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Abstract: FR-PO176

The Novel Dual-Effect Disintegrin, ARGD-RR, Attenuates AKI to CKD in Ischemic-Reperfusion Injury Models

Session Information

  • AKI: Mechanisms - II
    November 03, 2023 | Location: Exhibit Hall, Pennsylvania Convention Center
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms


  • Chiang, Chih-Kang, National Taiwan University College of Medicine, Taipei, Taipei, Taiwan
  • Liu, Shing-Hwa, National Taiwan University College of Medicine, Taipei, Taipei, Taiwan

Acute kidney injury (AKI) can lead to the development of renal fibrosis, ultimately resulting in chronic kidney disease (CKD) and end-stage renal disease (ESRD). Platelet activation has been identified as a key factor in the pathophysiology of AKI, triggering the formation of neutrophil extracellular traps (NETs), which exacerbate tubular necrosis and renal inflammation. Previous studies have demonstrated that antagonists or inhibitors of platelet activation hold promise as therapeutic interventions in AKI models induced by ischemia/reperfusion (I/R). Here, we tested whether the novel dual-effect disintegrin, ARGD-RR attenuated AKI to CKD in Ischemic-Reperfusion Injury.


In this study, we evaluated the therapeutic efficacy of a novel anti-platelet activation peptide called ARGDRR in a unilateral ischemic-reperfusion injury (uIRI) model. ARGDRR is a snake venom-derived dual-effect disintegrin-ARGDRR peptide that exhibits high affinity for binding to αIIbβ3 and αvβ3. Following ischemic-induced kidney injury, ARGDRR was administered, and we assessed renal dysfunction, renal fibrosis, and cell senescence after a 15-day period. Additionally, we examined the extent of platelet activation and NET formation in AKI.


The mRNA levels of platelet glycoprotein IIb-GPIIIa (Itga2b and Itgb3) progressively increased in the uIRI kidney from day 1 to day 15, accompanied by platelet aggregation and neutrophil infiltration. Administration of ARGDRR ameliorated renal dysfunction, fibrosis, and cell senescence in the transition from AKI to CKD. Moreover, ARGDRR modulated platelet-neutrophil interaction and inhibited NET formation in AKI.


Our findings provide compelling evidence that the disintegrin-ARGDRR peptide holds significant potential for renal protection in the transition from AKI to CKD by inhibiting platelet activation and NET formation. These results contribute to the advancement of therapeutic strategies for AKI and CKD treatment.


  • Government Support – Non-U.S.