[What's New in the CKD-BMD Therapy?].

The important advances in scientific knowledge have led to a notable enrichment of therapeutic offers in the field of CKD-MBD, which have allowed better control of the related biochemical parameters compared to the past. However, this has not corresponded to a tangible improvement in the clinical outcomes, both bone and cardiovascular, associated with CKD-MBD, nor has there been a significant drop in the number of pills that nephropathic patients must take, to keep the parameters controlled biochemicals, with the therapeutic cost of these interventions remaining high. All these unsatisfied needs continue to stimulate research to find new solutions that can improve one or more of these objectives not yet achieved.

Associations of Intact and C-Terminal FGF23 with Inflammatory Markers in Older Patients Affected by Advanced Chronic Kidney Disease.

: In patients with chronic kidney disease (CKD), Fibroblast Growth Factor 23 (FGF23) is markedly increased and has been proposed to interact with systemic inflammation. : In this cross-sectional study, we evaluated the correlations of intact FGF23, c-terminal FGF23, and the FGF23 ratio (c-terminal to intact) with some inflammatory cytokines in 111 elderly patients with advanced CKD not yet in dialysis. : Estimated glomerular filtration rate (eGFR) was inversely correlated with intact FGF23 and c-terminal FGF23, as well as with interleukin 6 (IL-6), tumor necrosis factor alpha (TNFα), and monocyte chemoattractant protein-1 (MCP-1).

Brain-Derived Neurotrophic Factor-Loaded Low-Temperature-Sensitive liposomes as a drug delivery system for repairing podocyte damage.

Podocytes, cells of the glomerular filtration barrier, play a crucial role in kidney diseases and are gaining attention as potential targets for new therapies. Brain-Derived Neurotrophic Factor (BDNF) has shown promising results in repairing podocyte damage, but its efficacy via parenteral administration is limited by a short half-life. Low temperature sensitive liposomes (LTSL) are a promising tool for targeted BDNF delivery, preserving its activity after encapsulation.

Targeted silencing of in a human model of osteoprogenitor cells results in the deregulation of the osteogenic differentiation program.

Introduction: The dysregulation of cell fate toward osteoprecursor cells associated with most -based disorders may lead to episodic extraskeletal or ectopic bone formation in subcutaneous tissues. The bony lesion distribution suggests the involvement of abnormal differentiation of mesenchymal stem cells (MSCs) and/or more committed precursor cells. Data from transgenic mice support the concept that is a crucial factor in regulating lineage switching between osteoblasts (OBs) and adipocyte fates.