Abstract

Background: Hcy is a sulfhydryl amino acid in the metabolism of methionine. It has been recognized as an independent risk factor for cardiovascular disease. In recent years, the relationship between hyperhomocysteinemia and renal disease has received attention from many researchers. However, the specific mechanisms by which Hcy plays a role in cardiovascular pathology in patients with chronic kidney disease are complex.
Methods: We consulted the relevant literature and sorted and summarized it.
Results: Multiple mechanisms of hyperhomocysteinemia-induced renal injury are summarized in detail from different perspectives, including oxidative stress, vascular endothelial damage, inflammatory response, cellular autophagy, apoptosis, fibrosis, and epigenetic regulation.
Conclusions: Hyperhomocysteinemia acts synergistically through multiple pathways, leading to glomerulosclerosis, tubular atrophy, and interstitial fibrosis, and ultimately accelerating renal failure. These mechanisms are complex and interrelated, suggesting that a comprehensive intervention strategy may achieve the ultimate goal of reducing renal injury.

DOI: 10.7754/Clin.Lab.2025.250335