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Chronic Kidney Disease: The State of the Art and Future Perspectives

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 October 2025 | Viewed by 4075

Special Issue Editor


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Guest Editor
SOC Nefrologia e Dialisi, Ospedale San Giovanni di Dio, 50143 Florence, Italy
Interests: renal transplantation; live donor; immunosuppression; chronic rejection, HLA antibodies; graft survival; kidney exchange programs; desensitization; marginal donor; renal donor biopsies

Special Issue Information

Dear Colleagues,

Chronic kidney disease (CKD) is a highly prevalent condition and is associated with a marked increase in the risk of death and cardiovascular events. Chronic kidney disease is expected to become one of the top five causes of death by 2040. The increase in prevalence observed in recent decades is mainly due to the increase in diabetes mellitus and cardiovascular diseases and to the aging of the population. The number of people receiving kidney replacement therapy (KRT) will continue to increase in the coming years, especially in developing countries. 

Recently, several new drugs have been introduced for the treatment of specific kidney diseases, for slowing the progression of chronic kidney disease, or for reducing CV risk. Even our understanding of the mechanisms underlying many kidney diseases, particularly immunologic or genetic diseases, has improved greatly, allowing for new treatment perspectives. There is hope that in the next few years, we will be able to reduce the number of new-incident patients who develop ESRD.

We are pleased to invite you to be part of this Special Issue on chronic kidney disease, which is a global health issue affecting approximately 700 million people. This Special Issue aims to improve treatment outcomes, benefiting patients and the broader society. We are looking for research articles and reviews focusing on CKD prevention, screening, and early treatment to prevent or delay CKD progression, thus reducing premature cardiovascular mortality and improving patients’ quality of life. Please note that manuscripts without molecular data will not be accepted.

Dr. Alberto Rosati
Guest Editor

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Keywords

  • glomerulonephritis
  • chronic kidney disease
  • prevention
  • screening
  • cardiovascular mortality
  • patient outcomes
  • CKD progression

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Published Papers (3 papers)

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Research

10 pages, 241 KiB  
Article
WT1 Gene Pathogenic Variants: Clinical Challenges and Treatment Strategies in Pediatric Nephrology—One Center Practice
by Artur Janek, Andrzej Badeński, Marta Badeńska, Martyna Szuster, Karolina Szymańska-Kurek, Elżbieta Trembecka-Dubel and Maria Szczepańska
Int. J. Mol. Sci. 2025, 26(8), 3642; https://doi.org/10.3390/ijms26083642 - 11 Apr 2025
Viewed by 258
Abstract
Pathogenic variants in the Wilms’ tumor suppressor gene 1 (WT1 gene) can lead to serious disorders within the kidney and urogenital system, including chronic kidney disease. There is still much uncertainty regarding the optimal management of diseases caused by WT1 dysfunction, posing [...] Read more.
Pathogenic variants in the Wilms’ tumor suppressor gene 1 (WT1 gene) can lead to serious disorders within the kidney and urogenital system, including chronic kidney disease. There is still much uncertainty regarding the optimal management of diseases caused by WT1 dysfunction, posing a challenge for physicians caring for these patients. The aim of our study is to present experiences related to the course and treatment of patients with confirmed WT1 pathogenic variants. Data from seven patients (five girls, two boys), who were at the age of 4.8 ± 5.1 years (0.3–14 years) at their first admission and were treated between 1997–2022, were analyzed. The analysis included each patient’s age at the day of diagnosis, anthropometric measurements, comorbidities, and laboratory and genetic test results, as well as their treatment, oncological procedures, and performed surgeries. Wilms’ tumor was the first manifestation of the disease in three patients. Arterial hypertension was diagnosed in three patients, and anemia in four. Treatment of patients with nephrotic syndrome included glucocorticosteroid therapy (GCS), calcineurin inhibitors (CNIs), and mycophenolate mofetil (MMF). Nephrectomy was performed in five children, while kidney transplantation was carried out in two patients. An interdisciplinary approach to WT1 gene pathogenic variants, including early diagnosis, individualization, regular monitoring of treatment, and oncological vigilance, is crucial for improving prognosis and ensuring proper care for patients with nephrological manifestations of WT1 gene region disorders. Furthermore, for a comprehensive understanding of the scope of this disease and the development of effective therapy methods, continued research on the clinical manifestations of WT1 pathogenic variants is essential. Full article
(This article belongs to the Special Issue Chronic Kidney Disease: The State of the Art and Future Perspectives)
12 pages, 2036 KiB  
Article
Effect of Buddleja cordata Leaf Extract on Diabetic Nephropathy in Rats
by Elizabeth Alejandrina Guzmán Hernández, Adriana Miranda Ocaña, Omar Ortiz Pedraza, María Eugenia Garín Aguilar, Rubén San Miguel Chávez, Martín Palomar Morales and David Segura Cobos
Int. J. Mol. Sci. 2024, 25(21), 11432; https://doi.org/10.3390/ijms252111432 - 24 Oct 2024
Cited by 2 | Viewed by 1124
Abstract
One of complications of diabetes mellitus is diabetic nephropathy. In Mexico, in traditional medicine, Buddleja cordata Humb. Bonpl. & Kunth, (“tepozán blanco”) is a shrub plant used for the treatment of rheumatic diseases, postpartum bath, stomachache, skin burns, diarrhea in children, sores, and [...] Read more.
One of complications of diabetes mellitus is diabetic nephropathy. In Mexico, in traditional medicine, Buddleja cordata Humb. Bonpl. & Kunth, (“tepozán blanco”) is a shrub plant used for the treatment of rheumatic diseases, postpartum bath, stomachache, skin burns, diarrhea in children, sores, and cancer. Objectives: We examined the effect of methanol extract of leaves of B. cordata on the expression of pro-inflammatory cytokines and its antioxidant effects in diabetic nephropathy. Methods: We used the streptozotocin-induced diabetes mellitus model in rats; these were treated with methanol extract from leaves of B. cordata at 50 and 100 mg/kg (orally) for 4 weeks. Kidney weight/total body weight ratio and proteins/DNA, proteinuria and creatinine clearance, Western blot of nuclear factor κΒ (NFkB) p65 (cytoplasm and nucleus), peroxisome proliferator activated receptor gamma (PPARγ), and activities of glutathione peroxidase, superoxide dismutase, and catalase were determined. Full article
(This article belongs to the Special Issue Chronic Kidney Disease: The State of the Art and Future Perspectives)
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19 pages, 5105 KiB  
Article
Hyperphosphatemia Contributes to Skeletal Muscle Atrophy in Mice
by Kylie Heitman, Seth Bollenbecker, Jordan Bradley, Brian Czaya, Abul Fajol, Sarah Madison Thomas, Qing Li, Svetlana Komarova, Stefanie Krick, Glenn C. Rowe, Matthew S. Alexander and Christian Faul
Int. J. Mol. Sci. 2024, 25(17), 9308; https://doi.org/10.3390/ijms25179308 - 28 Aug 2024
Cited by 1 | Viewed by 2042
Abstract
Chronic kidney disease (CKD) is associated with various pathologic changes, including elevations in serum phosphate levels (hyperphosphatemia), vascular calcification, and skeletal muscle atrophy. Elevated phosphate can damage vascular smooth muscle cells and cause vascular calcification. Here, we determined whether high phosphate can also [...] Read more.
Chronic kidney disease (CKD) is associated with various pathologic changes, including elevations in serum phosphate levels (hyperphosphatemia), vascular calcification, and skeletal muscle atrophy. Elevated phosphate can damage vascular smooth muscle cells and cause vascular calcification. Here, we determined whether high phosphate can also affect skeletal muscle cells and whether hyperphosphatemia, in the context of CKD or by itself, is associated with skeletal muscle atrophy. As models of hyperphosphatemia with CKD, we studied mice receiving an adenine-rich diet for 14 weeks and mice with deletion of Collagen 4a3 (Col4a3−/−). As models of hyperphosphatemia without CKD, we analyzed mice receiving a high-phosphate diet for three and six months as well as a genetic model for klotho deficiency (kl/kl). We found that adenine, Col4a3−/−, and kl/kl mice have reduced skeletal muscle mass and function and develop atrophy. Mice on a high-phosphate diet for six months also had lower skeletal muscle mass and function but no significant signs of atrophy, indicating less severe damage compared with the other three models. To determine the potential direct actions of phosphate on skeletal muscle, we cultured primary mouse myotubes in high phosphate concentrations, and we detected the induction of atrophy. We conclude that in experimental mouse models, hyperphosphatemia is sufficient to induce skeletal muscle atrophy and that, among various other factors, elevated phosphate levels might contribute to skeletal muscle injury in CKD. Full article
(This article belongs to the Special Issue Chronic Kidney Disease: The State of the Art and Future Perspectives)
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