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Cells
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Recent Advances in the Development and Progression of Kidney Diseases...
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Recent Advances in the Development and Progression of Kidney Diseases (Volume II)

A special issue of Cells (ISSN 2073-4409). This special issue belongs to the section "Cellular Pathology".

Deadline for manuscript submissions: closed (31 July 2024) | Viewed by 4524

Special Issue Editor

Prof. Dr. Akito Maeshima

E-Mail Website
Guest Editor
Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, 1981 Kamoda, Kawagoe, Saitama 350-8550, Japan
Interests: acute kidney injury; biomarker; renal stem cell; tubular regeneration; renal fibrosis; lupus nephritis; ANCA-associated vasculitis; activin–follistatin system; aging
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This is the expanded second edition of Recent Advances in Development and Progression of Kidney Diseases, the first edition of which published eleven papers.

Chronic kidney disease (CKD) and end-stage kidney disease (ESKD) are worldwide public health problems. The prevalence of ESKD could rise prominently over the next few decades, driven by the coming acceleration of global population aging and an increasing prevalence of diabetes and hypertension. To overcome this problem, it is indispensable for us to investigate the factors associated with the development of kidney diseases, to explore the mechanism of CKD to ESKD progression, and to search for better treatment options for various kidney diseases.

This Special Issue offers an open access forum that aims to gather a collection of original research and review articles addressing the cellular/molecular mechanism, diagnosis, evaluation, and treatment of kidney diseases, which include primary/secondary glomerulonephritis, rapidly progressive glomerulonephritis, nephrotic syndrome, acute kidney injury, diabetic nephropathy/diabetic kidney disease, chronic renal failure, renal fibrosis, and polycystic kidney disease.

We hope that this Special Issue will provide essential and insightful evidence for our understanding of the development and progression of various kidney diseases.

Prof. Dr. Akito Maeshima
Guest Editor

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Cells is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2700 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • nephrology
  • biomarker
  • inflammation
  • fibrosis
  • aging

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Published Papers (3 papers)

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Research

19 pages, 6046 KiB  
Article
Activation of Yes-Associated Protein Is Indispensable for Transformation of Kidney Fibroblasts into Myofibroblasts during Repeated Administration of Cisplatin
by Jia-Bin Yu, Babu J. Padanilam and Jinu Kim
Cells 2024, 13(17), 1475; https://doi.org/10.3390/cells13171475 - 2 Sep 2024
Viewed by 755
Abstract
Cisplatin is a potent chemotherapy medication that is used to treat various types of cancer. However, it can cause nephrotoxic side effects, which lead to acute kidney injury (AKI) and subsequent chronic kidney disease (CKD). Although a clinically relevant in vitro model of [...] Read more.
Cisplatin is a potent chemotherapy medication that is used to treat various types of cancer. However, it can cause nephrotoxic side effects, which lead to acute kidney injury (AKI) and subsequent chronic kidney disease (CKD). Although a clinically relevant in vitro model of CKD induced by repeated administration of low-dose cisplatin (RAC) has been established, its underlying mechanisms remain poorly understood. Here, we compared single administration of high-dose cisplatin (SAC) to repeated administration of low-dose cisplatin (RAC) in myofibroblast transformation and cellular morphology in a normal rat kidney fibroblast NRK-49F cell line. RAC instead of SAC transformed the fibroblasts into myofibroblasts as determined by α-smooth muscle actin, enlarged cell size as represented by F-actin staining, and increased cell flattening as expressed by the semidiameter ratio of attached cells to floated cells. Those phenomena, as well as cellular senescence, were significantly detected from the time right before the second administration of cisplatin. Interestingly, inhibition of the interaction between Yes-associated protein (YAP) and the transcriptional enhanced associated domain (TEAD) using Verteporfin remarkedly reduced cell size, cellular senescence, and myofibroblast transformation during RAC. These findings collectively suggest that YAP activation is indispensable for cellular hypertrophy, senescence, and myofibroblast transformation during RAC in kidney fibroblasts. Full article
(This article belongs to the Special Issue Recent Advances in the Development and Progression of Kidney Diseases (Volume II))
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12 pages, 1656 KiB  
Article
Potential Utility of Urinary Follistatin as a Non-Invasive Indicator of Acute Tubular Damage in Patients with Acute Kidney Injury
by Izumi Nagayama, Kaori Takayanagi, Daisuke Nagata, Hajime Hasegawa and Akito Maeshima
Cells 2024, 13(6), 525; https://doi.org/10.3390/cells13060525 - 16 Mar 2024
Cited by 1 | Viewed by 1360
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 [...] Read more.
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. Full article
(This article belongs to the Special Issue Recent Advances in the Development and Progression of Kidney Diseases (Volume II))
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16 pages, 1619 KiB  
Article
Acute Kidney Injury-Induced Circulating TNFR1/2 Elevations Correlate with Persistent Kidney Injury and Progression to Fibrosis
by Akshayakeerthi Arthanarisami, Yohei Komaru, Charikleia Katsouridi, Julian Schumacher, Deborah K. Verges, Liang Ning, Mai M. Abdelmageed, Andreas Herrlich and Eirini Kefaloyianni
Cells 2023, 12(18), 2214; https://doi.org/10.3390/cells12182214 - 5 Sep 2023
Cited by 1 | Viewed by 1791
Abstract
Elevated levels of circulating tumor necrosis factor receptors 1 and 2 (cTNFR1/2) predict chronic kidney disease (CKD) progression; however, the mechanisms of their release remain unknown. Whether acute kidney injury (AKI) drives cTNFR1/2 elevations and whether they predict disease outcomes after AKI remain [...] Read more.
Elevated levels of circulating tumor necrosis factor receptors 1 and 2 (cTNFR1/2) predict chronic kidney disease (CKD) progression; however, the mechanisms of their release remain unknown. Whether acute kidney injury (AKI) drives cTNFR1/2 elevations and whether they predict disease outcomes after AKI remain unknown. In this study, we used AKI patient serum and urine samples, mouse models of kidney injury (ischemic, obstructive, and toxic), and progression to fibrosis, nephrectomy, and related single-cell RNA-sequencing datasets to experimentally test the role of kidney injury on cTNFR1/2 levels. We show that TNFR1/2 serum and urine levels are highly elevated in all of the mouse models of kidney injury tested, beginning within one hour post injury, and correlate with its severity. Consistent with this, serum and urine TNFR1/2 levels are increased in AKI patients and correlate with the severity of kidney failure. Kidney tissue expression of TNFR1/2 after AKI is only slightly increased and bilateral nephrectomies lead to strong cTNFR1/2 elevations, suggesting the release of these receptors by extrarenal sources. The injection of the uremic toxin indoxyl sulfate in healthy mice induces moderate cTNFR1/2 elevations. Moreover, TNF neutralization does not affect early cTNFR1/2 elevations after AKI. These data suggest that cTNFR1/2 levels in AKI do not reflect injury-induced TNF activity, but rather a rapid response to loss of kidney function and uremia. In contrast to traditional disease biomarkers, such as serum creatinine or BUN, cTNFR1/2 levels remain elevated for weeks after severe kidney injury. At these later timepoints, cTNFR1/2 levels positively correlate with remaining kidney injury. During the AKI-to-CKD transition, elevations of TNFR1/2 kidney expression and of cTNFR2 levels correlate with kidney fibrosis levels. In conclusion, our data demonstrate that kidney injury drives acute increases in cTNFR1/2 serum levels, which negatively correlate with kidney function. Sustained TNFR1/2 elevations after kidney injury during AKI-to-CKD transition reflect persistent tissue injury and progression to kidney fibrosis. Full article
(This article belongs to the Special Issue Recent Advances in the Development and Progression of Kidney Diseases (Volume II))
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