Personalized Antifibrotic Therapy in CKD Progression.

Abstract

Chronic kidney disease (CKD) is a chronic disorder characterized by kidney fibrosis and extracellular matrix accumulation that can lead to end-stage kidney disease. Epithelial-to-mesenchymal transition, inflammatory cytokines, the TGF-β pathway, Wnt/β-catenin signaling, the Notch pathway, and the NF-κB pathway all play crucial roles in the progression of fibrosis. Current medications, such as renin-angiotensin-aldosterone system inhibitors, try to delay disease development but do not stop or reverse fibrosis. This review emphasizes the growing need for tailored antifibrotic medications for CKD treatment. Precision medicine, which combines proteomic, metabolomic, and genetic data, provides a practical way to personalize treatment regimens. Proteomic signatures, such as CKD273, and genetic markers, such as APOL1 and COL4A5, help in patient stratification and focused therapy development. Two recently developed antifibrotic medications, nintedanib and pirfenidone, have been proven to diminish fibrosis in preclinical animals. Additionally, research is being conducted on the efficacy of investigational drugs targeting CTGF and galectin-3 in the treatment of kidney fibrosis.