How to Escape from Primary Aldosteronism? News and Views on an Adrenal Disorder of Salt Retention

Abstract

The last years have seen substantial progress in primary aldosteronism (PA), which is the most common cause of secondary hypertension. Many programs have been established around the world to meet the needs in healthcare and the management of patients with PA according to published guidelines and clinical protocols. Systematic analysis of emerging data and meticulous scientific work have informed us on the molecular basis of the disease and helped to characterize hereditary forms of PA. Techniques have been developed to better diagnose PA and to establish genotype-phenotype relationships and their impact on hypertension. Studies have been undertaken to stratify patients for risk factors and to ensure quality of best medical treatment. This review focuses on some clinically relevant problems in characterizing autonomous aldosterone secretion and discusses testing and management strategies. Besides, this review puts the emphasis on some colorful studies not to pale soon beside an ever evolving painting background.

Mineralocorticoid Receptor Blockers and Aldosterone to Renin Ratio: A Randomized Controlled Trial and Observational Data

“…Moreover, it should also be emphasized that MR blockers are, apart from PA therapy, also considered and recommended as an effective third or fourth line therapy in essential hypertension and are an established treatment for heart failure [35]. Considering this along with the fact that it has not been clearly established that surgery of aldosterone producing adenomas is superior with regard to hard clinical endpoints compared to MR blocker treatment, it may for some patients with indications for PA diagnostics, be justified to remain on their MR blocker treatment without further diagnostic evaluation for PA [1,[36][37][38].…”

Diabetes Mellitus and Hypertension—A Case of Sugar and Salt?

“…On one hand, HTN in patients with DM is thought to arise from common risk factors related to the development of DM, e.g., genetic disposition, overactivity of the sympathetic nervous system, chronic inflammation, and excess adrenal steroid hormone secretion, along with RAAS activation as a consequence of surplus adipose tissue and a long list of factors generated by these fat cells [ 4 , 5 , 6 , 7 , 8 , 10 ]. On the other hand, HTN is also discussed to be already a consequence of diabetes with renal dysfunction, RAAS activation and abnormal renal sodium handling, endothelial dysfunction, blood vessel damage, and chronic inflammation [ 4 , 5 , 6 , 9 ]. A certain degree of vagueness may be the reason that until now, DM has not been considered a cause of secondary HTN [ 11 , 12 ].…”

“… Parallelisms in the regulation of glucose and salt blood concentrations. This figure is a further development of the scheme in [ 9 ]. Notably, both glucose and sodium are reclaimed in the kidney through the action of sodium-glucose cotransporters.…”

Aldosterone-Mediated Sodium Retention Is Reflected by the Serum Sodium to Urinary Sodium to (Serum Potassium)2 to Urinary Potassium (SUSPPUP) Index

“…Sodium retention is regulated by aldosterone which is secreted in dependency of potassium, angiotensin II and other stimuli [ 1 ]. Therefore, disturbed potassium and sodium chloride sensing in zona glomerulosa cells may result in autonomous secretion of aldosterone [ 2 , 3 , 4 , 5 , 6 , 7 , 8 ], termed primary aldosteronism (PA), which leads to sodium retention and through active mechanisms of water conservation to hypervolemic hypertension [ 9 ]. The conservation and dilution of sodium happens on the expense of potassium and protons which led to the classical description of PA as hypokalemic hypertension with metabolic alkalosis [ 10 ].…”