Abstract
Over the last decade, numerous studies have demonstrated that inflammation is involved in the cascade of events that lead to renal complications in patients with diabetic kidney disease [1]. Experimental studies highlighted the pathogenic role of inflammatory processes at the cellular and molecular levels. Observational studies have translated these findings to the human situation and have consistently shown that diabetic patients with higher levels of inflammatory markers in their blood or urine are at higher risk of renal function decline. These studies raise the possibility that anti-inflammatory interventions may slow the progression of diabetic kidney disease.
Highlights
Abbreviations CCL2 C-C motif chemokine ligand 2 CCR2 C-C motif chemokine receptor 2 MCP-1 Monocyte chemotactic protein-1 non-steroidal anti-inflammatory drugs (NSAIDs) Non-steroidal anti-inflammatory drugs
Whether anti-inflammatory properties contributed to the alleged long-term renoprotective effects of NSAIDs could not be determined at the time the studies were performed because specific assays for inflammatory markers were not available
In recent years various novel inflammatory components have been discovered. These inflammatory components often interact and collectively form a complex interplay through which inflammation contributes to the development and progression of diabetic kidney disease [1]
Summary
Abbreviations CCL2 C-C motif chemokine ligand 2 CCR2 C-C motif chemokine receptor 2 MCP-1 Monocyte chemotactic protein-1 NSAIDs Non-steroidal anti-inflammatory drugs. Whether anti-inflammatory properties contributed to the alleged long-term renoprotective effects of NSAIDs could not be determined at the time the studies were performed because specific assays for inflammatory markers were not available. The effects of emapticap on albuminuria persisted during the 12-week observational study period following the cessation of study medication [6].
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