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Comparative Proteomic Analysis of Whole Kidney, Medulla, and Cortical Tubules in Diabetic Pathogenesis of Kidney Injury in Mice
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The Mechanism of Contrast-Induced Acute Kidney Injury and Its Association with Diabetes Mellitus

Yanfei Li1, Ke Ren1

  • 1Department of Radiology, Xiang'an Hospital of Xiamen University, Xiamen 361102, China.

Contrast Media & Molecular Imaging
|August 14, 2020
PubMed

Insights

Diabetes mellitus and its kidney complication, diabetic nephropathy, increase the risk of contrast-induced acute kidney injury (CI-AKI). This review explores how high glucose status, immune responses, and signaling pathways contribute to CI-AKI in diabetic patients.

Area of Science:

  • Nephrology
  • Endocrinology
  • Immunology

Background:

  • Contrast-induced acute kidney injury (CI-AKI) is a significant hospital-acquired condition with adverse effects on patient prognosis, hospital stay, and costs.
  • Diabetic nephropathy (DN), a complication of diabetes mellitus (DM), is an independent risk factor for chronic kidney disease (CKD) and CI-AKI.
  • The incidence of CI-AKI is notably higher in patients with pre-existing renal injury, particularly those with DN.

Purpose of the Study:

  • To elucidate the mechanisms by which diabetes mellitus facilitates CI-AKI.
  • To review the pathophysiological, immunological, and signaling pathway aspects linking high-glucose status and CI-AKI.

Main Methods:

  • Review of existing literature on CI-AKI, diabetes mellitus, and diabetic nephropathy.
  • Analysis of pathophysiological changes in the kidney under high-glucose status (HGS).
  • Examination of immunological alterations in DM/DN that promote CI-AKI.
  • Investigation of signaling pathways common to both CI-AKI and DM.

Main Results:

  • High-glucose status exacerbates oxidative stress, increases reactive oxygen species (ROS), causes vasoconstriction, and impairs kidney oxygen supply, creating a detrimental cycle with CI-AKI.
  • Immune responses in DM/DN, involving innate immune cells and pattern recognition receptors (PRRs), may interact with damage-associated molecular patterns (DAMPs) during CI-AKI.
  • Signaling pathways implicated in CI-AKI are associated with apoptosis, inflammation, and ROS production, suggesting potential therapeutic targets.

Conclusions:

  • Diabetes mellitus significantly predisposes individuals to CI-AKI through complex pathophysiological and immunological mechanisms.
  • Understanding the interplay between high glucose, kidney injury, and immune activation is crucial.
  • Further research into shared signaling pathways is needed to develop novel strategies for preventing and treating CI-AKI in diabetic patients.

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