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Introduction:Hyponatremia is the most common electrolyte disorder in clinical practice, and it is associated with adverse outcomes. Severe hyponatremia can result in cerebral edema and hypoxia. Moreover, even mild hyponatremia can lead to gait instability and cognitive dysfunction, especially in the elderly. The main cause of hyponatremia is nonosmotic secretion of arginine vasopressin with resultant electrolyte-free water retention. Thus, the available management for chronic hyponatremia must increase solute-free water excretion, such as occurs with blocking vasopressin receptors with selective V2 antagonists.Areas covered:Several recent trials have assessed the efficacy and safety of hyponatremia treatment using vasopressin receptor antagonists (vaptans). These trials documented the efficacy of vaptans to reverse hyponatremia. Moreover, treatment of hypervolemic hyponatremia, such as in heart failure or liver cirrhosis, with vasopressin receptor antagonist results in increased solute-free excretion without activation of the neurohumoral systems. The current review covers results on management of hyponatremia with different vasopressin receptor antagonists.Expert opinion:Approaches, such as vasopressin receptor antagonists or urea, have been shown to reverse moderate hyponatremia. However, these agents have not been used to treat severe hyponatremia in clinical trials. Future studies in severe hyponatremic states are required to assess the impact of vaptans on clinically significant end points, such as morbidity and mortality.

Autosomal dominant polycystic kidney disease is the most frequent life-threatening hereditary disease. Prognostic factors for progressive renal impairment have been identified such as gender, race, age, proteinuria, hematuria, hypertension. Hypertension is the only risk factor for renal dysfunction in autosomal dominant polycystic kidney disease, which is presently treatable. Better understanding of the pathophysiology of hypertension will help in defining appropriate interventions. The renin-angiotensin-aldosterone-system is the pivotal factor in the pathogenesis of hypertension in autosomal dominant polycystic kidney disease. Basic research and clinical studies in autosomal dominant polycystic kidney disease implicated activation of the renin-angiotensin-aldosterone-system. Therapy of hypertension in autosomal dominant polycystic kidney disease with angiotensin-converting enzyme inhibitors or angiotensin receptor blocker has the potential to prevent cardiovascular complications and slow the progression of renal disease. The results of two large multicenter double-blind placebo controlled randomized clinical trials (the HALT-PKD trials) possibly will elucidate the beneficial effects of the renin-angiotensin-aldosterone-system inhibition in autosomal dominant polycystic kidney disease.