Abstract
Chronic kidney disease has become a major medical issue in recent years due to its high prevalence worldwide, its association with premature mortality, and its social and economic implications. A number of patients gradually progress to end-stage renal disease (ESRD), requiring then dialysis and kidney transplantation. Currently, approximately 40% of patients with diabetes develop kidney disease, making it the most prevalent cause of ESRD. Thus, more effective therapies for diabetic nephropathy are needed. In preclinical studies of diabetes, anti-inflammatory therapeutic strategies have been used to protect the kidneys. Recent evidence supports that immune cells play an active role in the pathogenesis of diabetic nephropathy. Th17 immune cells and their effector cytokine IL-17A have recently emerged as promising targets in several clinical conditions, including renal diseases. Here, we review current knowledge regarding the involvement of Th17/IL-17A in the genesis of diabetic renal injury, as well as the rationale behind targeting IL-17A as an additional therapy in patients with diabetic nephropathy.
Highlights
Diabetic nephropathy (DN) is a significant microvascular complication of diabetes
The epidemic of type 2 diabetes is the main cause of chronic kidney disease (CKD) worldwide, which leads to premature death and end-stage renal disease (ESRD)
Due to the complex mechanisms involved in the onset of renal injury in diabetes, it is highly unlikely that new anti-diabetic drugs, even when used appropriately and rationally, would halt the progression of DN, as evidenced by the persisting residual risk
Summary
The epidemic of type 2 diabetes is the main cause of chronic kidney disease (CKD) worldwide, which leads to premature death and end-stage renal disease (ESRD). In the absence of DN, mortality among diabetic patients is comparable to that of the general population [1,2]. CKD is expected to become the fifth global cause of death by 2040, and the second in long lived countries before the end of the century, mainly driven by DN [3,4]. We discuss the novel findings that support the contribution of an inflammatory microenvironment to the pathogenesis of DN. The potential for anti-inflammatory therapeutic strategies is discussed, remarking about the importance of Th17 mediated immune response and its effector cytokine, interleukin 17A (IL-17A)
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