The inflammatoryresponse dominated by NLRP3 inflammatoryvesicles, in combination with the inflammatory factorsIL-1β and IL-18, will promote the progression ofchronic kidney disease in diabetic patients [17], [18].Persistent glomerular and tubular injury in diabeticpatients dramatically aggravates renal impairment tothe point where the injury is irreversible, resulting inend-stage renal failure. Here, IL18 is linked to acute kidney injury.