Urinary albumin excretion, endothelial dysfunction and cardiovascular risk: study in Bartter's/Gitelman's syndromes and relevance for hypertension

Increased urinary albumin excretion in uncomplicated hypertension has been associated recently with impaired vascular reactivity ( nitric oxide (NO)-dependent and -independent vasodilation) 1 and increased levels of adhesion molecules, 2 thereby suggesting that endothelial dysfunction is responsible for the increased cardiovascular ( CV) risk associated with albuminuria. 1,2 In light of these reports, we have used our human model of vascular tone control, Bartter's/Gitelman's syndromes (BS/GS) patients who have biochemical and hormonal characteristics typical of hypertension, yet normotension/hypotension, hyporesponsiveness to pressors and have reduced vascular resistance,(3-5) to assess the urinary albumin/creatinine ratio (UACR) as a potential marker of endothelial dysfunction. We found that UACR in BS/GS did not differ from healthy subjects, contrary to that found in hypertensive patients, thereby indirectly providing further support for the fact that increased UACR reflects endothelial dysfunction and its associated increased CV risk.