Plasma and urine levels of resistin and adiponectin in chronic kidney disease

Subhashini Yaturu, Ramasubbareddy Dhanireddy, Justin Rains, Sushil K. Jain

Research output: Contribution to journalArticle

44 Citations (Scopus)

Abstract

Background: Subjects with chronic kidney disease (CKD) have an increased risk of developing coronary atherosclerosis. Adipocyte hormones, resistin and adiponectin are implicated in insulin resistance and atherosclerosis. However, few studies in the literature address the role of adipocyte hormones in CKD. The aim of this study was to compare the levels of resistin, adiponectin and other inflammatory markers in subjects with CKD with those of the control subjects. Materials and methods: In a cross-sectional study, we measured basal metabolic panel, fasting lipid panel and levels of glucose, resistin, adiponectin, insulin, C-reactive protein (CRP) and TNF-α in 43 subjects with CKD compared with those of 34 control subjects. We also measured the resistin and adiponectin levels in urine samples (16). Results: Subjects with CKD have increased insulin levels and insulin resistance index (IRI). Compared with controls, subjects with CKD had increased levels of resistin (5.12 ± 3.2 vs.7.5 ± 5.9; p < 0.05), CRP (1.7 ± 2.2 vs. 5.97 ± 6.0; p < 0.0005), and TNF-α (3.4 ± 2.0 vs. 5.2 ± 3.5; p < 0.005). Resistin levels correlate with CRP and TNF-α, even with BMI as a covariate. Although 60% of subjects with CKD have CAD, e plasma levels of adiponectin were not decreased in subjects with CKD compared with controls (17.02 ± 9.8 vs. 16.40 ± 9.0 with p value 0.78). Urinary adiponectin levels correlate inversely with GFR (r = -0.4; p < 0.05) and plasma adiponectin levels (r = 0.9; p < 0.0001). Conclusions: Subjects with CKD had normal levels of plasma adiponectin despite the adverse metabolic environment for CAD. In addition, this study demonstrates the relationship between resistin and TNF-α in subjects with CKD and suggests that resistin may play a role in the sub-clinical inflammation associated with CKD, suggesting that adiponectin clearance may be decreased as shown by the inverse correlation of urinary adiponectin with GFR.

Original languageEnglish (US)
Pages (from-to)1-5
Number of pages5
JournalCytokine
Volume37
Issue number1
DOIs
StatePublished - Jan 1 2007

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Resistin
Adiponectin
Chronic Renal Insufficiency
Urine
Plasmas
C-Reactive Protein
Insulin
Adipocytes
Insulin Resistance
Computer aided design
Hormones
Coronary Artery Disease
Fasting
Atherosclerosis
Cross-Sectional Studies

All Science Journal Classification (ASJC) codes

  • Immunology and Allergy
  • Immunology
  • Biochemistry
  • Hematology
  • Molecular Biology

Cite this

Plasma and urine levels of resistin and adiponectin in chronic kidney disease. / Yaturu, Subhashini; Dhanireddy, Ramasubbareddy; Rains, Justin; Jain, Sushil K.

In: Cytokine, Vol. 37, No. 1, 01.01.2007, p. 1-5.

Research output: Contribution to journalArticle

Yaturu, Subhashini ; Dhanireddy, Ramasubbareddy ; Rains, Justin ; Jain, Sushil K. / Plasma and urine levels of resistin and adiponectin in chronic kidney disease. In: Cytokine. 2007 ; Vol. 37, No. 1. pp. 1-5.
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AU - Yaturu, Subhashini

AU - Dhanireddy, Ramasubbareddy

AU - Rains, Justin

AU - Jain, Sushil K.

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N2 - Background: Subjects with chronic kidney disease (CKD) have an increased risk of developing coronary atherosclerosis. Adipocyte hormones, resistin and adiponectin are implicated in insulin resistance and atherosclerosis. However, few studies in the literature address the role of adipocyte hormones in CKD. The aim of this study was to compare the levels of resistin, adiponectin and other inflammatory markers in subjects with CKD with those of the control subjects. Materials and methods: In a cross-sectional study, we measured basal metabolic panel, fasting lipid panel and levels of glucose, resistin, adiponectin, insulin, C-reactive protein (CRP) and TNF-α in 43 subjects with CKD compared with those of 34 control subjects. We also measured the resistin and adiponectin levels in urine samples (16). Results: Subjects with CKD have increased insulin levels and insulin resistance index (IRI). Compared with controls, subjects with CKD had increased levels of resistin (5.12 ± 3.2 vs.7.5 ± 5.9; p < 0.05), CRP (1.7 ± 2.2 vs. 5.97 ± 6.0; p < 0.0005), and TNF-α (3.4 ± 2.0 vs. 5.2 ± 3.5; p < 0.005). Resistin levels correlate with CRP and TNF-α, even with BMI as a covariate. Although 60% of subjects with CKD have CAD, e plasma levels of adiponectin were not decreased in subjects with CKD compared with controls (17.02 ± 9.8 vs. 16.40 ± 9.0 with p value 0.78). Urinary adiponectin levels correlate inversely with GFR (r = -0.4; p < 0.05) and plasma adiponectin levels (r = 0.9; p < 0.0001). Conclusions: Subjects with CKD had normal levels of plasma adiponectin despite the adverse metabolic environment for CAD. In addition, this study demonstrates the relationship between resistin and TNF-α in subjects with CKD and suggests that resistin may play a role in the sub-clinical inflammation associated with CKD, suggesting that adiponectin clearance may be decreased as shown by the inverse correlation of urinary adiponectin with GFR.

AB - Background: Subjects with chronic kidney disease (CKD) have an increased risk of developing coronary atherosclerosis. Adipocyte hormones, resistin and adiponectin are implicated in insulin resistance and atherosclerosis. However, few studies in the literature address the role of adipocyte hormones in CKD. The aim of this study was to compare the levels of resistin, adiponectin and other inflammatory markers in subjects with CKD with those of the control subjects. Materials and methods: In a cross-sectional study, we measured basal metabolic panel, fasting lipid panel and levels of glucose, resistin, adiponectin, insulin, C-reactive protein (CRP) and TNF-α in 43 subjects with CKD compared with those of 34 control subjects. We also measured the resistin and adiponectin levels in urine samples (16). Results: Subjects with CKD have increased insulin levels and insulin resistance index (IRI). Compared with controls, subjects with CKD had increased levels of resistin (5.12 ± 3.2 vs.7.5 ± 5.9; p < 0.05), CRP (1.7 ± 2.2 vs. 5.97 ± 6.0; p < 0.0005), and TNF-α (3.4 ± 2.0 vs. 5.2 ± 3.5; p < 0.005). Resistin levels correlate with CRP and TNF-α, even with BMI as a covariate. Although 60% of subjects with CKD have CAD, e plasma levels of adiponectin were not decreased in subjects with CKD compared with controls (17.02 ± 9.8 vs. 16.40 ± 9.0 with p value 0.78). Urinary adiponectin levels correlate inversely with GFR (r = -0.4; p < 0.05) and plasma adiponectin levels (r = 0.9; p < 0.0001). Conclusions: Subjects with CKD had normal levels of plasma adiponectin despite the adverse metabolic environment for CAD. In addition, this study demonstrates the relationship between resistin and TNF-α in subjects with CKD and suggests that resistin may play a role in the sub-clinical inflammation associated with CKD, suggesting that adiponectin clearance may be decreased as shown by the inverse correlation of urinary adiponectin with GFR.

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