The Role of Alterations in Alpha-Klotho and FGF-23 in Kidney Transplantation and Kidney Donation

Area of Science:

• Endocrinology
• Nephrology
• Cardiovascular Medicine

Background:

• Cardiovascular disease and mineral bone disorders are significant causes of mortality in chronic kidney disease patients, often persisting post-kidney transplant (KT).
• Hormonal imbalances after KT are linked to graft dysfunction and adverse outcomes.
• Fibroblast growth factor 23 (FGF-23) and its co-receptor α-Klotho play critical roles in integrating atherosclerosis, vascular calcification, mineral disorders, and osteodystrophy.

Purpose of the Study:

• To review and summarize current data on the role of FGF-23 and α-Klotho in the endocrine response to KT.
• To examine the impact of living kidney donation on these hormonal factors.
• To highlight research areas for enhancing diagnostics and therapeutics in KT recipients and donors.

Main Methods:

• Literature review and synthesis of existing data.
• Analysis of the integrated roles of FGF-23 and α-Klotho in post-transplant complications.
• Identification of knowledge gaps regarding long-term hormonal alterations.

Main Results:

• FGF-23 and α-Klotho are central to the pathophysiology of mineral and bone disorders and cardiovascular complications in CKD and post-KT.
• Kidney donation involves endocrine and metabolic adaptations, including transient FGF-23 increases and α-Klotho decreases.
• The long-term clinical relevance of these alterations in donors and recipients remains to be fully determined.

Conclusions:

• FGF-23 and α-Klotho are critical endocrine factors in the context of kidney transplantation and donation.
• Further research is needed to elucidate the long-term impact and clinical significance of FGF-23 and α-Klotho alterations.
• Targeting FGF-23 and α-Klotho pathways may offer novel diagnostic and therapeutic strategies for kidney transplant recipients and living donors.