Key result
Bartter's and Gitelman's syndromes are linked to ~3-fold higher TNF-alpha levels versus controls.
Why the study?
The relationship between inflammation and high angiotensin II levels in Bartter's and Gitelman's syndromes, which do not develop hypertension or cardiovascular remodeling, was unclear.
Observational
Absolute Event Rate: 10.5% vs 3.68%
p-value: p=0.0001
Despite high angiotensin II levels, patients with Bartter's and Gitelman's syndromes do not show generalized increases in inflammatory markers, except for TNF-alpha, providing insight into vascular biology and hypertension.
TNF-α elevation in Bartter's/Gitelman's syndromes should not change practice; leaves open selective inflammatory pathways in high-angiotensin states.
BACKGROUND: Inflammation has been increasingly recognized as playing a critical role in hypertension and atherosclerosis as reflected by overexpression and increased production of a variety of pro-inflammatory mediators. As angiotensin II (Ang II) also plays a major role in these diseases, the relationship between inflammation and Ang II has drawn increasing scrutiny. This study explores Ang II effects in Bartter's and Gitelman's syndromes (BS/GS) which do not develop hypertension and related cardiovascular remodelling and atherosclerosis, in spite of high Ang II levels and activation of the renin-angiotensin-aldosterone system while the NO system is up-regulated. METHODS: We evaluated the plasma levels of inflammation-associated markers, C-reactive protein (CRP), serum amyloid A (SAA), vascular cell adhesion molecules (VCAM) and intercellular adhesion molecules (ICAM), and the inflammation-related cytokines interleukin-6 (IL-6) and tumour necrosis factor-alpha (TNF-alpha) using immunonephelometric and ELISA-based assays. RESULTS: The study demonstrated that all markers of inflammation except TNF-alpha, were unchanged in BS/GS (2.51+/-0.62 mg/l in BS/GS vs 1.7+/-0.6 in controls for CRP; 4.56+/-1.09 mg/l in BS/GS vs 4.51+/-1.0 for SAA; 1.84+/-0.27 ng/l in BS/GS vs 2.1+/-0.3 for IL-6; 449+/-83 ng/ml in BS/GS vs 410+/-92 for VCAM and 234+/-26 ng/ml in BS/GS vs 185+/-22 for ICAM), while TNF-alpha was increased (10.5+/-2.03 vs 3.68+/-0.2, P = 0.0001). CONCLUSIONS: The results of this study stress the critical role played by Ang II in controlling vascular biology including inflammation-related processes as well as highlighting the utility of BS/GS in investigating these pathways.
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Davis et al. (2006) conducted an observational in Bartter's and Gitelman's syndromes. Bartter's and Gitelman's syndromes vs. Controls was evaluated on Plasma levels of TNF-alpha (p=0.0001). Patients with Bartter's and Gitelman's syndromes had significantly increased levels of TNF-alpha (10.5 vs 3.68, P=0.0001) compared to controls, while other inflammatory markers remained unchanged.
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