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Nephrol Dial Transplant (2002) 17: 539-542
© 2002 European Renal Association-European Dialysis and Transplant Association

Editorial Comment

Mineralocorticoid receptor malfunction: further insights from rare forms of hypertension

Markus G. Mohaupt and Felix J. Frey

Division of Nephrology/Hypertension, University Hospital of Berne, Berne, Switzerland

Keywords: aldosterone; epithelial sodium channel; 11ß-hydrosteroid dehydrogenase; hypertension; pregnancy

Introduction

Monogenic diseases enhance the understanding of mechanisms for arterial hypertension. All genetic forms so far identified induce hypertension by increased renal sodium reabsorption [1,2]. Recently a novel form of genetically determined renal sodium retention due to a gain-of-function mutation of the mineralocorticoid receptor (MR) has been described. This mutation causes activation of the MR in the absence of aldosterone [3]. Therefore, this disease potentially provides a clue to understand the pathomechanisms in the large number of patients with low renin-low aldosterone hypertension [4].

Mechanisms for enhanced sodium retention in the cortical collecting duct

The mechanism of sodium reabsorption in the principal cells of the cortical collecting duct is depicted in Figure 1Go. Sodium enters the cell via the epithelial sodium channel (ENaC). Gain-of-function mutations of the ENaC . . . [Full Text of this Article]

Activating mineralocorticoid receptor mutation

Conclusion and perspectives

Acknowledgments

Notes

References


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