Since muscles are the major source of pGSN biosynthesis, and patients with end-stage renal disease (ESRD) often exhibit muscle depletion, malnutrition, hypoalbuminemia, and diffuse tissue injury, it is suggested that extracellular gelsolin declines due to both impaired synthesis and accelerated actin-related clearance of pGSN [75]. This evidence concerns the gene GSN and chronic kidney disease.