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Urinary renin-angiotensin markers in polycystic kidney disease.

American journal of physiology. Renal physiology (2017-07-28)
Mahdi Salih, Dominique M Bovée, Lodi C W Roksnoer, Niek F Casteleijn, Stephan J L Bakker, Ronald T Gansevoort, Robert Zietse, A H Jan Danser, Ewout J Hoorn
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In autosomal dominant polycystic kidney disease (ADPKD), activation of the renin-angiotensin aldosterone system (RAAS) may contribute to hypertension and disease progression. Although previous studies have focused on circulating RAAS components, preliminary evidence suggests that APDKD may increase urinary RAAS components. Therefore, our aim was to analyze circulating and urinary RAAS components in ADPKD. We cross-sectionally compared 60 patients with ADPKD with 57 patients with non-ADPKD chronic kidney disease (CKD). The two groups were matched by sex, estimated glomerular filtration rate (eGFR), blood pressure, and RAAS inhibitor use. Despite similar plasma levels of angiotensinogen and renin, urinary angiotensinogen and renin excretion were five- to sixfold higher in ADPKD (

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