Adipokines and their Relation to Endothelial Dysfunction in Patients with Chronic Kidney Disease

Madhusudan Ambarkar1, Srinivasarao V L N Pemmaraju2, Sivakrishna Gouroju3

  • 1PhD Scholar, Department of Biochemistry, Sri Venkateswara Institute of Medical Sciences (SVIMS) , Alipiri Road, Tirupati, Andhra Pradesh, India .

Insights

Chronic kidney disease (CKD) is linked to cardiovascular issues due to altered adipokines and inflammation. Increased interleukin-6 (IL-6) in CKD negatively impacts nitric oxide (NO) levels, contributing to endothelial dysfunction.

Area of Science:

  • Nephrology
  • Cardiology
  • Biochemistry

Background:

  • Chronic Kidney Disease (CKD) patients face elevated cardiovascular disease (CVD) risks.
  • Reduced nitric oxide (NO) bioavailability and inflammation are key factors in CKD-associated endothelial dysfunction (ED) and CVD.
  • Adipose tissue-derived factors (adipokines) are implicated in inflammation and ED within CKD.

Purpose of the Study:

  • To compare adipokine, inflammatory, and ED marker concentrations in CKD patients versus healthy controls.
  • To investigate the associations between adipokines, inflammation, and ED in CKD patients across different disease stages.

Main Methods:

  • 120 CKD patients were categorized into three groups based on Glomerular Filtration Rate (GFR) (Stages I-V), alongside 40 healthy controls.
  • Measurements included adiponectin, leptin, Interleukin-10 (IL-10), Interleukin-6 (IL-6), tumor necrosis factor-alpha (TNF-α) via ELISA, high-sensitivity C-reactive protein (hsCRP) via immunoturbidimetry, and NO via Griess method.
  • Statistical analyses included Mann-Whitney U, ANOVA, Kruskal-Wallis, Spearman's rank correlation, and linear regression.

Main Results:

  • CKD patients exhibited significantly higher leptin, IL-6, TNF-α, IL-6/IL-10 ratio, and hsCRP, with lower adiponectin, IL-10, and NO compared to controls (p<0.05).
  • Within CKD groups, adiponectin, leptin, IL-6, IL-6/IL-10 ratio, and TNF-α increased, while IL-10 decreased progressively with declining GFR (p<0.05).
  • Interleukin-6 (IL-6) showed a significant negative correlation with NO (r=-0.557; p=0.005) and a negative association in linear regression (B±SE=-0.038±0.11; p=0.002) in advanced CKD stages.

Conclusions:

  • Altered adipokine profiles in CKD, progressing with renal dysfunction, contribute to inflammation.
  • This inflammatory state, coupled with adipokine changes, exacerbates endothelial dysfunction (ED).
  • The study highlights a pathway linking altered adipokines and inflammation to ED and cardiovascular events in CKD patients.
Abstract

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