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GW23-e1041
CORRELATION OF RENAL RESISTIVE INDEX, TUMOUR NECROSIS α AND INTERLEUKIN 10 WITH HYPERTENSIVE RENAL DAMAGE
  1. Yang Zhen1,
  2. Yu Xin2,
  3. Wang Xue-zhong1,
  4. Sha Yong1,
  5. Wang Jing-jing1,
  6. Jia Shao-bin1
  1. 1Heart Center, the General Hospital of Ningxia Medical University
  2. 2School of Laboratory Medicine, Ningxia Medical University

    Abstract

    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.

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