Disturbed tumor necrosis factor system is linked with lower eGFR and chronic inflammation in hypertension

Insights

In hypertension, the tumor necrosis factor (TNF) system is linked to chronic inflammation and mild renal dysfunction. This disturbed TNF system appears more related to inflammation than insulin resistance in hypertensive patients.

Area of Science:

  • Cardiovascular Research
  • Metabolic Syndrome
  • Inflammation Biology

Background:

  • The link between tumor necrosis factor (TNF)-related factors and cardiorenal metabolic parameters in hypertension remains unclear.
  • Essential hypertension is associated with metabolic disturbances and inflammation.

Purpose of the Study:

  • To investigate the relationship between TNF-related parameters and cardiorenal metabolic factors in normotensive and hypertensive men.
  • To explore the association of TNF system with insulin resistance and chronic inflammation in essential hypertension.

Main Methods:

  • Cross-sectional study comparing normotensive men (NT, n=60) and treated essential hypertensive men (HT, n=89).
  • Analysis of TNF-related parameters (soluble TNF receptor 1 and 2, TNF-α) and cardiorenal metabolic factors.
  • Regression analysis to determine relationships between TNF parameters and clinical factors.

Main Results:

  • Hypertensive individuals exhibited higher insulin resistance and chronic inflammation than normotensive individuals.
  • Soluble TNF receptor levels were elevated in hypertensive men, while TNF-α levels were paradoxically lower.
  • TNF-related parameters correlated with renal dysfunction in both groups and with inflammation in hypertensive individuals.

Conclusions:

  • The dysregulated TNF system in hypertension is primarily associated with chronic inflammation.
  • The TNF system's link to insulin resistance in hypertension is less pronounced than its association with inflammation.
  • Renin-angiotensin system inhibitors improved insulin resistance but did not alter TNF-related parameters in hypertensive patients.
Abstract

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