A New Surgical Approach to the Treatment of Renovascular Hypertension by Intervention on the Renal Vein. An Experimental Study

Abstract

Renovascular hypertension produced by stenosis of the renal artery and its branches is the most common curable form of secondary hypertension. The pathophysiological background is based on activation of the renin-angiotensin-aldosterone system (RAAS), with imbalance between renin production by the kidney and renin degradation by the liver. The aim of this experimental study was to examine whether deviation of renin-rich blood from the renal vein of the affected kidney into the portal circulation by splenorenal venous anastomosis can ameliorate renovascular hypertension. Pigs were used as the experimental model because, in addition to the similarity to humans of their anatomy and physiology, they have been found capable of developing chronic renovascular hypertension. After the establishment of unilateral left renal artery stenosis and hypertension in the pigs, we created a renal-portal venous shunt by means of a splenorenal anastomosis. Ultrasonography (U/S) and angiography were used to evaluate the renal artery stenosis and the renal-portal shunt. Successive measurement was made of arterial blood pressure (BP) and the level of renin in blood samples collected at every stage of the experiment, to evaluate the effectiveness of the procedure. Histological examination was used to evaluate the effects of the renal-portal shunt on the kidney and the liver two months after the surgical procedure. Following the creation of the left renal artery stenosis, both blood renin levels and mean BP increased, as expected, from 1.23±0.06 ng/ml/h and 85.6±0.5 mm Hg at baseline to 4.59±0.02 ng/ml/h and 126±1.76 mm Hg, respectively. After deviation of the renal vein the blood renin levels returned to normal (1.59±0.07 ng/ml/h) with a concomitant reduction of the mean BP to 91±2 mm Hg. Significant correlation was observed between changes in renin levels and mean BP. Both the kidney and the liver remained macroscopically and histologically intact at the end of the experiment. Deviation into the portal system of the renal venous blood from the kidney affected by renal artery stenosis can result in total degradation by the liver of the high amounts of renin generated by the RAAS and ameliorate renovascular hypertension. This surgical strategy could be of benefit to individuals with fibromuscular or atheromatous lesions in the distal region of the renal artery or its branches, which are not amenable to balloon angioplasty or surgical revascularization.