Abstract
Currently available treatments of diabetic kidney disease (DKD) remain limited despite improved understanding of DKD pathophysiology. The complement system is a central part of innate immunity, but its dysregulated activation is detrimental and results in systemic diseases with overt inflammation. Growing evidence suggests complement activation in DKD. With existent drugs and clinical success of treating other kidney diseases, complement inhibition has emerged as a potential novel therapy to halt the progression of DKD. This article will review DKD, the complement system's role in diabetic and non-diabetic disease, and the potential benefits of complement targeting therapies especially for DKD patients.
Highlights
Diabetic kidney disease (DKD) is a common microvascular complication of diabetes mellitus
Diabetic kidney disease is a frequent complication of diabetes and the leading cause of chronic kidney disease worldwide
The complement system is hyper-activated in DKD and has been recognized as the main mechanism of disease progression
Summary
Diabetic kidney disease (DKD) is a common microvascular complication of diabetes mellitus. The success of C5 blockade by eculizumab in atypical HUS [6] has tremendously improved clinical outcomes, and the preliminary data on other glomerular diseases such as ANCA-associated vasculitis (AAV) is encouraging [7] Both mice and human data suggested the role of complement activation in the development of acute and chronic kidney injury. Animal models of diabetes have illuminated a deeper understanding of the potential role for the complement system in disease pathogenesis [See [40] for an extensive review; Table 1] These preclinical studies reported an association between intrarenal C3 deposition and DKD in both T1D [45, 46] and T2D models [47].
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