alexa Fluvastatin Increases AQP2 Urine Excretion in a Dyslipi
ISSN: 2155-6156

Journal of Diabetes & Metabolism
Open Access

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Research Article

Fluvastatin Increases AQP2 Urine Excretion in a Dyslipidemic Patient with Nephrogenic Diabetes Insipidus: An In Vivo and In Vitro Study

Giuseppe Procino1*, Maiolo D2, Barbieri C1, Milano S1, Carmosino M1, Squatrito S2, Svelto M1,3 and Gullo D2

1Department of Biosciences, Biotechnologies and Biopharmaceutics, University of Bari, Italy

2Endocrinology Unit, Garibaldi-Nesima Hospital, University of Catania Medical School, Catania, Italy

3The National Research Council (CNR), Bari, Italy

*Corresponding Author:
Giuseppe Procino
Department of Biosciences
Biotechnologies and Biopharmaceutics
Via Amendola 165/A 70126, Bari, Italy
Tel: +39 0805443414
Fax: +39 0800000000
E-mail: [email protected]

Received date: June 05, 2014; Accepted date: July 26, 2014; Published date: August 03, 2014

Citation: Procino G, Maiolo D, Barbieri C, Milano S, Carmosino M, et al. (2014) Fluvastatin Increases AQP2 Urine Excretion in a Dyslipidemic Patient with Nephrogenic Diabetes Insipidus: An In Vivo and In Vitro Study. J Diabetes Metab 5:408 doi: 10.4172/2155-6156.1000408

Copyright: © 2014 Procino G, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

 

Abstract

Objective: Among the pleiotropic effects of statins, we have previously reported that fluvastatin increases the amount of plasma membrane-expressed AQP2 in renal collecting duct cells both in vitro and in vivo, independently of vasopressin. This effect may be of potential clinical significance for the treatment of patients affected by nephrogenic diabetes insipidus forms caused by inactivating mutations of the vasopressin type 2 receptor. Here we report the effect of fluvastatin on AQP2 plasma membrane abundance on an adult male XNDI patient treated with statins.

Methods: An adult male NDI patient, carrying an inactivating mutation of the V2R, under conventional treatment to reduce polyuria, was also treated with fluvastatin because of high levels of blood cholesterol. AQP2 plasma membrane expression in the kidney was monitored by measuring urinary excreted AQP2 (u-AQP2), before starting fluvastatin treatment and during a three months follow-up period. The effect of fluvastatin was also tested in vitro in mouse kidney cortical collecting duct MCD4 cells.

Results: u-AQP2 increased in a time- and dose-dependent manner after treatment with 40 and 80 mg/day of fluvastatin for 90 days. However, at this drug dosage, increased uAQP2 was not accompanied by reduction of diuresis and increase of urine osmolality. The effect of fluvastatin on AQP2 excretion was confirmed in vitro in cultured renal cells.

Conclusions: We first demonstrate that the use of fluvastatin increased AQP2 plasma membrane expression in an NDI dyslipidemic patient. This observation was confirmed by in vitro studies using mouse cultured renal cells treated with fluvastatin. Although a clinical relevant effect of fluvastatin on total diuresis and urine osmolality was not observed at the used dosages, these results suggest further investigation on the possible role of HMG CoA reductase inhibitors to improve the efficacy of the current NDI therapy.

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