P-398: Loss of renal reserve in obese hypertensive patients

To demonstrate the effects of obesity on renal hemodynamics and the role of renal kallikrein (rKal) and nitric oxide (NO) on renal response to oral protein load (renal reserve, RR), we studied 14 obese (BMI: 32.9 ±1.1, age: 50.5 ±0.9 yrs, SBP: 152.8 ±2.4mmHg, DBP 96.2 ±2.2mmHg, 5 males and 9 females) and 9 non obese hypertensive patients (BMI=22.9±1.1, age 50.6±2.7yrs, SBP=151.2±2.8 mmHg, DBP: 97.9±2.1mmHg, 4 males and 5 females). Hemodynamic and metabolic evaluations were conducted at basal conditions and after protein challenge moment (1g/kg of weight). Glomerular filtration rate (GFR) was estimated by clearance of inulin, and renal plasma flow (RPF) was calculated by the clearance of 131 orthoiodohippurate. We measured the levels of serum NO by the Griess reaction modified, and the urinary excretion of Kallikrein (Kal) by chromogenic substrate. After protein load there were significant increases of urinary Kal /Creat in both obese individuals (0.12±0.04 vs 0.29±0.06, p=0.002) and lean subjects (0.052±0.008 vs 0.22±0.02, p