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Kidney Week

Abstract: TH-PO797

Gadolinium-Based Contrast Agents Are Metabolic Disruptors in the Kidney and Exacerbate Obesity- and Diabetes-Induced Kidney Injury

Session Information

Category: Glomerular Diseases

  • 1201 Glomerular Diseases: Fibrosis and Extracellular Matrix


  • Wagner, Brent, Kidney Institute of New Mexico and the University of New Mexico Health Science Center, Albuquerque, New Mexico, United States
  • Lee, Doug Yoon, University of Texas Health Science Center, San Antonio, Texas, United States
  • Tan, Chunyan, University of Texas Health Science Center, San Antonio, Texas, United States
  • Do, Catherine, University of Texas Health Science Center, San Antonio, Texas, United States
  • Gorin, Yves C., University of Texas Health Science Center, San Antonio, Texas, United States

Obesity-related renal injury and diabetic kidney disease are characterized by activation of glomerular mesangial cells and podocyte damage with alteration of lipid metabolism/lipid accumulation in both cell types resulting in matrix accumulation and eventual progression to glomerulosclerosis with loss of renal function. We examined the consequences of gadolinium-based contrast agent (GBCA) treatment in the kidney from mice with normal kidney function and the potential interplay between obese and diabetic states and GBCA exposure.


GBCA was administered for 4 weeks (as previously described); Metabolomics was by Metabolon. Obesity and diabetes (T1D) were induced by high fat diet (HFD, 60% kcal saturated fat) or streptozoticin, respectively (22 week durations of each condition). Obese and T1D mice in the GBCA groups were treated for 4 weeks prior to sacrifice.


GBCA caused renal fibrotic lesions and podocyte injury that correlate with metabolic disorders as evidenced by increased serum triglyceride/cholesterol levels and insulin resistance. GBCA also induced expression of fatty acid translocase FAT/CD36—an indicator of fatty acid uptake—and lipogenic enzymes ATP citrate lyase (ACLY) and fatty acid synthase (FASN), indicators of de novo lipid synthesis. Metabolomic analysis indicated that renal lipid metabolism and metabolic markers of collagen turnover were significantly altered by GBCA.
HFD- and T1D-induced fibrotic and podocyte injuries are worsened by GBCA. GBCA exacerbated 1) HFD-mediated hyperlipidemia, 2) CD36/ACLY/FASN upregulation, and 3) lipid metabolism as assessed by metabolomics.


Our work provides the first evidence that GBCA causes significant metabolic disorders and kidney injury in mice without renal insufficiency. These injurious actions of GBCA are amplified in obese and T1D.
The understanding of the functional interplay between GBCA and diabetes/obesity will allow the development of therapeutic interventions or the establishment of effective preventive measures to reduce GBCA- and diabetes/obesity-mediated renal pathologies. This will help break the vicious cycle in which GBCA exposure in patients with normal kidney function or in obese or diabetic patients that may be more susceptible to GBCA-mediated renal pathologies.


  • NIDDK Support