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 X

Kidney Week

Please note that you are viewing an archived section from 2022 and some content may be unavailable. To unlock all content for 2022, please visit the archives.

Abstract: SA-PO984

Suppressing Delayed Rectifier Potassium Channels (Kv1.3) in T Lymphocytes and Its Therapeutic Efficacy in Rats With CKD

Session Information

  • CKD: Pathobiology - II
    November 05, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: CKD (Non-Dialysis)

  • 2203 CKD (Non-Dialysis): Mechanisms


  • Kazama, Itsuro, Miyagi Daigaku, Kurokawa-gun, Miyagi, Japan

T lymphocytes predominantly express delayed rectifier K+-channels (Kv1.3) in their plasma membranes. In our previous study, we revealed that the overexpression of lymphocyte Kv1.3-channels contributed to the progression of chronic kidney disease (CKD) by promoting cellular proliferation and interstitial fibrosis. On the other hand, by suppressing the lymphocyte Kv1.3-channels, some drugs exert immunosuppressive properties.


Employing the standard patch-clamp whole-cell recording technique in murine thymocytes, we examined the effects of commonly used drugs, such as anti-hypertensive drugs, on Kv1.3-channel currents. Additionally, using male Sprague-Dawley rats that underwent 5/6 nephrectomy followed by a 14-week recovery period, we actually examined the therapeutic efficacy of these drugs in advanced CKD.


In addition to some anti-hypertensive drugs, non-steroidal anti-inflammatory drugs, antibiotics and anti-cholesterol drugs, effectively suppressed the Kv1.3-channel currents in murine thymocytes. Among them, benidipine, a long-acting 1,4-dihydropyridine Ca2+ channel blocker, most effectively and persistently inhibited the channel currents. Therefore, using the rat model with advanced CKD, we examined the effects of benidipine (5mg/kg) on the histopathological features of the kidneys, cellular proliferation of leukocytes and the cortical expression of pro-inflammatory cytokines. In the cortical interstitium of advanced CKD rat kidneys, benidipine significantly ameliorated the progression of renal fibrosis without affecting glomerular injury. This drug also reduced the number of proliferating leukocytes with a significant decrease in the pro-inflammatory cytokine expression.


Taken together, these in vitro and in vivo findings suggested the therapeutic potency of Kv1.3-channel inhibitors, such as benidipine, in the treatment or prevention of CKD.