COL4A5 and chronic kidney disease: Emerging evidence indicates that AS progression shares pathological mechanisms with other CKDs, including inflammation, fibrosis, oxidative stress, and mitochondrial dysfunction9 A notable large-scale whole exome sequencing study has revealed that mutations in COL4A3, COL4A4, and COL4A5 collectively account for nearly 30% of all monogenic CKD cases, establishing AS as the second most common hereditary nephropathy after autosomal dominant polycystic kidney disease10.