Special Issue "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: 31 March 2024 | Viewed by 1321

Special Issue Editor

University Hospital of Split, University of Split School of Medicine, Spinciceva 1, 21000 Split, Croatia
Interests: nephrology; dialysis: critical care nephrology: intensive care; toxicology

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

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 100 words) can be sent to the Editorial Office for announcement on this website.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-blind peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Medicina is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 1800 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.


  • phosphate
  • PTH
  • vascular calcification
  • arteriosclerosis
  • cholecalciferol
  • VDR
  • cardiovascular disease
  • renal osteodystrophy
  • aging

Published Papers (1 paper)

Order results
Result details
Select all
Export citation of selected articles as:


11 pages, 356 KiB  
Association between the Polymorphisms rs2070744, 4b/a and rs1799983 of the NOS3 Gene with Chronic Kidney Disease of Uncertain or Non-Traditional Etiology in Mexican Patients
Medicina 2023, 59(5), 829; https://doi.org/10.3390/medicina59050829 - 24 Apr 2023
Viewed by 1084
Background and Objectives: Chronic Kidney Disease of uncertain or non-traditional etiology (CKDnT) is a form of chronic kidney disease of undetermined etiology (CKDu) and is not associated with traditional risk factors. The aim of this study was to investigate the association of [...] Read more.
Background and Objectives: Chronic Kidney Disease of uncertain or non-traditional etiology (CKDnT) is a form of chronic kidney disease of undetermined etiology (CKDu) and is not associated with traditional risk factors. The aim of this study was to investigate the association of polymorphisms rs2070744, 4b/a and rs1799983 of the NOS3 gene with CKDnT in Mexican patients. Materials and Methods: We included 105 patients with CKDnT and 90 controls. Genotyping was performed by PCR-RFLP’s, genotypic and allelic frequencies were determined and compared between the two groups using χ2 analysis, and differences were expressed as odd ratios with 95% confidence intervals (CI). Values of p < 0.05 were considered statistically significant. Results: Overall, 80% of patients were male. The rs1799983 polymorphism in NOS3 was found to be associated with CKDnT in the Mexican population (p = 0.006) (OR = 0.397; 95% CI, 0.192–0.817) under a dominant model. The genotype frequency was significantly different between the CKDnT and control groups (χ2 = 8.298, p = 0.016). Conclusions: The results of this study indicate that there is an association between the rs2070744 polymorphism and CKDnT in the Mexican population. This polymorphism can play an important role in the pathophysiology of CKDnT whenever there is previous endothelial dysfunction. Full article
(This article belongs to the Special Issue Chronic Kidney Disease and Mineral Bone Disorders)
Back to TopTop