Inflammatory Cell Markers as Indicators of Atherosclerotic Renovascular Disease

Endothelial Outgrowth Cells Shift Macrophage Phenotype and Improve Kidney Viability in Swine Renal Artery Stenosis

“…Several studies indicate that inflammation portends stenotic-kidney injury by increasing production and activity of cytokines, leading to microvascular damage, collagen deposition, matrix accumulation, and fibrosis 6, 24, 25 . Interstitial macrophage accumulation in swine RAS stimulates fibrosis and vascular rarefaction 7 .…”

“…Mounting data highlight inflammatory cells as important mediators of irreversible kidney damage 6 , which may contribute to the limited response to revascularization observed in RVH. We have previously shown in experimental renovascular disease increased stenotic-kidney expression of the pro-inflammatory cytokine monocyte-chemoattractant-protein (MCP-1), accompained by macrophage infiltration and microvascular rarefaction 7 .…”

When stenting in renal artery stenosis? Update on pathophysiology of ischemic nephropathy and management strategies

“…48 Furthermore, it is recognized that AT2 is a potent activator of inflammation 49 because the AT1R activation of T cells is capable of activating chemokine pathways, leading to inflammation. 50,51 Therefore, when the activation of IRAS takes place, it may trigger off a cascade of events that end up in glomerular and tubulo-interstitial fibrosis and in micro-vessel loss which is no longer reversible (Figure 4). 52 The importance of the role of imbalance, at medullary level, between O 2 supply and tubular work, correlated with the IRAS activation, can explain an apparent paradox which at times occurs in clinical practice: a rapid decrease in GFR can play a protective role and can favor the functional recovery after the revascularization, as reported by Murray et al, 53 who found that the faster the decline in GFR before revascularization, the better the renal function recovery after revascularization.…”

Diagnostic criteria for renovascular disease: where are we now?

“…Biopsy samples from advanced disease demonstrate progressive accumulation of inflammatory cells and interstitial fibrosis [44]. AT1 receptor activation of T cells is capable of activating sympathoadrenergic and chemokine pathways leading to vasoconstriction and inflammation [45]. Murine 2-kidney-1-clip hypertension models are characterized by stimulation of TGF-β and recruitment of other inflammatory cells as a consequence of the kidney injury [46].…”