The renal angiotensin system does not reveal its secrets with a cross-sectional analysis of urinary angiotensinogen levels

Abstract

The renal angiotensin system does not reveal its secrets with a cross-sectional analysis of urinary angiotensinogen levels Branko Braam I have been puzzled by the findings and the interpretation thereof presented by Zou et al.[1] in the Journal. Briefly, they report a positive correlation between sodium excretion and urinary angiotensinogen levels. Moreover, urine angiotensinogen levels were correlated with blood pressure. We were not informed about the clinical characteristics of the patients with higher versus lower blood pressure, and kidney function was not mentioned. This being said, as a pioneer in the intraluminal renin-angiotensin system dynamics [2-5], I am baffled by the interpretation of the results.The authors conclude that 'it is very likely that increased dietary sodium intake activates the intrarenal reninangiotensin system (RAS), as reflected by increased urinary angiotensinogen levels, and in turn increased BP'. There are dozens of studies indicating that low and not high sodium increases renal renin release, and this interpretation is completely at odds. There are two possible alternative explanations. One is that a high sodium diet decreases the luminal conversion angiotensinogen to angiotensins I and II, resulting in more shedding of angiotensinogen in the urine. This would be a protective mechanism. The other is that the group with the (salt-sensitive) higher blood pressure has an inappropriately elevated RAS.Anyhow, are we going to discard strong evidence for a reciprocal (renal) renin release with sodium intake? Evaluating urinary angiotensinogen levels as 'accurate read out' for the intrarenal RAS obviously leads to inconsistencies in the interpretation that warrant more thoughts. NavarLG, Lewis L, Hymel A, Braam B, Mitchell KD. Tubular fluid concentrations and kidney contents of angiotensins I and II in anesthetized rats.

Urinary Angiotensinogen Could Be a Prognostic Marker of the Renoprotection of Olmesartan in Metabolic Syndrome Patients

“…Others and we have previously reported that the urinary AGT excretion rate could be a marker of intrarenal RAS status in hypertension [9,16,17,18], as well as in CKD [7,19,20,21,22]. However, the effect of ARB on urinary AGT has not yet been examined in patients with metabolic syndrome.…”