FN1 and diabetic kidney disease: (45) showed that both pharmacological blockade and genetic deficiency of CCR2 could alleviate renal tissue injury in diabetic mice by reducing albuminuria, blood urea nitrogen (BUN), plasma creatinine, histological changes, kidney fibronectin expression, macrophage recruitment, and inflammatory cytokine production in Ins2Akita and STZ-induced diabetic kidney disease.