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Chronic Kidney Disease: From Molecular Mechanisms to Therapeutic Approaches
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Chronic Kidney Disease: From Molecular Mechanisms to Therapeutic Approaches

A special issue of International Journal of Molecular Sciences (ISSN 1422-0067). This special issue belongs to the section "Molecular Biology".

Deadline for manuscript submissions: 20 August 2026 | Viewed by 10929

Special Issue Editor

Prof. Dr. Ligia Petrica

E-Mail Website
Guest Editor
Department of Nephrology, Centre for Molecular Research in Nephrology and Vascular Disease, "Victor Babes" University of Medicine and Pharmacy Timisoara, Timisoara, Romania
Interests: chronic kidney disease; diabetic kidney disease; epigenetics; proteomics; lipidomics; metabolomics; mitochondrial dysfunction
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

This Special Issue, entitled “Chronic Kidney Disease: From Molecular Mechanisms to Therapeutic Approaches”, provides an in-depth exploration of the pathophysiological processes underlying chronic kidney disease (CKD) and the latest advances in potential therapeutic strategies. Contributions from leading researchers in the field present cutting-edge insights into the molecular mechanisms that drive CKD progression, including inflammation, fibrosis, and mitochondrial dysfunction, alongside novel biomarkers for early detection and disease monitoring.

This Special Issue also highlights the roles of genetic and epigenetic factors in CKD susceptibility and progression, providing a comprehensive understanding of the intricate interplay between genetic predisposition and environmental influences. Regarding therapeutics, this Special Issue delves into promising approaches, such as targeted drug therapies, gene editing, stem cell treatments, and precision medicine, for improving patient outcomes.

By combining basic research with clinical applications, this Special Issue acts as an essential resource for researchers, clinicians, and healthcare professionals working to tackle the global burden of CKD and develop effective, personalized therapeutic interventions.

Prof. Dr. Ligia Petrica
Guest Editor

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Keywords

  • genetics
  • epigenetics
  • inflammation
  • metabolomics
  • oxiative stress

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Published Papers (6 papers)

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Research

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19 pages, 2821 KB  
Article
Endocannabinoid System-Related Inflammation and Progression of Autosomal Dominant Polycystic Kidney Disease
by Paulina Simankowicz, Barbara Dołęgowska, Małgorzata Marchelek-Myśliwiec, Katarzyna Dołęgowska, Jacek Różański and Joanna Stępniewska
Int. J. Mol. Sci. 2026, 27(9), 4087; https://doi.org/10.3390/ijms27094087 - 2 May 2026
Viewed by 383
Abstract
The endocannabinoid system is a complex regulatory network whose functioning is associated with maintaining homeostasis and regulating immune response. The aim of this study was to evaluate the relationship between endocannabinoid system activity, inflammation, and the progression of chronic kidney disease (CKD) in [...] Read more.
The endocannabinoid system is a complex regulatory network whose functioning is associated with maintaining homeostasis and regulating immune response. The aim of this study was to evaluate the relationship between endocannabinoid system activity, inflammation, and the progression of chronic kidney disease (CKD) in patients with autosomal dominant polycystic kidney disease (ADPKD). The study included 105 participants: 60 individuals with ADPKD and 45 healthy volunteers. From a single venous blood draw, concentrations of anandamide (AEA), 2-arachidonoylglycerol (2-AG), tumor necrosis factor α (TNF-α), and interleukin 6 (IL-6) were measured in EDTA plasma. Basic laboratory parameters were also assessed, including complete blood count, iron metabolism indices, electrolyte panel, and azotemia parameters. There were statistically significant differences in the concentrations of both endocannabinoids, with higher mean values observed in the control group (p < 0.001). IL-6 concentrations were significantly higher in the ADPKD group compared with controls (p < 0.001). Although TNF-α concentrations were higher in the ADPKD group than in the control group, these differences did not reach statistical significance. Statistically significant correlations were also identified between inflammatory markers, endocannabinoid concentrations, and indices of renal function. Patients with ADPKD exhibit an altered endocannabinoid profile characterized by reduced AEA and 2-AG concentrations, which correlates with disease progression and poorer kidney function. The endocannabinoid system may modulate inflammation in ADPKD. Full article
(This article belongs to the Special Issue Chronic Kidney Disease: From Molecular Mechanisms to Therapeutic Approaches)
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16 pages, 1225 KB  
Article
Gut-Derived Uremic Toxins as a Risk Factor for Vascular Damage in Patients with Chronic Kidney Disease
by María Carmen Ruiz Fuentes, Mahsa Rashki, Noelia Risquez Chica, Elena Clavero García, Elisa B. Pereira Pérez, María José Espigares Huete and Rosemary Wangensteen
Int. J. Mol. Sci. 2026, 27(8), 3487; https://doi.org/10.3390/ijms27083487 - 13 Apr 2026
Viewed by 738
Abstract
Patients with chronic kidney disease (CKD) have a markedly increased cardiovascular risk that is not fully explained by traditional risk factors. Gut-derived uremic toxins, indoxyl sulfate (IS), indole-3-acetic acid (IAA), and p-cresyl sulfate (pCS), are poorly cleared by dialysis and may contribute to [...] Read more.
Patients with chronic kidney disease (CKD) have a markedly increased cardiovascular risk that is not fully explained by traditional risk factors. Gut-derived uremic toxins, indoxyl sulfate (IS), indole-3-acetic acid (IAA), and p-cresyl sulfate (pCS), are poorly cleared by dialysis and may contribute to vascular damage. This cross-sectional observational study included 70 patients with CKD under different clinical conditions (pre-dialysis, peritoneal dialysis, hemodialysis, and kidney transplantation) and 17 healthy controls. Serum levels of IS, IAA, pCS and Klotho were measured, and vascular damage was assessed by carotid intima–media thickness (IMT) using ultrasound. CKD patients showed higher concentrations of IS, IAA, and pCS compared with controls, with the highest levels observed in hemodialysis patients. Peritoneal dialysis was associated with elevated IS and pCS, whereas in kidney transplantation, IS and IAA levels did not differ significantly from controls, and pCS remained elevated. Carotid IMT was higher in patients with diabetes and those undergoing hemodialysis. IAA correlated significantly with left/mean IMT, and mean IMT was the only parameter associated with previous cardiovascular events. These findings suggest that gut-derived uremic toxins, particularly IAA, might be associated with subclinical vascular damage in advanced CKD, although larger studies are needed to confirm these associations. Full article
(This article belongs to the Special Issue Chronic Kidney Disease: From Molecular Mechanisms to Therapeutic Approaches)
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19 pages, 946 KB  
Article
Targeted Analysis of Serum and Urinary Metabolites for Early Chronic Kidney Disease
by Mihaela-Roxana Glavan, Carmen Socaciu, Andreea Iulia Socaciu, Oana Milas, Florica Gadalean, Octavian M. Cretu, Adrian Vlad, Danina M. Muntean, Flaviu Bob, Anca Suteanu, Dragos Catalin Jianu, Maria Stefan, Lavinia Marcu, Silvia Ienciu and Ligia Petrica
Int. J. Mol. Sci. 2025, 26(7), 2862; https://doi.org/10.3390/ijms26072862 - 21 Mar 2025
Cited by 2 | Viewed by 2553
Abstract
Chronic kidney disease (CKD) has become one of the most rapidly advancing diseases of the century, contributing significantly to increased mortality and morbidity. Metabolomics presents a promising approach to understanding CKD pathogenesis and identifying novel biomarkers for early diagnosis. This study evaluated serum [...] Read more.
Chronic kidney disease (CKD) has become one of the most rapidly advancing diseases of the century, contributing significantly to increased mortality and morbidity. Metabolomics presents a promising approach to understanding CKD pathogenesis and identifying novel biomarkers for early diagnosis. This study evaluated serum and urine metabolomic profiles in CKD patients with declining glomerular filtration rates (eGFR). Using targeted metabolomics, we quantified seven potential metabolites in blood and urine samples from 20 healthy individuals and 99 CKD patients staged by eGFR according to the KDIGO guidelines. The analysis was conducted using ultra-high performance liquid chromatography combined with electrospray ionization quadrupole time-of-flight mass spectrometry. The metabolites investigated included L-phenylalanine, L-methionine, arginine, indoxyl sulfate, kynurenic acid, and L-acetylcarnitine. Quantitative assessments were performed using pure standards and validated through methods such as the limit of detection (LOD) and limit of quantification (LOQ). The findings identified potential biomarkers for early CKD diagnosis: in serum, L-phenylalanine, L-methionine, arginine, kynurenic acid, and indoxyl sulfate, while L-acetylcarnitine was significant in urine. These biomarkers could provide valuable insights into CKD progression and support in developing more effective diagnostic tools for early intervention. Full article
(This article belongs to the Special Issue Chronic Kidney Disease: From Molecular Mechanisms to Therapeutic Approaches)

Review

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15 pages, 522 KB  
Review
Apolipoproteins in Chronic Kidney Disease and Kidney Transplant: A Long Unfinished Story
by Carmine Secondulfo, Carmine Izzo, Nicoletta Vecchione, Gianmarco Minelli, Dora Russo, Donatella Russo, Rossella Barra, Gabriella Molinaro, Luca Apicella, Candida Iacuzzo, Antonio Pisani, Sarah Hamzeh, Maria Amicone, Massimo Cirillo and Giancarlo Bilancio
Int. J. Mol. Sci. 2025, 26(19), 9664; https://doi.org/10.3390/ijms26199664 - 3 Oct 2025
Cited by 5 | Viewed by 2150
Abstract
Chronic kidney disease (CKD) is a growing global health burden, strongly associated with cardiovascular disease, the leading cause of mortality in this population. Dyslipidemia is a key metabolic abnormality in CKD, but traditional lipid measures such as total cholesterol, LDL cholesterol, HDL cholesterol, [...] Read more.
Chronic kidney disease (CKD) is a growing global health burden, strongly associated with cardiovascular disease, the leading cause of mortality in this population. Dyslipidemia is a key metabolic abnormality in CKD, but traditional lipid measures such as total cholesterol, LDL cholesterol, HDL cholesterol, and triglycerides often fail to capture the complexity of lipid disturbances in CKD and after kidney transplantation. Apolipoproteins have emerged as more reliable markers of cardiovascular and renal risk. Elevated apolipoprotein B (ApoB), reduced apolipoprotein A1 (ApoA1), and a higher ApoB/ApoA1 ratio are linked to CKD progression, cardiovascular events, and post-transplant complications, including post-transplant diabetes mellitus. Lipoprotein(a), a genetically determined atherogenic lipoprotein, accumulates in CKD due to impaired clearance and further increases cardiovascular risk. Other apolipoproteins, such as APOL1 and APOE, modulate CKD susceptibility through lipid-dependent and independent mechanisms. In addition, proprotein convertase subtilisin/kexin type 9 (PCSK9) has been identified as an important regulator of lipid metabolism, and PCSK9 inhibitors may represent a promising therapeutic option, though evidence in advanced CKD and transplant recipients is still limited, especially regarding their effects on apolipoproteins. This review summarizes current evidence on apolipoproteins and PCSK9 in CKD and transplantation, with attention to their potential as biomarkers and therapeutic targets. Full article
(This article belongs to the Special Issue Chronic Kidney Disease: From Molecular Mechanisms to Therapeutic Approaches)
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29 pages, 2454 KB  
Review
The Non-Traditional Cardiovascular Culprits in Chronic Kidney Disease: Mineral Imbalance and Uremic Toxin Accumulation
by Yue Lu, Linlin Meng, Xinlu Wang, Yun Zhang, Cheng Zhang and Meng Zhang
Int. J. Mol. Sci. 2025, 26(16), 7938; https://doi.org/10.3390/ijms26167938 - 17 Aug 2025
Cited by 6 | Viewed by 3607
Abstract
Chronic kidney disease (CKD) is associated with a significantly elevated mortality rate, primarily due to cardiovascular disease (CVD), highlighting a complex bidirectional relationship between the two conditions. Life-threatening cardiovascular events occur despite control of the traditional risk factors, emphasizing the underlying role of [...] Read more.
Chronic kidney disease (CKD) is associated with a significantly elevated mortality rate, primarily due to cardiovascular disease (CVD), highlighting a complex bidirectional relationship between the two conditions. Life-threatening cardiovascular events occur despite control of the traditional risk factors, emphasizing the underlying role of non-traditional risk factors. CKD, causing mineral imbalance and the accumulation of uremic toxins due to a compromised ability to excrete waste products, imposes extra pressure on the cardiovascular system. The retention of mineral and uremic toxins, in turn, aggravates the progression of CKD. This review aims to elucidate the pathophysiological connections between CKD and CVD, with a particular focus on the metabolic regulatory mechanisms influenced by minerals such as calcium and phosphate, as well as uremic toxins. We review how these factors contributed to accelerated multi-organ damage through mechanisms such as inflammation, endothelial dysfunction, oxidative stress, and vascular calcification. In addition, we discuss the therapeutic strategies for specific uremic toxins and proposed directions for future investigations. This review provides insights into the complex interplay between metabolic dysregulation and cardiovascular outcomes in CKD patients, promoting the development of innovative therapeutic interventions, ultimately improving the prognosis and quality of life for patients affected by these interconnected conditions. Full article
(This article belongs to the Special Issue Chronic Kidney Disease: From Molecular Mechanisms to Therapeutic Approaches)
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Other

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16 pages, 14227 KB  
Brief Report
High Glucose-Induced Alterations in Regucalcin Expression in Podocytes and Their Potential Consequences
by Olga Żołnierkiewicz and Dorota Rogacka
Int. J. Mol. Sci. 2026, 27(3), 1602; https://doi.org/10.3390/ijms27031602 - 6 Feb 2026
Viewed by 635
Abstract
Regucalcin (RGN) is a multifunctional regulator of intracellular calcium signaling, implicated in cellular homeostasis and stress responses. While aberrant RGN activity has been associated with diabetic kidney disease (DKD), existing studies have primarily focused on its role in proximal tubular cells. Whether RGN [...] Read more.
Regucalcin (RGN) is a multifunctional regulator of intracellular calcium signaling, implicated in cellular homeostasis and stress responses. While aberrant RGN activity has been associated with diabetic kidney disease (DKD), existing studies have primarily focused on its role in proximal tubular cells. Whether RGN is expressed in podocytes and how its expression responds to diabetic-like stimuli remain largely unexplored. Podocyte injury under diabetic conditions is a critical event in DKD pathogenesis. Therefore, in this study, we aimed to investigate whether podocytes express RGN and how its expression is affected under high-glucose (HG) conditions. To address these questions, we employed quantitative real-time PCR, Western blotting, fluorescence-based protein staining, and immunohistochemical analysis of renal sections. Our results confirmed RGN expression in podocytes and revealed its dysregulation at both the mRNA and protein levels under HG conditions. Additionally, we identified the subcellular localization of RGN and a significant association with sarco/endoplasmic reticulum calcium ATPase (SERCA), a key enzyme regulating endoplasmic reticulum (ER) calcium storage and the ER stress response. Altered RGN expression in podocytes exposed to HG concentrations may contribute to the progression of DKD, possibly through the disruption of intracellular calcium homeostasis. Full article
(This article belongs to the Special Issue Chronic Kidney Disease: From Molecular Mechanisms to Therapeutic Approaches)
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