title: Interleukin-18 contributes more closely to the progression of diabetic nephropathy than other diabetic complications.
abstract: Diabetic complication is comprised of a wide variety of pathophysiological factors involving proinflammatory cytokines, adipokines, and oxidative stress, among others. Each of these complications differs in their incidence and the stage of their occurrence. We examined cytokines and stress markers in 48 patients with type 2 diabetes mellitus and compared the difference of their contribution to pathogenesis between nephropathy and other diabetic complications. Hemoglobin A1c correlated with the level of low-density lipoprotein-cholesterol, and significantly elevated in the severe macroangiopathy group. Cystatin C increased in the severe microangiopathy groups but did not increase in the macroangiopathy group. The levels of interleukin 18 (IL-18), high-sensitive CRP (H-CRP), liver-type fatty acid binding protein, and 8-hydroxy-2-deoxyguanosine increased in the severe microangiopathy group. These data suggest the participation of proinflammatory signaling and oxidative stress in the progression of microangiopathy. In particular, IL-18 and H-CRP were significantly elevated only in the severe nephropathy group but did not significantly elevate in other complications. These data suggest another effect of IL-18 on glomerulus in addition to its proinflammatory effect. In conclusion, we propose that IL18 has a specific role that contributes more closely to the progression of diabetic nephropathy than other diabetic complications.
authors.affiliation: Department of Nephrology, Hypertension and Endocrinology, Nihon University School of Medicine, Itabashiku, Tokyo, Japan. tfujita@med.nihon-u.ac.jp
authors.forename: Takayuki
authors.initials: T
authors.lastname: Fujita
authors.forename: Norikazu
authors.initials: N
authors.lastname: Ogihara
authors.forename: Yumi
authors.initials: Y
authors.lastname: Kamura
authors.forename: Atsushi
authors.initials: A
authors.lastname: Satomura
authors.forename: Yoshinobu
authors.initials: Y
authors.lastname: Fuke
authors.forename: Chie
authors.initials: C
authors.lastname: Shimizu
authors.forename: Yuki
authors.initials: Y
authors.lastname: Wada
authors.forename: Koichi
authors.initials: K
authors.lastname: Matsumoto
mesh_terms: D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002097:C-Reactive Protein / Q000276:immunology; D048909:Diabetes Complications / Q000209:etiology / Q000276:immunology / Q000473:pathology; D003924:Diabetes Mellitus, Type 2 / Q000150:complications*; D003928:Diabetic Nephropathies / Q000209:etiology / Q000276:immunology* / Q000473:pathology; D018450:Disease Progression; D005260:Female; D006801:Humans; D018836:Inflammation Mediators / Q000276:immunology*; D020382:Interleukin-18 / Q000276:immunology*; D008297:Male; D008875:Middle Aged
chemical_list: D018836:Inflammation Mediators; D020382:Interleukin-18; D002097:C-Reactive Protein