keiichiro, additional, Yamashita, Shin, additional, Nakasatomi, Masao, additional, Miya, Masaaki, additional, Sakurai, Noriyuki, additional, Sakairi, Toru, additional, Ikeuchi, Hidekazu, additional, Hiromura, Keiju, additional, Hasegawa, Yoshihisa, additional, Kojima, Itaru, additional, and Nojima, Yoshihisa, additional

Published
2014
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46. SIRPα signaling regulates podocyte structure and function

Author

Takahashi, Satoshi, primary, Tomioka, Mai, additional, Hiromura, Keiju, additional, Sakairi, Toru, additional, Hamatani, Hiroko, additional, Watanabe, Mitsuharu, additional, Ikeuchi, Hidekazu, additional, Kaneko, Yoriaki, additional, Maeshima, Akito, additional, Aoki, Takeo, additional, Ohnishi, Hiroshi, additional, Matozaki, Takashi, additional, and Nojima, Yoshihisa, additional

Published
2013
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47. Nephrotic Syndrome Caused by Immune-Mediated Acquired LCAT Deficiency

Author

Takahashi, Satoshi, primary, Hiromura, Keiju, additional, Tsukida, Mayuko, additional, Ohishi, Yuko, additional, Hamatani, Hiroko, additional, Sakurai, Noriyuki, additional, Sakairi, Toru, additional, Ikeuchi, Hidekazu, additional, Kaneko, Yoriaki, additional, Maeshima, Akito, additional, Kuroiwa, Takashi, additional, Yokoo, Hideaki, additional, Aoki, Takeo, additional, Nagata, Michio, additional, and Nojima, Yoshihisa, additional

Published
2013
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