Diabetic kidney disease (DKD) is one of the most common complications in diabetes mellitus and accounts for a large proportion of clinical nephrology practice. Studies have shown that the kallikrein–kinin system (KKS) may be involved in several pathogenic mechanisms that contribute to DKD, including oxidative stress, inflammatory cytokines, and profibrotic autacoids. This review focuses on recent research advance on the potential role of the KKS in the development of DKD and its clinical relevance.
A number of recent studies support the idea that there is a protective role of the KKS in diabetes. For example, agents that activate the KKS have shown strong renal protective effects that might highlight its potential to change the clinical practice. In addition, diabetic mice lacking both bradykinin B2 and B1 receptors have worse kidney lesions as compared with wild-type diabetic mice.
Current basic research has demonstrated that pharmacological activation of the KKS improves renal outcomes in diabetes. These findings suggest that this system may be a therapeutic target in preventing and treating DKD.
aDivision of Endocrinology and Metabolism, Huashan Hospital, Fudan University, Shanghai, China
bRenal Division, Joslin Diabetes Center, One Joslin Place, Boston, Massachusetts, USA
cInstitute of Endocrinology and Diabetology, Fudan University, Shanghai, China
Correspondence to Zhaoyun Zhang, MD, PhD, Division of Endocrinology and Metabolism, Huashan Hospital, Fudan University, 12 Wulumuqi Road, Shanghai 200040, China. Tel: +86 15000275016; fax: +86 21 52888286; e-mail: firstname.lastname@example.org