K036: Angiotensin II modulates the changes in renal hemodynamic induced by angioplasty of renal artery stenosis

The beneficial effects on glomerular filtration rate (GFR) induced by angioplasty (PTRA) of renal artery stenosis (RAS) are thought to derive from an increase in renal plasma flow (RPF); however it is possible that the modifications in the activity of the renin angiotensin system following PTRA partecipate in modulating renal hemodynamics both in the stenotic kidney (SK) and in the contralateral normal kidney (CK). In 14 patients (5 mononephric) we measured mean arterial pressure (MAP, mmHg) and, by radioisotopic techniques, RPF (ml/min), glomerular filtration rate (GFR, ml/min), filtration fraction (FF) and renal resistance (RR) in 16 SK, 7 CK and in 18 normal kidneys (NK) from patients with essential hypertension. In those patients with SK who were not on treatment with ACE inhibitors, we collected blood samples from the renal veins and from the aorta for the measurement of plasma renin activity (PRA, ng/ml/h) and of angiotensin II (AII, pg/ml) and calculated the veno-arterial difference (V − A) for both across SK and CK; the renin secretion rate (RSR, ng AI/ml) was also calculated multiplying (V − A) by RPF. All these studies were repeated within 7 days after a technically successful PTRA which reduced the average degree of RAS from 82% to 7% and the MAP from 116 ± 3 to 109 ± 3 mmHg. (See Table) SK (n = 16) RPF GFR FF RR RSR ΔAII before PTRA 138 ± 14 34 ± 4 25 ± 2 1.1 ± 0.1 220 ± 84 1.6 ± 3.8 after PTRA 185* ± 14 42* ± 4 23 ± 2 0.7* ± 0.1 63* ± 19 −4.6 ± 2.4 CK (n = 7) RPF GFR FF RR RSR ΔAII before PTRA 213° ± 21 62° ± 10 29 ± 3 0.6° ± 0.1 −25° ± 28 −4.8 ± 3.4 after PTRA 235° ± 24 58° ± 8 25 ± 4 0.5 ± 0.1 34* ± 16 −6.3 ± 4.3 *p < 0.05 before vs after PTRA °p < 0.05 SK vs CK. In NK GFR and FF were significantly lower than in CK (41 ± 3 ml/min and 25% respectively, p < 0.05 for both), whereas RPF and RR were similar (182 ± 12 ml/min and 0.7 respectively). In SK the percent increase in GFR and RPF induced by PTRA were respectively 36% and 50% whereas the FF and RR were decreased by 4% and 28%; also in CK inspite of an increase in RPF of 15% and a decrease of RR by 12%, the GFR and FF were reduced respectively by 4% and 11%. These results suggest that in SK the amelioration in GFR induced by PTRA is lower than that expected from the increase in RPF because of the fall in FF which most likely is derived from the withdrawal of the effects of AII on postglomerular efferent arteriole.