38 research outputs found
Influence of vegetated bed material on erosional patterns of meandering rivers: preliminary experimental results
Lateral variation in gravelly sediments and processes in an alluvial fan-fan-delta setting, north of Durgapur
A method for the analysis of pulse-height spectra containing gain-shift and zero-drift compensation
The Robustness of One-Dimensional, Time-Dependent, Ice-Flow Models: A Case Study from Storglaciären, Northern Sweden
Engaging Undergraduates in Soil Sustainability Decision-Making Through an InTeGrate Module
Waveform Optimization for Integrated Radar and Communication Systems Using Meta-Heuristic Algorithms
Changes of river bed pattern of a lowland river: effect of natural processes or anthropogenic intervention?
Dynamical stress in force chains of granular media traveling on a bumpy terrain and the fragmentation of rock avalanches
The relationship between albuminuria, MCP-1/CCL2 and interstitial macrophages in chronic kidney disease
Glomerular-derived proteins may activate tubular cells to express the macrophage-directed chemokine monocyte chemoattractant protein-1 (MCP-1/CCL2). Macrophages at interstitial sites have a central role in directing renal scarring. We have prospectively assessed the relationship between albuminuria, urinary MCP-1/CCL2, interstitial macrophage infiltration, in situ damage, and clinical outcomes in a large group of patients with chronic kidney disease. We studied 215 patients and quantified albumin–creatinine ratio (ACR), urinary MCP-1/CCL2, interstitial macrophage numbers, and in situ damage. ACR correlated with urinary MCP-1/CCL2 (correlation 0.499; P<0.001), interstitial macrophage numbers (correlation 0.481; P<0.001), and index of chronic damage (correlation 0.363; P<0.001). Macrophage numbers closely correlated with in situ damage (correlation 0.755; P<0.001). By multivariate analysis ACR, urinary MCP-1/CCL2, and interstitial macrophage numbers were interdependent. By Kaplan–Meier survival analysis albuminuria, urinary MCP-1/CCL2, interstitial macrophages, and chronic damage predict the outcome. ACR, macrophage numbers, chronic damage, and creatinine independently predicted renal survival. The association of ACR with other variables was strongest in patients with less advanced disease states. There is a close association between albuminuria, urinary MCP-1/CCL2, and interstitial macrophage infiltration with in situ damage and clinical outcomes. These findings support the hypothesis that albuminuria triggers tubular MCP-1/CCL2 expression with subsequent macrophage infiltration. These processes may represent the dominant pathway for the progression of renal injury before the establishment of advanced renal scarrin