Role of renal nerves in renal sodium retention of nephrotic syndrome

Abstract

To define the role of the renal nerves in the renal sodium retention of the nephrotic syndrome, experiments were conducted in rats given adriamycin to produce nephrotic syndrome. All rats developed proteinuria and hypoalbuminemia and exhibited edema formation. Adriamycin-injected nephrotic rats were subjected to bilateral renal denervation (ADRIADNX) or sham renal denervation (ADRIASHAM). Rats injected with adriamycin vehicle were subjected to bilateral renal denervation (DNX) or sham renal denervation (SHAM). Metabolic balance studies were carried out in all rats beginning on the 8th day after bilateral or sham renal denervation. Dietary sodium content was 210 meq/kg Na on days 8-12 and days 24-26 and was 10 meq/kg Na on days 13-23. Nephrotic rats demonstrated significantly greater overall (19 days) cumulative sodium balance than vehicle control rats, ADRIASHAM 8.47 +/- 0.81 vs. SHAM 5.74 +/- 0.34 meq Na, P less than 0.01. Bilateral renal denervation did not significantly affect overall cumulative sodium balance in the vehicle control rats, DNX 6.15 +/- 0.71 vs. SHAM 5.74 +/- 0.34 meq Na. However, bilateral renal denervation significantly decreased overall cumulative sodium balance in the nephrotic rats, ADRIADNX 6.59 +/- 0.56 vs. ADRIASHAM 8.47 +/- 0.81 meq Na, P less than 0.01. Results indicated that the increased renal sodium retention characteristic of nephrotic syndrome is dependent, in large part, on increased efferent renal sympathetic nerve activity.