Association between Hypertension, Kidney Disease & Obesity Samir T. Kumar, M. D. Nephrology Associates of Northern Illinois Certified Clinical Hypertension Specialist

JNC-7: Scathing Assessment 122 million Americans are overweight or obese. Mean sodium intake is approximately 4100mg for men and 2750 mg/day, 75% of which comes from processed foods Fewer than 20% of Americans engage in regular physical activity and fewer than 25% consume 5 or more servings of fruits and vegetables daily

Obesity and Hypertension More than 30% of US adult population is obese (BMI > 30) Any weight gain, even to a level that is not obese, is associated with increased risk of Hypertension BMI > 30 is a significant predictor of incident Hypertension Hypertensive effect of weight gain is related to increased abdominal visceral fat.

Obesity and Hypertension Each 10% increase in BMI is associated with a 3.9mm increase in SBP Dose dependent relationship between severity of obesity and risk of hypertension Obesity ClassOdds ratio of HTN Overweight1.7 Class 12.6 Class 23.7 Class 34.8

Obesity and Hypertension Africans in rural Cameroon – 10%, BMI is 22 Jamaica – 25%, BMI 25 African Americans in Illinois – 40% BMI 35

Obesity and Hypertension Adipose tissue is not just for storage Release of “Adipokines” (Leptin, Angiotensinogen, etc) Sympathetic over activity, blunted production of adiponectin, RAAS over activity Retention of salt and water, and oxidative stress leads to endothelial dysfunction and vascular proliferation

Trial of non-pharmacologic Interventions in the Elderly –TONE (Whelton et al, JAMA 1998) 975 men and women age years; hypertension controlled with 1 med Randomized to reduce sodium intake, weight loss, both or none After 3 months, antihypertensives were withdrawn 30 month follow up – number of normotensives 44% with both interventions, 35% with one, 16% with neither

Fructose and HTN Some data suggest than fructose intake may be a component of HTN in obesity and the metabolic syndrome American diets are high in sucrose (50% fructose) and high fructose corn syrup (55% fructose) Not confirmed in all studies Fructose appears to enhance sodium absorption in the intestine

Trials of Hypertension: Prevention II Study (Stevens et al Annals of Internal Med 2001) 595 moderate obese patients – 10-65% above IBW High normal DBP’s (83-89 mm Hg) Intense weight loss program 595 controls – observed 4.5 kg weight loss Significant reduction in BP and 65% lower risk of hypertension

Diet better than weight loss medications No. of RCTs No. of PtsChange in SBP (mmHg) Change in DBP (mmHg) Change in Body Weight (kg) Diet Orlistat Sibutramine

Does diet alone work for Hypertension? Sacks et al, NEJM 2001 – 412 patients average age 48 – SBP /DBP randomized to typical US diet US DASH diet, additionally 3 levels of sodium intake 30 days – significant benefit to both DASH and low sodium diets PREMIER trial – (Elmer et al, Annals of Int Med 2006) DASH diet vs Normal Pts prepared their own meals Only 1.1/0.9 difference in BP between the 2 groups

How about Bariatric Surgery? Batsis et al, Mayo Clinic proceedings 2008 Retrospective study 180 patients with bariatric surgery vs 157 without surgery Surgical group had 7/6 mm greater reduction in BP compared to non surgical group at 3.4 year follow up

How about Bariatric Surgery? Swedish obese subjects bariatric intervention Initial BP reduction of 4.4/5.5 mm Hg Did not persist 10 years out

Obesity/Sleep Apnea and HTN Sleep heart health study 2470 pts without HTN at enrollment Stratified by AHI (Apnea Hypopnia Index) AHIOdds Ratio for HTN events/hr events/hr1.54 >30 events/hr2.19

Treatment of Sleep Apnea Treatment with CPAP very effective for OSA symptoms Treatment with CPAP has had mixed results in pts with HTN, ineffective in several studies Pts with OSA who underwent weight loss had decrease in BP Relationship between OSA and HTN may be largely related to obesity Younger pts < 50 with resistant HTN respond better to CPAP.

Obesity and Focal Sclerosis Focal and Segmental glomerulosclerosis – is the most aggressive primary idiopathic Nephrotic syndrome Affects predominantly African Americans, untreated, almost 90% will have ESRD in 10 years Secondary FSGS – Obesity is an important cause Treatment of Obesity reduces proteinurea and stabilizes or improves renal function

Obesity and Chronic kidney disease Obesity accelerates progression of chronic kidney disease by increasing insulin resistance, increasing sympathetic activity and activating renin angiotensin aldosterone system ACE inhibitor therapy appears to be more effective in reducing risk of progression of chronic kidney disease in obese pts, highlighting the effects of activation of RAAS

Obesity and Chronic kidney disease Obesity is a well recognized risk factor for progression of chronic kidney disease, regardless of etiology KDIGO guidelines 2013 Undertake physical activity compatible with cardiovascular health and tolerance (aiming for at least 30 mins, 5 times/wk) Achieve a healthy weight (BMI kg/m2) Stop smoking