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Article ; Online: Potential Utility of Urinary Follistatin as a Non-Invasive Indicator of Acute Tubular Damage in Patients with Acute Kidney Injury.

Nagayama, Izumi / Takayanagi, Kaori / Nagata, Daisuke / Hasegawa, Hajime / Maeshima, Akito

2024 Volume 13, Issue 6

Abstract: Activin A is known to impede tubular repair following renal ischemia, whereas exogenous follistatin, an activin A antagonist, has been shown to ameliorate kidney damage in rats. Despite these findings, the precise role of endogenous follistatin in the ... ...

Abstract	Activin A is known to impede tubular repair following renal ischemia, whereas exogenous follistatin, an activin A antagonist, has been shown to ameliorate kidney damage in rats. Despite these findings, the precise role of endogenous follistatin in the kidney has yet to be elucidated. In this study, we investigated the localization of follistatin in the normal human kidney and its potential utility as a marker for acute kidney injury (AKI). In a total of 118 AKI patients and 16 healthy adults, follistatin levels in serum and urine were quantified using ELISA, and correlations with clinical parameters were analyzed. Follistatin-producing cells were positive for Na-Cl co-transporter and uromodulin, but negative for aquaporin 1 and aquaporin 2. Unlike healthy adults, urinary follistatin significantly increased in AKI patients, correlating positively with AKI severity. Urinary follistatin levels were notably higher in patients needing renal replacement therapy. Significant correlations were observed with urinary protein, α1 microglobulin, and urinary NGAL, but not with urinary KIM-1, urinary L-FABP, urinary NAG, urinary β2 microglobulin, or serum creatinine. Interestingly, no correlation between urinary and serum follistatin levels was identified, indicating a renal origin for urinary follistatin. In conclusion, follistatin, produced by distal tubules, is detectable in the urine of AKI patients, suggesting its potential as a valuable marker for monitoring acute tubular damage severity in AKI.
MeSH term(s)	Adult ; Animals ; Humans ; Rats ; Acute Kidney Injury ; Creatinine ; Follistatin/metabolism ; Ischemia/metabolism ; Kidney/metabolism
Chemical Substances	Creatinine (AYI8EX34EU) ; Follistatin ; FST protein, human
Language	English
Publishing date	2024-03-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells13060525
Database	MEDical Literature Analysis and Retrieval System OnLINE

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

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

Diagnostics (Basel, Switzerland)

2024 Volume 14, Issue 5

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 ... ...

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 m
Language	English
Publishing date	2024-02-23
Publishing country	Switzerland
Document type	Case Reports
ZDB-ID	2662336-5
ISSN	2075-4418
ISSN	2075-4418
DOI	10.3390/diagnostics14050476
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Article ; Online: Tubule-Derived Follistatin Is Increased in the Urine of Rats with Renal Ischemia and Reflects the Severity of Acute Tubular Damage.

Nagayama, Izumi / Takayanagi, Kaori / Hasegawa, Hajime / Maeshima, Akito

Cells

2023 Volume 12, Issue 5

Abstract: Activin A, a member of the TGF-beta superfamily, is a negative regulator of tubular regeneration after renal ischemia. Activin action is controlled by an endogenous antagonist, follistatin. However, the role of follistatin in the kidney is not fully ... ...

Abstract	Activin A, a member of the TGF-beta superfamily, is a negative regulator of tubular regeneration after renal ischemia. Activin action is controlled by an endogenous antagonist, follistatin. However, the role of follistatin in the kidney is not fully understood. In the present study, we examined the expression and localization of follistatin in normal and ischemic rat kidneys and measured urinary follistatin in rats with renal ischemia to assess whether urinary follistatin could serve as a biomarker for acute kidney injury. Using vascular clamps, renal ischemia was induced for 45 min in 8-week-old male Wistar rats. In normal kidneys, follistatin was localized in distal tubules of the cortex. In contrast, in ischemic kidneys, follistatin was localized in distal tubules of both the cortex and outer medulla. Follistatin mRNA was mainly present in the descending limb of Henle of the outer medulla in normal kidneys but was upregulated in the descending limb of Henle of both the outer and inner medulla after renal ischemia. Urinary follistatin, which was undetectable in normal rats, was significantly increased in ischemic rats and peaked 24 h after reperfusion. There was no correlation between urinary follistatin and serum follistatin. Urinary follistatin levels were increased according to ischemic duration and were significantly correlated with the follistatin-positive area as well as the acute tubular damage area. These results suggest that follistatin normally produced by renal tubules increases and becomes detectable in urine after renal ischemia. Urinary follistatin might be useful to assess the severity of acute tubular damage.
MeSH term(s)	Animals ; Male ; Rats ; Follistatin/metabolism ; Ischemia/metabolism ; Kidney/metabolism ; Kidney Tubules/metabolism ; Rats, Wistar
Chemical Substances	Follistatin ; Fst protein, rat
Language	English
Publishing date	2023-03-04
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12050801
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Article ; Online: Tubule-Derived Follistatin Is Increased in the Urine of Rats with Renal Ischemia and Reflects the Severity of Acute Tubular Damage

Izumi Nagayama / Kaori Takayanagi / Hajime Hasegawa / Akito Maeshima

Cells, Vol 12, Iss 801, p

2023 Volume 801

Abstract	Activin A, a member of the TGF-beta superfamily, is a negative regulator of tubular regeneration after renal ischemia. Activin action is controlled by an endogenous antagonist, follistatin. However, the role of follistatin in the kidney is not fully understood. In the present study, we examined the expression and localization of follistatin in normal and ischemic rat kidneys and measured urinary follistatin in rats with renal ischemia to assess whether urinary follistatin could serve as a biomarker for acute kidney injury. Using vascular clamps, renal ischemia was induced for 45 min in 8-week-old male Wistar rats. In normal kidneys, follistatin was localized in distal tubules of the cortex. In contrast, in ischemic kidneys, follistatin was localized in distal tubules of both the cortex and outer medulla. Follistatin mRNA was mainly present in the descending limb of Henle of the outer medulla in normal kidneys but was upregulated in the descending limb of Henle of both the outer and inner medulla after renal ischemia. Urinary follistatin, which was undetectable in normal rats, was significantly increased in ischemic rats and peaked 24 h after reperfusion. There was no correlation between urinary follistatin and serum follistatin. Urinary follistatin levels were increased according to ischemic duration and were significantly correlated with the follistatin-positive area as well as the acute tubular damage area. These results suggest that follistatin normally produced by renal tubules increases and becomes detectable in urine after renal ischemia. Urinary follistatin might be useful to assess the severity of acute tubular damage.
Keywords	follistatin ; acute kidney injury ; ischemia reperfusion ; Biology (General) ; QH301-705.5
Subject code	630
Language	English
Publishing date	2023-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article: Urinary Activin A: A Novel Biomarker for Human Acute Kidney Injury.

Nagayama, Izumi / Maeshima, Akito / Nagata, Daisuke

Diagnostics (Basel, Switzerland)

2022 Volume 12, Issue 3

Abstract: Activin is a multifunctional cytokine belonging to the transforming growth factor (TGF)-β superfamily that regulates the growth and differentiation of cells in various organs. We previously reported that activin A, which is absent in normal kidneys, was ... ...

Abstract	Activin is a multifunctional cytokine belonging to the transforming growth factor (TGF)-β superfamily that regulates the growth and differentiation of cells in various organs. We previously reported that activin A, which is absent in normal kidneys, was significantly increased in the ischemic kidney, and that the blockade of activin action by follistatin, an activin antagonist, significantly enhanced tubular regeneration after renal ischemia, suggesting that activin A acts as an endogenous inhibitor of tubular repair after kidney injury in rodents. However, the role of activin A in human acute kidney injury (AKI) remains unclear. In this analysis, we measured serum and urinary activin A in human AKI (n = 39) and tested if activin A might serve as a biomarker for AKI. Urinary activin A, which was undetectable in healthy controls, was significantly increased in AKI (0.0 ± 0.0 vs. 173.4 ± 58.8 pg/mL, p < 0.05). The urinary activin A level in patients with AKI stage 3, was significantly higher than that in patients with AKI stages 1 and 2. Patients who required renal replacement therapy (RRT) had a significantly higher urinary activin A level than patients who did not require RRT. Urinary activin A might be a useful non-invasive biomarker for the severity of AKI.
Language	English
Publishing date	2022-03-09
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2662336-5
ISSN	2075-4418
ISSN	2075-4418
DOI	10.3390/diagnostics12030661
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Article ; Online: Urinary Activin A

Izumi Nagayama / Akito Maeshima / Daisuke Nagata

Diagnostics, Vol 12, Iss 661, p

A Novel Biomarker for Human Acute Kidney Injury

2022 Volume 661

Abstract	Activin is a multifunctional cytokine belonging to the transforming growth factor (TGF)-β superfamily that regulates the growth and differentiation of cells in various organs. We previously reported that activin A, which is absent in normal kidneys, was significantly increased in the ischemic kidney, and that the blockade of activin action by follistatin, an activin antagonist, significantly enhanced tubular regeneration after renal ischemia, suggesting that activin A acts as an endogenous inhibitor of tubular repair after kidney injury in rodents. However, the role of activin A in human acute kidney injury (AKI) remains unclear. In this analysis, we measured serum and urinary activin A in human AKI ( n = 39) and tested if activin A might serve as a biomarker for AKI. Urinary activin A, which was undetectable in healthy controls, was significantly increased in AKI (0.0 ± 0.0 vs. 173.4 ± 58.8 pg/mL, p < 0.05). The urinary activin A level in patients with AKI stage 3, was significantly higher than that in patients with AKI stages 1 and 2. Patients who required renal replacement therapy (RRT) had a significantly higher urinary activin A level than patients who did not require RRT. Urinary activin A might be a useful non-invasive biomarker for the severity of AKI.
Keywords	activin A ; acute kidney injury ; urinary biomarker ; Medicine (General) ; R5-920
Subject code	616
Language	English
Publishing date	2022-03-01T00:00:00Z
Publisher	MDPI AG
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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Article ; Online: Fyn Phosphorylates Transglutaminase 2 (Tgm2) and Modulates Autophagy and p53 Expression in the Development of Diabetic Kidney Disease.

Uehara, Ryota / Yamada, Eijiro / Okada, Shuichi / Bastie, Claire C / Maeshima, Akito / Ikeuchi, Hidekazu / Horiguchi, Kazuhiko / Yamada, Masanobu

Cells

2023 Volume 12, Issue 8

Abstract: Autophagy is involved in the development of diabetic kidney disease (DKD), the leading cause of end-stage renal disease. The Fyn tyrosine kinase (Fyn) suppresses autophagy in the muscle. However, its role in kidney autophagic processes is unclear. Here, ... ...

Abstract	Autophagy is involved in the development of diabetic kidney disease (DKD), the leading cause of end-stage renal disease. The Fyn tyrosine kinase (Fyn) suppresses autophagy in the muscle. However, its role in kidney autophagic processes is unclear. Here, we examined the role of Fyn kinase in autophagy in proximal renal tubules both in vivo and in vitro. Phospho-proteomic analysis revealed that transglutaminase 2 (Tgm2), a protein involved in the degradation of p53 in the autophagosome, is phosphorylated on tyrosine 369 (Y369) by Fyn. Interestingly, we found that Fyn-dependent phosphorylation of Tgm2 regulates autophagy in proximal renal tubules in vitro, and that p53 expression is decreased upon autophagy in Tgm2-knockdown proximal renal tubule cell models. Using streptozocin (STZ)-induced hyperglycemic mice, we confirmed that Fyn regulated autophagy and mediated p53 expression via Tgm2. Taken together, these data provide a molecular basis for the role of the Fyn-Tgm2-p53 axis in the development of DKD.
MeSH term(s)	Mice ; Animals ; Diabetic Nephropathies/metabolism ; Protein Glutamine gamma Glutamyltransferase 2 ; Tumor Suppressor Protein p53/metabolism ; Proteomics ; Autophagy ; Diabetes Mellitus
Chemical Substances	Protein Glutamine gamma Glutamyltransferase 2 (EC 2.3.2.13) ; Tumor Suppressor Protein p53
Language	English
Publishing date	2023-04-20
Publishing country	Switzerland
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2661518-6
ISSN	2073-4409 ; 2073-4409
ISSN (online)	2073-4409
ISSN	2073-4409
DOI	10.3390/cells12081197
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Article: Label-retaining cells in the kidney: origin of regenerating cells after renal ischemia.

Maeshima, Akito

Clinical and experimental nephrology

2007 Volume 11, Issue 4, Page(s) 269–274

Abstract: The kidney is capable of regeneration. In response to a variety of insults, renal epithelial tubular cells dedifferentiate into an immature phenotype, proliferate, migrate to the injured area, and redifferentiate into mature polarized epithelial cells. ... ...

Abstract	The kidney is capable of regeneration. In response to a variety of insults, renal epithelial tubular cells dedifferentiate into an immature phenotype, proliferate, migrate to the injured area, and redifferentiate into mature polarized epithelial cells. In animal models of acute kidney injury induced by renal ischemia or renal toxins, various growth factors, transcription factors, chemokines, and extracellular matrix components have been demonstrated to be involved in the regeneration process. Recent research has suggested the existence of renal stem/progenitor cells in the kidney and their involvement in renal regeneration. In this review, we will focus on the mechanisms of tubular regeneration after kidney injury, particularly on label-retaining cells actively engaged in this process, and discuss their potential as targets of regenerative therapy for various kidney diseases.
MeSH term(s)	Animals ; Cell Differentiation ; Cell Movement ; Cell Proliferation ; Cell Transdifferentiation ; Epithelial Cells/pathology ; Fibrosis ; Humans ; Ischemia/pathology ; Ischemia/physiopathology ; Kidney/blood supply ; Kidney/pathology ; Kidney/physiopathology ; Kidney Tubules/pathology ; Kidney Tubules/physiopathology ; Regeneration ; Stem Cells/pathology
Language	English
Publishing date	2007-12-21
Publishing country	Japan
Document type	Journal Article ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	1338768-6
ISSN	1342-1751
ISSN	1342-1751
DOI	10.1007/s10157-007-0500-9
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Pregnancy outcomes in patients with systemic lupus erythematosus with or without a history of lupus nephritis.

Oishi, Yuko / Ikeuchi, Hidekazu / Hamatani, Hiroko / Nakasatomi, Masao / Sakairi, Toru / Kaneko, Yoriaki / Maeshima, Akito / Iwase, Akira / Hiromura, Keiju

Clinical and experimental nephrology

2021 Volume 25, Issue 8, Page(s) 835–843

Abstract: Background: Pregnancy is an important issue for many women with systemic lupus erythematosus (SLE). This study examined maternal and fetal outcomes among SLE women with or without a history of lupus nephritis (LN).: Methods: We retrospectively ... ...

Abstract	Background: Pregnancy is an important issue for many women with systemic lupus erythematosus (SLE). This study examined maternal and fetal outcomes among SLE women with or without a history of lupus nephritis (LN). Methods: We retrospectively analyzed 98 pregnancies in 57 women previously diagnosed with SLE who gave birth at our hospital. Results: There were 44 pregnancies in women with a history of LN and 54 pregnancies in those without. Fetal loss was observed in 16.1% of SLE pregnancies when excluding induced abortion, and preeclampsia and SLE flare were observed in 12.2 and 6.1% of SLE pregnancies, respectively. No significant differences were evident between women with or without LN in rate of fetal loss, preeclampsia or SLE flare. Women with a history of LN exhibited a significantly shorter duration of gestation (37.0 weeks vs. 38.4 weeks, P = 0.006) and lower birth weight (2484 g vs. 2746 g, P = 0.007) than those without LN. Multivariate analysis revealed glucocorticoid dose but not history of LN, as an independent risk factor for preterm delivery and low birth weight. Conclusion: This study was unable to conclude that a history of LN predicted pregnancy outcomes among SLE women. Instead, a higher dose of glucocorticoid at conception was unexpectedly associated with preterm delivery and low birth weight. Further studies are awaited to verify the relationship.
MeSH term(s)	Adult ; Birth Weight ; Female ; Humans ; Infant, Low Birth Weight ; Infant, Newborn ; Japan/epidemiology ; Lupus Nephritis/epidemiology ; Pregnancy ; Pregnancy Complications/epidemiology ; Pregnancy Outcome/epidemiology ; Premature Birth/epidemiology ; Retrospective Studies ; Risk Factors
Language	English
Publishing date	2021-06-24
Publishing country	Japan
Document type	Journal Article
ZDB-ID	1338768-6
ISSN	1437-7799 ; 1342-1751
ISSN (online)	1437-7799
ISSN	1342-1751
DOI	10.1007/s10157-020-02017-0
Database	MEDical Literature Analysis and Retrieval System OnLINE

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Article ; Online: Combating Kidney Fibrosis

Keizo Kanasaki / Akito Maeshima / Gangadhar Taduri / Ignacio Revuelta

BioMed Research International, Vol

2014 Volume 2014

Keywords	Medicine ; R
Language	English
Publishing date	2014-01-01T00:00:00Z
Publisher	Hindawi Limited
Document type	Article ; Online
Database	BASE - Bielefeld Academic Search Engine (life sciences selection)

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