Extract

As clinicians, we often feel disarmed in front of the relentless decline of renal function in patients with diabetes despite optimal medical treatment.

In the last decade, inflammation and ways to target it have become probably the most promising therapeutic approach to tackle diabetic nephropathy (DN).

Research studies in experimental animal model of diabetes have implicated the innate immunity as an important pathogenic mechanism driving the development and progression of DN [1]. The innate immunity is a non-specific defence mechanism characterized by up-regulation of monocyte chemoattractant protein-1 (MCP-1) paralleled by an increase in macrophage infiltration in the glomeruli and tubular interstitium.

MCP-1 is an inflammatory cytokine that binds to its receptor CCR2, expressed mainly on monocytes and macrophages. The chronic activation of the MCP-1/CCR2 system, driven by the metabolic and haemodynamic perturbations seen in diabetes, is an important player in the pathogenesis of diabetic chronic microvascular complications and, specifically in the kidney, drives renal inflammation (macrophage tissue infiltration), fibrosis and ultimately loss of renal function.

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