New Development in Pharmacotherapy of Kidney Diseases

A special issue of Pharmaceuticals (ISSN 1424-8247). This special issue belongs to the section "Pharmacology".

Deadline for manuscript submissions: 25 November 2025 | Viewed by 671

Special Issue Editor


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Guest Editor
Division of Nephrology, Department of Internal Medicine, Kaohsiung Chang Gung Memorial Hospital, Kaohsiung, Taiwan
Interests: chronic kidney disease (CKD); acute kidney injury (AKI); cardiovascular protection; kidney protection

Special Issue Information

Dear Colleagues,

We are pleased to invite you to submit your research papers for a Special Issue of our journal, focusing on recent advances in pharmacotherapy for patients with kidney disease. This Special Issue aims to highlight the latest developments and innovations in the treatment of patients with both chronic and acute kidney disease, with an emphasis on cardiovascular and kidney protection, as well as the improvement of quality of life. Additionally, it will cover therapies that benefit bone health, endocrine function, electrolyte/mineral balance, gastrointestinal health, hematology, metabolism, neuromuscular function, and nutrition. We also welcome submissions on therapies that address specific symptoms and procedures related to kidney disease, such as uremic pruritus and the survival of dialysis access. We believe that your contributions will significantly enhance the understanding and management of kidney disease, ultimately improving patient outcomes and quality of life. We look forward to receiving your submissions and to the valuable insights your research will bring to this Special Issue.

Dr. Chihchao Yang
Guest Editor

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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.

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Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 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

  • chronic kidney disease (CKD)
  • acute kidney injury (AKI)
  • pharmacotherapy
  • cardiovascular protection
  • kidney protection
  • bone health
  • endocrine function
  • gut health
  • metabolism
  • neuromuscular function
  • nutrition
  • symptom management
  • sodium-glucose cotransporter-2 (SGLT-2) inhibitors
  • glucagon-like peptide-1 (GLP-1) receptor agonists
  • non-steroidal mineralocorticoid receptor antagonists (MRA)
  • endothelin receptor antagonists
  • anemia management
  • electrolyte abnormalities
  • dialysis
  • nephrotoxicity
  • drug interactions
  • uremic toxin
  • clinical trials
  • innovative therapies
  • protein-energy wasting
  • chronic kidney disease and bone mineral disease
  • inflammation
  • oxidation
  • diabetes
  • hypertension
  • obesity
  • hyperlipidemia
  • pruritus
  • osteoporosis
  • fracture
  • sarcopenia
  • protein-energy wasting

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Published Papers (1 paper)

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Research

24 pages, 21945 KiB  
Article
Drug Pair of Astragali Radix–Ligustri Lucidi Fructus Alleviates Acute Kidney Injury in Mice Induced by Ischemia–Reperfusion Through Inhibiting Ferroptosis
by Xuanhe Liu, Dan Zhang, Yuting Xie, Mengdan Wang, Xiaochun Chen, Weijie Yu, Yuming Ma, Jia Zeng, Qixuan Long, Guangrui Huang, Jie Geng and Anlong Xu
Pharmaceuticals 2025, 18(6), 789; https://doi.org/10.3390/ph18060789 - 25 May 2025
Viewed by 381
Abstract
Background: Acute kidney injury (AKI), characterized by high morbidity and mortality, is primarily caused by renal ischemia–reperfusion injury (RIRI). Ferroptosis plays a key role in RIRI, yet its underlying mechanisms remain unclear. The drug pair of Astragali Radix–Ligustri Lucidi Fructus (DAL) shows promise [...] Read more.
Background: Acute kidney injury (AKI), characterized by high morbidity and mortality, is primarily caused by renal ischemia–reperfusion injury (RIRI). Ferroptosis plays a key role in RIRI, yet its underlying mechanisms remain unclear. The drug pair of Astragali Radix–Ligustri Lucidi Fructus (DAL) shows promise in renal diseases, but its protective effects against RIRI and associated molecular pathways via ferroptosis inhibition are unknown. This study aimed to investigate DAL’s therapeutic effects on RIRI and its mechanisms. Methods: A mouse model of bilateral renal ischemia–reperfusion was established. Renal function (serum creatinine, Scr; blood urea nitrogen, BUN), inflammatory cytokines (TNF-α, IFN-γ, IL-6), ferroptosis markers (GPX4, MDA, GSH, tissue iron), and pathological damage were evaluated. Transcriptomic sequencing and electron microscopy analyzed gene pathways and mitochondrial structure. In HK-2 cells, oxygen–glucose deprivation/reoxygenation (OGD/R) and RSL3-induced ferroptosis models were used to assess DAL-containing serum effects via cell viability, GPX4 expression, and mitochondrial morphology. LC-MS analyzed DAL’s chemical components, and network pharmacology predicted ferroptosis-related targets. Results: DAL significantly reduced Scr/BUN levels, alleviated tubular injury, fibrosis, and apoptosis, and downregulated inflammatory cytokines and damage markers. It inhibited ferroptosis by upregulating GPX4, decreasing MDA/tissue iron, and increasing GSH. Transcriptomics revealed enrichment in lipid metabolism pathways. DAL restored the mitochondrial cristae structure; DAL-containing serum improved cell viability, blocked RSL3-induced GPX4 downregulation, and mitigated mitochondrial dysfunction. Network pharmacology identified DAL’s potential active components and targets. Molecular docking validated binding affinity and interaction patterns of active components with targets. Conclusions: DAL protects against RIRI by upregulating GPX4, preserving the mitochondrial structure, and inhibiting ferroptosis, highlighting its therapeutic potential for AKI prevention and treatment. Full article
(This article belongs to the Special Issue New Development in Pharmacotherapy of Kidney Diseases)
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