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There was significantly higher usage of both loop diuretics and aldosterone antagonist in the group with persistent hyponatraemia. Is it possible that one of the clinical manifestation of RV dysfunction, i.e peripheral oedema, led to an increased use of diuretic in this group and hence hyponatraemia as a complication of this treatment? Over diuresis in this scenario leads to activation of the RAAS which in turn worsens pulmonary hypertension and tricuspid regurgitation. The consequence of this is worsening peripheral oedema and the tendency to increase the diuretic dose.Hyponatraemia therefore may not be an independent predictor of outcome as stated.