2007
DOI: 10.1097/maj.0b013e3180959e4e
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Obesity-Hypertension: Emerging Concepts in Pathophysiology and Treatment

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Cited by 34 publications
(24 citation statements)
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“…In the current analysis, we adjusted for many metabolic risk factors at baseline; this fully attenuated the relationship between BMI and development of kidney disease while the relationship between WHR and kidney disease remained robust, suggesting that WHR identifies additional risk beyond that suggested by pre-existing diabetes, hypertension and dyslipidemia. Additionally other unmeasured factors associated more with visceral obesity than subcutaneous obesity, including leptin, plasminogen activator inhibitor-1, and angiotensinogen, may contribute to incident kidney disease (24). The differences in our study between WHR and BMI may reflect the fact that they assess different features of obesity and potentially different forms of fat (central obesity and visceral fat with WHR versus subcutaneous and total fat with BMI).…”
Section: Discussioncontrasting
confidence: 39%
“…In the current analysis, we adjusted for many metabolic risk factors at baseline; this fully attenuated the relationship between BMI and development of kidney disease while the relationship between WHR and kidney disease remained robust, suggesting that WHR identifies additional risk beyond that suggested by pre-existing diabetes, hypertension and dyslipidemia. Additionally other unmeasured factors associated more with visceral obesity than subcutaneous obesity, including leptin, plasminogen activator inhibitor-1, and angiotensinogen, may contribute to incident kidney disease (24). The differences in our study between WHR and BMI may reflect the fact that they assess different features of obesity and potentially different forms of fat (central obesity and visceral fat with WHR versus subcutaneous and total fat with BMI).…”
Section: Discussioncontrasting
confidence: 39%
“…Several previous studies showed that being obese or overweight increased the risk of cardiovascular disease, diabetes, hypertension, dyslipidemia, and renal dysfunction (Mokdad et al 2003;Qureshi et al 2005;Gu et al 2008). The relationship between increased BMI and blood pressure may incorporate other non-traditional risk factors not examined in this report, including increased C-reactive protein (Ridker et al 2002), amyloid A (Poitou et al 2006), hyperlipidemia (Qureshi et al 2005;Gu et al 2008), cytokines (Honda et al 2006), homocysteine (Homocysteine Studies Collaboration 2002), oxidative stress (Drüeke et al 2002), hyperleptinemia (Mathew et al 2007), increased sympathetic activity (Masuo et al 2000), renal hyperfiltration (Knight and Imig 2007) and gamma-glutamyl transferase activity (Kawamoto et al 2008) caused by insulin resistance, and the renin-angiotensin system (Engeli et al 1999). All these risk factors result in atherosclerosis, and prehypertension and hypertension may be complicated by both the severity and duration of atherosclerosis, and vice versa.…”
Section: Discussionmentioning
confidence: 85%
“…BMI is the most important determinant of insulin resistance, while TG and HDL-C levels might be good markers of insulin resistance in non-obese patients with type 2 diabetes mellitus in Korea (Chang et al 2004). Moreover, Increased BMI and insulin resistance may be associated with other non-traditional risk factors not examined in this study, including low-grade inflammation (i.e., C-reactive protein) (Visser et al 1999), oxidative stress (Krzystek-Korpacka et al 2008), dyslipidemia (Kishimoto et al 2009), hyperleptinemia (Mathew et al 2007), increased sympathetic activity (Masuo et al 2000), hyperfiltration caused by insulin resistance (Knight and Imig 2007), renin-angiotensin system (Rossi et al 2008), and elevated cytokines (Khaodhiar et al 2004). All these risk factors that are induced by increased BMI result in insulin resistance.…”
Section: Discussionmentioning
confidence: 99%