Interleukin-18 contributes more closely to the progression of diabetic nephropathy than other diabetic complications

• Published in: Acta diabetologica Vol. 49; no. 2; pp. 111 - 117
• Main Authors: Fujita, Takayuki, Ogihara, Norikazu, Kamura, Yumi, Satomura, Atsushi, Fuke, Yoshinobu, Shimizu, Chie, Wada, Yuki, Matsumoto, Koichi
• Format: Journal Article
• Language: English
• Published: Milan Springer Milan 01-04-2012; Springer Nature B.V
• Subjects: Adult; Aged; Aged, 80 and over; C-Reactive Protein - immunology; cystatin C; Cytokines; Data processing; Diabetes; Diabetes Complications - etiology; Diabetes Complications - immunology; Diabetes Complications - pathology; Diabetes mellitus; Diabetes Mellitus, Type 2 - complications; Diabetic Nephropathies - etiology; Diabetic Nephropathies - immunology; Diabetic Nephropathies - pathology; Diabetic neuropathy; Disease Progression; Fatty acid-binding protein; Female; Glomerulus; Hemoglobin; Humans; Immune system; Inflammation; Inflammation Mediators - immunology; Interleukin 18; Interleukin-18 - immunology; Internal Medicine; Male; Medicine; Medicine & Public Health; Metabolic Diseases; Middle Aged; Nephropathy; Original Article; Oxidative stress; Oxidative stress; Diabetic nephropathy; Adipokine; Proinflammatory cytokine; High-sensitive CRP; Interleukin 18
• ISSN: 0940-5429; 1432-5233
• DOI: 10.1007/s00592-010-0178-4

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.