Metabolic syndrome (MS) is characterized by the clustering of obesity, hypertension (HTN), insulin resistance and lipid abnormalities, and increases future risk of Type 2 diabetes mellitus (T2DM) and cardiovascular disease (CVD). Despite the growing prevalence of MS, i.e. >40% of the US adult population above age 40 meets criteria, little is understood regarding the pathophysiology of the progression from MS to T2DM and/or CVD. Clustering of these risk factors, often initiated by excessive weight gain, increases CVD risk above that expected due to the risk factors alone, which suggests synergistic risk. In addition to atherosclerotic risk, the component parts of metabolic syndrome are associated with increased vascular stiffness, increased aortic pulsatility, and increased risk for renal dysfunction. Glomerular hyperfiltration, combined with increased arterial pulsatility, may lead to renal damage by transmission of pulsatile pressure to the renal capillary bed. This barotrauma may disturb the integrity of the renal membrane and lead to early proteinuria. Because of a unique combination of risks and pathophysiology, MS patients may be uniquely susceptible to hemodynamically mediated kidney damage, which if undetected becomes irreversible. This study will test the hypothesis that the renal damage in metabolic syndrome is related to aortic pulsatility via altered renal hemodynamics and oxidative stress. We will also test the hypothesis that early vascular and renal abnormalities, if detected, are reversible with aggressive lifestyle intervention and have the potential to be therapeutic targets in this population.
The PI of this project was: Nancy Sweitzer, MD, PhD
This project was funded by: Department of Medicine
The term of this project was: April 2011 to March 2020
The number of subjects scanned during this project was: 120