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Recent Advances in Molecular Mechanisms Underlying Kidney Diseases: Pathophysiology and Therapeutic Targets, 2nd Edition

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Pathology, Diagnostics, and Therapeutics".

Deadline for manuscript submissions: 20 July 2025 | Viewed by 2144

Special Issue Editor

Dr. George J. Dugbartey

E-Mail Website
Guest Editor
Department of Surgery, London Health Sciences Center, University of Western Ontario, London, ON N6A 5C1, Canada
Interests: kidney diseases; pharmacotherapy; kidney transplantation; cellular and molecular mechanisms; renal protection
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

Kidney diseases remain a major public health concern associated with the increasing morbidity and mortality of millions of people globally. Unfortunately, the prevalence of kidney diseases has increased significantly in recent times. The hallmarks of this important human pathology include the excessive accumulation and deposition of extracellular matrix, mesangiolysis, glomerular basement membrane thickening, tubulointerstitial fibrosis and many more, which eventually lead to loss of kidney function. As the pathogenesis of different forms of kidney diseases is multifactorial, several experimental models have recently been developed to mimic clinical situations and provide a mechanistic understanding of the various pathologies of kidney diseases, with the ultimate goal of identifying and developing potential therapeutic targets. These experimental models have identified several molecular mechanisms underlying various forms of kidney diseases. These mechanisms include:

  • PI3K/Akt/mTOR pathway;
  • Jak/Stat and inflammatory signaling pathways;
  • Induction of oxidative stress and apoptotic pathways;
  • Upregulation of renal transforming growth factor beta-1 expression;
  • Activation of fibroblast and renin-angiotensin-aldosterone system;
  • Mitochondrial dysfunction and depletion of adenosine triphosphate.

Targeting various molecular mechanisms underlying the pathophysiology of the different forms of kidney diseases has shown to be beneficial, and offers a huge potential to be explored that is amenable to novel therapies. This Special Issue focuses on recent research developments in the pathophysiology of kidney diseases and their therapeutic targets for diagnosis and treatment.

Original papers, review articles, and perspectives from experts in the field are welcome.

Dr. George J. Dugbartey
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. International Journal of Molecular Sciences is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. There is an Article Processing Charge (APC) for publication in this open access journal. For details about the APC please see here. 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

  • kidney diseases
  • pathophysiology
  • molecular mechanisms
  • therapeutic targets
  • acute kidney injury
  • chronic kidney disease
  • polycystic kidney disease
  • end-stage renal disease
  • IgA nephropathy
  • diabetic nephropathy
  • hypertensive nephropathy
  • renal cancer
  • kidney infarction
  • kidney infection
  • kidney failure
  • kidney stones
  • renal tubular acidosis
  • renal artery stenosis
  • acute tubular necrosis
  • glomerulopathy
  • interstitial nephritis
  • nephrotic syndrome
  • simple kidney cyst

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Published Papers (2 papers)

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Research

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20 pages, 5057 KiB  
Article
Chemoprotective Mechanism of Sodium Thiosulfate Against Cisplatin-Induced Nephrotoxicity Is via Renal Hydrogen Sulfide, Arginine/cAMP and NO/cGMP Signaling Pathways
by George J. Dugbartey, Karl K. Alornyo, Ismaila Adams, Samuel Adjei, Daniel Amoah and Richard Obeng-Kyeremeh
Int. J. Mol. Sci. 2025, 26(1), 384; https://doi.org/10.3390/ijms26010384 - 4 Jan 2025
Viewed by 611
Abstract
Cisplatin is a common and highly effective chemotherapeutic agent whose nephrotoxic side effect is well-characterized. Sodium thiosulfate (STS), an FDA-approved hydrogen sulfide (H2S) donor drug, is emerging as a chemoprotective agent against cisplatin-induced nephrotoxicity (CIN). In this study, we investigated the [...] Read more.
Cisplatin is a common and highly effective chemotherapeutic agent whose nephrotoxic side effect is well-characterized. Sodium thiosulfate (STS), an FDA-approved hydrogen sulfide (H2S) donor drug, is emerging as a chemoprotective agent against cisplatin-induced nephrotoxicity (CIN). In this study, we investigated the chemoprotective mechanism of STS in a rat model of CIN. Twenty-five male Sprague Dawley rats were randomly assigned to the following groups: HC: Healthy control (received 10 mL/kg/day of 0.9% saline intraperitoneally (ip), [n = 5]), CIN: Cisplatin (received single dose of 7 mg/kg cisplatin ip [n = 5]); CIN + PAG: Cisplatin and daily ip administration of 40 mg/kg of the H2S inhibitor, DL-propargylglycine (PAG) for 28 days (n = 5); CIN + PAG + STS: Cisplatin and daily PAG and STS (150 µM) ip injection for 28 days; CIN + STS: Cisplatin and daily STS ip administration for 28 days (n = 5). Rats in each group were kept in metabolic cages for 24 h on day 0, 14 and 29 after cisplatin administration for urine collection. Rats were then euthanized, and kidney and blood samples were collected for analysis. Histologically, CIN was characterized by glomerular and tubular injury and significant macrophage influx and tubular apoptosis, as well as markedly increased levels of plasma and renal IL-1β, IL-6 and TNF-α and impaired renal antioxidant status compared to HC rats (p < 0.001). These pathological changes were exacerbated in CIN + PAG rats and were strongly reduced in CIN + PAG + STS rats relative to CIN + PAG rats (p < 0.01), while superior renal protection was observed in CIN + STS rats. Functionally, CIN was evidenced by markedly increased levels of serum creatinine and BUN, and significantly decreased urine creatinine, renal creatinine clearance, as well as electrolyte imbalance and urinary concentrating defect in comparison with HC (p < 0.01). These functional changes worsened significantly in CIN + PAG rats (p < 0.05) but improved in CIN + PAG + STS rats, with further improvement in CIN + STS rats to levels comparable to HC rats. Mechanistically, STS increased renal and plasma levels of H2S, arginine, cAMP, nitric oxide (NO) and cGMP as well as SIRT3 and PGC-1α. We have shown for the first time that STS provides chemoprotection against CIN by activating renal arginine/cAMP and NO/cGMP signaling pathways and their downstream mechanisms through increased renal H2S production. Full article
(This article belongs to the Special Issue Recent Advances in Molecular Mechanisms Underlying Kidney Diseases: Pathophysiology and Therapeutic Targets, 2nd Edition)
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Review

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18 pages, 669 KiB  
Review
Exploring the Efficacy and Safety of Ketamine for Managing Acute Renal Colic in Emergency Departments: A Systematic Review of Recent Clinical Trials
by Shiryn D. Sukhram, Grozdena Yilmaz, Stephanie Erichsen and Sergey Vassilevich
Int. J. Mol. Sci. 2025, 26(1), 371; https://doi.org/10.3390/ijms26010371 - 4 Jan 2025
Viewed by 862
Abstract
Kidney stones typically present as renal colic in emergency departments (EDs), where patients experience severe pain and often require parenteral therapy for symptom management. The economic burden associated with managing kidney stones exceeds USD 5 billion annually in the US and accounts for [...] Read more.
Kidney stones typically present as renal colic in emergency departments (EDs), where patients experience severe pain and often require parenteral therapy for symptom management. The economic burden associated with managing kidney stones exceeds USD 5 billion annually in the US and accounts for more than a million visits to EDs each year. There is clear evidence emphasizing the need for innovative and alternative pain control options for patients with renal colic. Recent randomized controlled trials suggest that intranasal (IN) and intravenous (IV) ketamine are as effective as parenteral NSAIDs and opioids in treating renal colic. However, the limited studies available show inconsistent results regarding the analgesic effects of ketamine. In this study, we reviewed the mechanism of action of ketamine for kidney stones, its efficacy in treating acute renal colic, and the potential adverse side effects of ketamine treatment. A population, intervention, comparison, and outcome (PICO)-related question was formulated to guide our research inquiry: “What are the effects of IV or IN ketamine, as a single agent or as an adjuvant (I), in adult patients diagnosed with acute renal colic (P) on pain scale scores and adverse side effects (O) compared to NSAIDs and/or opioids (C)?” Full article
(This article belongs to the Special Issue Recent Advances in Molecular Mechanisms Underlying Kidney Diseases: Pathophysiology and Therapeutic Targets, 2nd Edition)
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