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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: 31 October 2024 | Viewed by 1268

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 (1 paper)

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Research

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
Viewed by 955
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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