Abstract
Excerpt: Fibrosis of the kidney is the hallmark and the final common pathway of chronic kidney disease (CKD) progression, regardless of underlying etiology. Fibrosis is characterized by excessive production and deposition of extracellular matrix (ECM) proteins mainly in the kidney interstitium and results in structural damage, impairment of renal function, and eventually end-stage renal disease (ESRD). The most abundant collagens in the interstitial matrix of the kidney are collagen type I (COL I) and III (COL III). In renal fibrosis, these collagens are upregulated and the activity of the proteases responsible for their remodeling is altered. In this study, we used a sub-cohort of the Chronic Renal Insufficiency Cohort (CRIC) to examine the association of serum PRO-C6, a biomarker for type VI collagen formation and urine C3M, a biomarker for type III collagen degradation with a composite endpoint (ESRD or 50% decline in eGFR).