ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005

email@asn-online.org

202-640-4660

The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2020 and some content may be unavailable. To unlock all content for 2020, please visit the archives.

Abstract: PO0195

Role of Glomerular Filtration Rate (GFR)-Modifying Drugs in Prevention of Anticoagulant-Related Nephropathy (ARN)

Session Information

  • AKI Mechanisms - 2
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms

Authors

  • Brodsky, Sergey V., The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
  • Medipally, Ajay kumar, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
  • Xiao, Min, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
  • Satoskar, Anjali A., The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
  • Nadasdy, Tibor, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
  • Hebert, Lee A., The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
Background

Acute kidney injury (AKI) with red blood cell (RBC) tubular casts secondary to different anticoagulants has been recognized as ARN. ARN is seen in patients with underlying kidney diseases. 5/6 nephrectomy (5/6NE) animal model reproduces morphologic features of ARN. One of the possible pathogenetic mechanisms of ARN proposed to be increased GFR.
Aim of the current study was to investigate the role of GFR-modifying drugs in prevention of ARN.

Methods

5/6NE rats 3 weeks after the surgery were treated with direct thrombin inhibitor dabigatran (150mg/kg/day) and with GFR-reducing Enalapril (1.5mg/kg/dl) or GFR-increasing Albuterol (4mg/kg/day) for 7 days. Daily monitoring of serum creatinine (SCr), blood pressure and hematuria was performed. Morphology of the kidney was evaluated at day 7 after animals were euthanized .

Results

Dabigartan resulted in gradual increase in SCr (Fig 1), hematuria, acute tubular necrosis (ATN) and RBC tubular casts in all treatment groups. Neither of GFR-modifying drugs significantly changed there parameters. ATN was 0.75±0.27, 0.67±0.25 and 0.79±0.27 in Dabigatran, Dabigatran + Enalapril and Dabigartan + Albuterol treatment groups, respectively. Systolic blood pressure was reduced with Enalaprilbut did not change significanlty with Albuterol. Diastolyc blood presuure was not changed significantly with either treatment.

Conclusion

Our data indicate that GFR-modifying drugs do not prevent or aggravate ARN at least secondary to direct thrombin inhibitor.

Funding

  • NIDDK Support