“…Activation of the reninangiotensin system (RAS) causes secondary hyperfiltration, pressure diuresis, and sodium loss from the contralateral, nonstenotic kidney. Renal handling of other solutes is also affected by this hyperfiltration state, as reflected by findings of hypokalemia, alkalosis, hypercalciuria, glycosuria, and proteinuria, sometimes within the nephrotic range [2,4,8,10]. Several authors reported reversible cortical hyperechogenicity of the nonstenotic kidney, probably a consequence of hyperfiltration and tubulointerstitial damage [10,14].…”