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Kidney Week

Abstract: FR-PO1010

Insulin Resistance and Intermuscular Adipose Tissue (IMAT) in Patients with CKD

Session Information

Category: CKD (Non-Dialysis)

  • 2303 CKD (Non-Dialysis): Mechanisms


  • Dilaver, Ragibe Gulsah, Vanderbilt University Division of Nephrology and Hypertension, Nashville, Tennessee, United States
  • Roshanravan, Baback, University of California Davis, Division of Nephrology, Sacramento, California, United States
  • Ikizler, Talat Alp, Vanderbilt University Division of Nephrology and Hypertension, Nashville, Tennessee, United States
  • Gamboa, Jorge, Vanderbilt University Medical Center, Division of Clinical Pharmacology, Nashville, Tennessee, United States

Insulin resistance (IR) is commonly observed in CKD and plays a critical role in protein energy wasting (PEW). We have found that patients with moderate to advanced CKD have increased IMAT accumulation. In this study, we hypothesized that the extent of IMAT is associated with homeostatic model assessment of insulin resistance (HOMA-IR), a measure of insulin resistance and systemic inflammation


In this cross-sectional study, we included 46 patients (21 control, 25 with CKD stage 3-5). Anthropometry, inflammatory biomarkers, and HOMA-IR) were measured in all participants. Quadriceps IMAT was analyzed with magnetic resonance imaging (MRI) of the thigh.


The control and CKD groups were matched by gender and body mass index. There was no difference in HOMA-IR, glucose, or insulin levels between the groups. Quadriceps IMAT accumulation was higher in patients with Stage 3-5 CKD compared to the control group (Figure 1A). Higher insulin resistance was associated with greater IMAT accumulation (rho=0.55, p<0.001, Figure 1B). Greater IMAT accumulation was associated with increased levels of tumor necrosis factor-alpha (TNFα) (rho=0.16, p=0.005, Figure 1C).


In patients with stage 3-5 CKD, there is greater accumulation of IMAT that associates with insulin resistance and increased TNFα levels compared to controls. IMAT accumulation may contribute to skeletal muscle insulin resistance by promoting a local inflammatory milieu. Further studies should evaluate if IMAT reduction may improve insulin sensitivity in CKD.


  • NIDDK Support