CORRELATION OF RENAL RESISTIVE INDEX, TUMOUR NECROSIS [alpha] AND INTERLEUKIN 10 WITH HYPERTENSIVE RENAL DAMAGE

• Published in: Heart (British Cardiac Society) Vol. 98; p. E69
• Main Authors: Zhen, Yang, Xin, Yu, Xue-zhong, Wang, Yong, Sha, Jing-jing, Wang, Shao-bin, Jia
• Format: Journal Article
• Language: English
• Published: London BMJ Publishing Group LTD 01.10.2012
• ISSN: 1355-6037; 1468-201X
• DOI: 10.1136/heartjnl-2012-302920a.173

Objectives To investigate the changes of renal resistive index (RRI) and the serum levels of necrosis α (TNF-α) and interleukin 10 (IL-10) in patients with hypertensive renal damage, whereby to explore the correlation of RRI, TNF-α and IL-10 with the hypertensive renal damage. Methods Seventy three patients with primary hypertension were divided into two groups according to their urinary albumin excretion rate (UAER): normal buminuric hypertensive group (n=37), hypertensive renal damage group (n=36). RRI was measured using Doppler ultrasonography, serum TNF-α and IL-10 using radioimmune assay. Thirty normotensive healthy persons were selected as normotensive control group. Results RRI and TNF-α were significantly higher and IL-10 significantly lower in patients with essential hypertension than those in normotensive control group p<0.5), and in patients with hypertension, those with renal damage had higher RRI and TNF-α and a lower IL-10 than those without p<0.5), with a statistically significant difference among groups p<0.5). RRI, TNF-α and IL-10 were found to have correlations with UAER (r=0.801, p<0.01; r=0.703, p<0.01; r=-0.613, p<0.01), but no correlation with the level of blood pressure, and RRI positively correlated with TNF-α (r=0.609, p<0.001), negatively with IL-10 (r=-0.533, p<0.01). Conclusions RRI is remarkably increased in patients with hypertensive renal damage, whereby can be used as a parameter, together with UAER, in evaluating hypertensive renal damage. TNF-α is increased and IL-10 decreased significantly in patients with hypertensive renal damage, indicating that the imbalanced cytokine network may play a role in the pathological mechanisms of hypertensive renal damage.