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Abstract: PO0649

Renal Expression of L-Type Fatty Acid Binding Protein in Addition to Angiotensin II Type 1a Receptor Loss Ameliorates Chronic Tubulointerstitial Damage After Renal Ischemia Reperfusion

Session Information

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

Category: CKD (Non-Dialysis)

  • 2103 CKD (Non-Dialysis): Mechanisms

Authors

  • Fujita, Yoko, Division of Nephrology and Hypertension, Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan
  • Sugaya, Takeshi, Division of Nephrology and Hypertension, Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan
  • Ichikawa, Daisuke, Division of Nephrology and Hypertension, Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan
  • Tanabe, Jun, Division of Nephrology and Hypertension, Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan
  • Kimura, Kenjiro, JCHO Tokyo Takanawa Hospital, Tokyo, Japan
  • Shibagaki, Yugo, Division of Nephrology and Hypertension, Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan
  • Ikemori, Atsuko, Division of Nephrology and Hypertension, Department of Internal Medicine, St. Marianna University School of Medicine, Kawasaki, Kanagawa, Japan
Background

Although angiotensin II (Ang II) type 1 receptor blocker was reported to attenuate chronic tubulointerstitial damage (TID) after renal ischemia reperfusion (IR), its effect is limited. We had revealed the importance of renal L-type fatty acid binding protein (L-FABP) with antioxidative effect in various renal disease models. Therefore, the aim of this study is to elucidate the renoprotective effect of renal L-FABP and Ang II type 1a receptor (AT1a) loss against chronic TID after renal IR.

Methods

To induce severe chronic TID after renal IR, unilateral renal ischemia for 60 min was performed via clamping of right renal pedicle using four types of male mice; wild type mice (hL-FABP-/-AT1a+/+), human L-FABP chromosomal transgenic mice (hL-FABP+/-AT1a+/+), AT1a knockdown homo mice (hL-FABP-/-AT1a-/-), and generated hL-FABP+/-AT1a-/- mice. Right and left kidneys were removed at 10 weeks after IR.

Results

While marked renal atrophy and progressive TID were found in each IR-kidney of hL-FABP-/-AT1a+/+, hL-FABP+/-AT1a+/+ and hL-FABP-/-AT1a-/- mice, the degrees of both atrophy and TID were significantly ameliorated in the IR-kidneys of the hL-FABP+/-AT1a-/- mice. Systolic blood pressure levels in the hL-FABP+/-AT1a-/- mice were similar to the hL-FABP-/-AT1a-/- mice. These results suggested that antioxidative effect of L-FABP in addition to AT1a loss may be related to suppression of chronic TID after IR.

Conclusion

Increased expression of renal L-FABP in addition to suppressed activity of AT1a may be a useful strategy for prevention of AKI-to-CKD transition.

Funding

  • Private Foundation Support