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Abstract: PO2145

Effect of Dietary Magnesium Supplementation on Tubulointerstitial Damages in Angiotensin II-Induced Hypertensive Rats

Session Information

Category: Hypertension and CVD

  • 1403 Hypertension and CVD: Mechanisms

Authors

  • Takayanagi, Kaori, Ishikawa Kinenkai Kawagoe Ekimae Clinic, Kawagoe, Japan
  • Shimizu, Taisuke, Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, Kawaoe, Japan
  • Iwashita, Takatsugu, Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, Kawaoe, Japan
  • Hara, Hiroaki, Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, Kawaoe, Japan
  • Kurosawa, Akira, Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, Kawaoe, Japan
  • Terao, Masaaki, Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, Kawaoe, Japan
  • Hasegawa, Hajime, Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, Kawaoe, Japan
Background

Recently, it has been epidemiologically suggested that Mg deficiency promotes progressive renal damage, and conversely, it has been reported that Mg load to Cyclosporine A-induced renal damage models attenuates renal impairment. This study aimed to investigate the ameliorating effect of high Mg diet on the renal impairment by use of hypertensive nephrosclerosis model.

Methods

Eight-week-old SD rats were subjected to continuous infusion of Angiotensine II by subcutaneously placed osmotic minipumps for 2 weeks (435 ng/kg/min) and then housed for 6 weeks. The food for animals was normal Mg diet (NMD): 4% NaCl+0.05% Mg or high Mg diet (HMD): 4% NaCl+0.5% Mg. PicroSirius Red staining was used to assess fibrosis, and immunostaining of claudin-16, which is known to be down-reguglated in the renal interstitial damage was also performed.

Results

No significant difference in mean blood pressure was seen between two groups (NMD: 97.8±7.6 mmHg vs HMD: 94.2±9.0 mmHg, n=4), and serum Mg was elevated in HMD group (NMD: 1.63±0.19 mg/dL vs HMD: 2.48±0.09 mg/dL, n=4). Analysis of PicroSirius Red staining positive area by semi-quantification showed that positive area in outer medullary resion was significantly reduced in HMD group (NMD: 1.61±0.15% vs HMD: 1.11±0.10%, n=4). Positive area of claudin-16 immunostaining in HMD was greater than NMD (NMD: 1.52±0.13% vs HMD: 1.70±0.15%, n=4).

Conclusion

Hypertensive nephrosclerosis is one of the major causes of end-stage renal failure, and its suppression is important. It was confirmed that the outermedullary fibrosis was inhibited by high Mg diet, while there was no change in the blood pressure, indicating that anti-fibrotic effect of high Mg diet seemed to be an independent mechanism from the blood pressure. We report the fact that claudin-16 expression is reduced and Mg excretion is increased in the interstitial fibrosis model (Shimizu, Magnesium Res 2018). These results suggest that high Mg diet has an inhibitory effect on fibrogenesis through suppressing the increased Mg-excretion.