Beer Potomania: A View on the Dynamic Process of Developing Hyponatremia

Abstract

Poor solute intake has been ascribed to hyponatremia seen in patients with beer potomania, an uncommon etiology of hyponatremia. Our current understanding of how hyponatremia develops in these patients is derived only from individual cases described in the literature. In these case reports, the pathophysiology of beer potomania is explained exclusively by the concept of solute-free water clearance in the kidney. Specifically, low solute intake reduces urinary excretion of osmoles, thereby capping a ceiling on the renal capacity of free water excretion. A positive water balance follows an excess of water intake, causing dilutional hyponatremia. We propose that further inquiry is needed to explain how water is retained by the kidney. From reviewing the clinical data of these case reports, it is evident that there is a broad range of urine osmolality, ranging from levels below to above plasma osmolality. This finding is consistent with a dynamic course of vasopressin secretion during the development of hyponatremia. Vasopressin raises epithelial permeability to water in the collecting duct; the amount of luminal osmoles then determines the osmotic gradient for water transport. At a certain degree of hyponatremia, vasopressin secretion may cease and profound water diuresis ensues. Unfortunately, the status of vasopressin release is rarely investigated. We propose that in patients with beer potomania detailed fluid balance studies, sequential observations of changes in urine and plasma osmolality corresponding to dynamics of vasopressin release would advance our understanding of its pathophysiology.