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


The Latest on Twitter

Kidney Week

Abstract: TH-PO091

AKI to CKD Transition After Acute Cardiorenal Syndrome in the Mouse

Session Information

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms


  • Matsushita, Katsuyuki, Oregon Health & Science University, Portland, Oregon, United States
  • Saritas, Turgay, Oregon Health & Science University, Portland, Oregon, United States
  • McCormick, James A., Oregon Health & Science University, Portland, Oregon, United States
  • Hutchens, Michael, Portland VA Medical Center, Portland, Oregon, United States

Acute cardiorenal syndrome (CRS type 1, CRS1) is an common cause of acute kidney injury (AKI) with high mortality and significant potential to transition to chronic kidney disease (CKD). Mechanistic data from translational models is lacking. We report AKI-to-CKD transition following CRS1 in a mouse model, accompanied by long-term renal inflammation.


CRS1 was modeled in male C57BL/6 mice (n=16) using potassium-induced 8 minute cardiac arrest followed by cardiopulmonary resuscitation (CA/CPR) and compared with sham (n=8). α-smooth muscle antibody, KIM-1, cleaved caspase-3, Ki-67, macrophage F4/80, and CD3 were quantified from immunohistology 1, 7, 14, and 60 days later. Glomerular filtration rate (GFR) was measured by FITC-sinistrin transcutaneous clearance and serum urea nitrogen by autoanalyzer.


Sham survival was 100%. 24h survival after CA/CPR was 100% and 60 day survival was 88%. CA/CPR induced severe AKI with near-zero GFR at 24h, and early macrophage infiltration demonstrated by robust F4/80 signal. 7 days after CA/CPR, KIM-1, F4/80, and CD3 revealed severe tubular injury, predominantly of proximal tubules, and inflammation with extensive cell proliferation, although GFR was recovering. At 14 days, GFR had normalized, but at 60 days GFR was again significantly below baseline, accompanied by elevated serum urea nitrogen, continued macrophage and t-cell infiltrate, apoptotic cell death, and widespread tubulointerstitial fibrosis.


Acute cardiorenal syndrome induces extensive tubular injury and inflammation in the renal cortex and outer medulla which progresses to renal fibrosis and chronic kidney disease despite initial functional recovery. We present a clinically relevant mouse model of AKI-CKD transition which we expect to provide insight into the the mechanisms underlying renal sequelae of cardiac arrest.


  • NIDDK Support