Effect of salt load on the intrarenal angiotensin activity and receptor-mediated prorenin system in kidney fibrosis

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Although activation of intrarenal renin angiotensin system (RAS) is involved in the progression of kidney fibrosis, it is unknown how salt load that suppresses circulating RAS aggravates kidney fibrosis. This study demonstrated that high salt intake increased the apical membranous transition of (pro)renin receptor in collecting ducts and connecting tubules, resulting in the increased binding of prorenin and renin proteins without concomitant renin mRNA expression, followed by non-proteolytic activation of prorenin and angiotensin II generation, with resultant worsening of renal fibrosis in chronic anti-thymocyte serum nephritis on high salt intake.