ASN's Mission

ASN leads the fight to prevent, treat, and cure kidney diseases throughout the world by educating health professionals and scientists, advancing research and innovation, communicating new knowledge, and advocating for the highest quality care for patients.

learn more

Contact ASN

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


The Latest on Twitter

Kidney Week

Abstract: PO0219

Ascending Vasa Recta Responsible for Medullary Vascular Congestion

Session Information

  • AKI Mechanisms - 3
    October 22, 2020 | Location: On-Demand
    Abstract Time: 10:00 AM - 12:00 PM

Category: Acute Kidney Injury

  • 103 AKI: Mechanisms


  • Ray, Sarah C., Augusta University Medical College of Georgia, Augusta, Georgia, United States
  • O'Connor, Paul, Augusta University Medical College of Georgia, Augusta, Georgia, United States

Vascular congestion of the renal medulla is common in acute kidney injury and has been shown to prolong ischemia and promote injury. We have reported that pretreatment with low dose lipopolysaccharide (LPS) attenuates ischemia reperfusion (IR) induced congestion. The temporal localization of congestion during IR and how LPS prevents congestion remains unknown. We hypothesized that ‘vascular congestion originates in the medullary vasa recta (VR) prior to the peritubular (PT) capillary plexus, and that pretreatment with low dose LPS aids in early VR reperfusion’.


To test this hypothesis, male WKY rats (10wks) were pretreated (i.p) with 1000µg/kg LPS or saline daily for 3 days and a 45-minute warm, bilateral ischemia was performed. Rats were randomized to 0, 1, 2, 6, 10, or 24 hour(s) of reperfusion (n=4-6/group). Congestion of the medullary VR and PT capillaries was assessed in histological sections (scale: 0-5, 0=0%, 5=100% congestion).


At time 0 (no reperfusion), congestion of the medullary VR averaged 80% in both saline and LPS treated rats. Following reperfusion for 1, 2, 6, and 10 hours, VR congestion was >60% in saline treated rats. In contrast, VR congestion in LPS rats rapidly declined within 1 hour (<20%) and remained lower than saline scores through 24 hours (pTREATMENT<0.0001). In both groups, PT congestion was less than 20% at time 0 (no reperfusion) but rapidly increased in saline treated rats to >60% by 6 hours of reperfusion. Conversely, in LPS treated rats, PT congestion remained low (average 13.4%, pINTERACTION=0.0144) across the 24-hour reperfusion period. Immunofluorescent staining of neural-glial antigen 2 (NG2) and urea transporter (UTB) localized initial congestion to the ascending VR (AVR).


Our data provides the first evidence that congestion originates in the medullary AVR during the ischemic period and that blockage of AVR drives congestion in the PT capillary plexus during reperfusion by preventing drainage of the renal medullary circulation. Rapid reperfusion of the AVR (LPS group) prevented congestion of the PT capillaries. These data provide new insight into the pathophysiology of vascular congestion following ischemia and identify the AVR as the renal defect responsible for PT congestion. Understanding the mechanisms by which LPS aids in AVR reperfusion may be critical in order to find therapeutic targets for vascular congestion.


  • Other NIH Support