IL1B and diabetes mellitus: The high glucose environment induces RANK expression in glomerular podocytes, which mediates the development of diabetic nephropathy by promoting the production of ROS, TNF-α, Gal-3, and IL-1β.432 Kidney risk inflammatory signature (KRIS) consisting of 17 systemic proteins enriched in TNFR superfamily members has been identified to be associated with a 10-year risk of end-stage renal disease from both three independent cohorts of patients with type 1 and type 2 diabetes mellitus.435 Metabolic insufficiency due to mitochondrial damage is also a possible mechanism of nephritis.