Chronic Kidney Disease and Mineral Bone Disorders
A special issue of Medicina (ISSN 1648-9144). This special issue belongs to the section "Urology & Nephrology".
Deadline for manuscript submissions: closed (31 March 2024) | Viewed by 2829
Special Issue Editor
Special Issue Information
Dear Colleagues,
Chronic kidney disease-mineral bone disorder (CKD-MBD) is a syndrome characterized by alterations in the homeostasis of calcium, phosphate, PTH, fibroblast growth factor-23 (FGF-23), Klotho, and vitamin D. Important features of CKD-MBD are vascular and soft tissue calcification, with a greater prevalence in low turnover renal osteodystrophy. The progression of CKD is associated with an early increase in FGF-23, PTH, and serum phosphates. FGF-23 binds to FGFR-1 and 3 receptors and the co-receptor Klotho. The Klotho gene encodes a protein that, in rodents, causes a premature aging-like phenotype (atherosclerosis, osteoporosis, and cardiovascular calcifications). Numerous evidences of a link between bone fragility, osteoporosis, and vascular calcification point to a shared pathophysiology between human aging and CKD-MBD. Clarification of phenotypic differentiation from vascular to bone cells has recently become the focus of scientific efforts. The most important promoter of vascular calcification is phosphorus, exerting its effects through osteopontin, osteocalcin, BMP-2, BMP4, bone sialoprotein, etc. Vascular calcification inhibitors are fetuin-A, osteoprotegerin, BMP-7, sclerosin, etc. Recently, exciting insights into monocytes/macrophages and their role in vascular calcification in CKD patients have made this field extremely dynamic.
All of these aspects of CKD-MBD are covered in this Special Issue of Medicina, which is entirely dedicated to scientific and clinical efforts to understand pathophysiology and improve the outcomes of patients with CKD-MBD.
Dr. Vedran Kovačić
Guest Editor
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Keywords
- CKD-MBD
- phosphate
- PTH
- vascular calcification
- arteriosclerosis
- cholecalciferol
- VDR
- cardiovascular disease
- renal osteodystrophy
- aging
