John Libbey Eurotext

Magnesium Research

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Down-regulation of magnesium transporting molecule, claudin-16, as a possible cause of hypermagnesiuria with the development of tubulo-interstitial nephropathy Volume 31, numéro 1, January-February-March 2018

Illustrations

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Tableaux

Auteurs
1 Department of Nephrology and Hypertension, Saitama Medical Center, Saitama Medical University, Kawagoe, Saitama, Japan
2 Saitama Cardiovascular and Respiratory Center, Saitama, Japan
3 IshikawaKinenkai, Kawagoe Ekimae Clinic, Saitama, Japan
4 Laboratory of Biochemistry, Gifu Pharmaceutical University, Gifu, Japan
5 Department of Pharmacology, Graduate School of Medicine, Chiba University, Chiba, Japan
* Correspondence: Hajime Hasegawa, Professor and Chairman, Department of Nephrology and Hypertension, Center of Blood Purification, Saitama Medical Center, Saitama Medical University, 1981 Kamoda, Kawagoe, Saitama 350-8550, Japan.
  • Mots-clés : interstitial nephropathy, claudin-16, TRPM6, magnesium
  • DOI : 10.1684/mrh.2018.0434
  • Page(s) : 11-23
  • Année de parution : 2018

Background/Aims

Tubulo-interstitial nephropathy (TIN) is a critical pathological setting for the renal prognosis, and an increase in the urine magnesium excretion is a well-known characteristic feature as one of clinical parametets for the assessment of TIN. We examined the correlation between the development of TIN and the changes in the mRNA expression of renal magnesium-transporting molecules in rats with unilateral ureter obstruction (UUO).