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New Insights into Molecular Mechanisms of Chronic Kidney Disease

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Dear Colleagues,

Chronic kidney disease (CKD) is increasing in prevalence worldwide and represents a major cause of morbidity and mortality. The pathogenesis of CKD is multifactorial, including complex mechanisms involving numerous genetic factors and molecules involved in inflammation, fibrosis, oxidative stress, endothelial dysfunction, hypoxia, or tubular and podocyte injury. Recent advances in proteomic and molecular technology have identified numerous signaling pathways involved in CKD, including the hyperactivity of the renin-angiotensin (RAS)-aldosterone system, osmotic sodium retention, endothelial dysfunction, dyslipidemia, the RAS/RAF/extracellular-signal-regulated kinase pathway, alterations in the purinergic system, phosphatidylinositol 3-kinase (PI 3-kinase)-dependent signaling pathways, and inflammation, all leading to morphological changes at the vascular and renal levels. Deciphering the molecular mechanisms will allow the development of targeted therapies.

In this Special Issue, we welcome original contributions and scientific reviews on the cellular and molecular aspects of CKD and its complications. We hope the papers published in our journal will significantly contribute to CKD patients.

Dr. Lǎcrǎmioara Ionela Butnariu
Guest Editor

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28 pages, 1104 KB

Open AccessArticle

The Importance of Molecular Testing in the Diagnosis of Genetic Syndromes with Chronic Kidney Disease: Genotype–Phenotype Correlations

by Lăcrămioara Ionela Butnariu, Radu Russu, Ramona Geanina Babici, Aurora Băgiag, Laura Mihaela Trandafir, Elena Țarcă, Paula Popovici, Nicoleta Gimiga and Iuliana Magdalena Starcea

Int. J. Mol. Sci. 2026, 27(5), 2362; https://doi.org/10.3390/ijms27052362 - 3 Mar 2026

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Abstract

Globally, chronic kidney disease (CKD) affects over 800 million individuals and is characterized by significant genetic complexity. More than 600 genes are associated with hereditary kidney disease, which may manifest as isolated kidney issues or as part of a syndrome that also includes extrarenal manifestations. The aim of this study was to identify genetic variants in a group of ten patients who presented with clinical signs suggestive of genetic syndromes associated with CKD, or who were asymptomatic but had a positive family history of CKD. Extensive genetic testing (targeted gene panels and whole-exome sequencing—WES) identified a mutation in the PKD1 gene in 3 out of 10 cases. In one patient, a known mutation in the PKD2 gene was identified. Another four patients were diagnosed with Alport syndrome: three of these presented with de novo missense mutations in the COL4A5 gene, and one patient had a mutation in the COL4A3 gene. One patient was diagnosed with MODY5, caused by a known mutation in the HNF1B gene, and one patient was diagnosed with Bartter syndrome type 1, resulting from a known mutation in the SLC12A1 gene. We present genotype–phenotype correlations, highlighting the particularities of each patient within their family context. Our findings emphasize the importance of genotype–phenotype correlations in refining diagnosis, personalizing therapeutic management, and providing essential genetic counseling for at-risk relatives. Full article

(This article belongs to the Special Issue New Insights into Molecular Mechanisms of Chronic Kidney Disease)

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34 pages, 1034 KB

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Chronic Kidney Disease and Cellular Senescence

by Marya Morevati, Juliette Tavenier, Morten Scheibye-Knudsen, Morten Baltzer Houlind, Aram Hedayati and Mads Hornum

Int. J. Mol. Sci. 2026, 27(7), 3205; https://doi.org/10.3390/ijms27073205 - 1 Apr 2026

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Abstract

Chronic kidney disease (CKD) and kidney aging share many pathological and molecular features, with cellular senescence emerging as a potentially important contributor to disease progression. Senescent cells accumulate in the kidneys due to persistent stressors, contributing to chronic inflammation and fibrosis via the senescence-associated secretory phenotype (SASP). This review explores the intersection between CKD and renal aging, focusing on the mechanisms driving senescence, its impact on kidney function, and potential therapeutic interventions. We explore various senotherapeutic approaches, such as senolytics, senomorphics, and rejuvenating agents, and highlight the increasing role of artificial intelligence (AI) and machine learning (ML) in detecting and monitoring senescent cells, enabling high-throughput and precise assessment across experimental and clinical settings. Understanding these mechanisms offers new avenues for developing targeted treatments to slow CKD progression and improve patient outcomes. Full article

(This article belongs to the Special Issue New Insights into Molecular Mechanisms of Chronic Kidney Disease)

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