Der Internist
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Arterial hypertension is a real global burden with a very high prevalence. In the last decades, many pharmaceutical approaches have been successfully developed for treating hypertension. Currently, novel medications for influencing blood pressure are not in sight. ⋯ In very systematic sham-controlled, blinded studies in patients with hypertension but without medication a robust blood pressure reducing effect of RDN could be shown, which corresponded to the effect of a blood pressure-reducing drug. It is obvious that larger studies and also long-term studies have to sustainably confirm this effect. In recent years, active and passive stimulation of the baroreceptors could also be established as a blood pressure reducing principle, at least in studies but the evidence is still very low.
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Aldosterone is produced in the adrenal cortex and governs volume and electrolyte homeostasis. Hyperaldosteronism can occur either as primary aldosteronism (renin-independent) or secondary aldosteronism (renin-dependent). As the commonest cause of secondary hypertension, primary aldosteronism is associated with increased cardiovascular risk. ⋯ Over the past 10 years, somatic mutations in ion channels or transporters have been identified as causes of aldosterone-producing adenomas and so-called aldosterone-producing cell clusters (potential precursors of adenomas and correlates of bilateral hyperplasia, but also of subclinical hyperaldosteronism). In addition, germline mutations in overlapping genes cause familial hyperaldosteronism. Secondary hyperaldosteronism can occur in patients with hypertension treated with diuretics or in renal artery stenosis.
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Severe arteriosclerotic stenosis of the renal artery with at least 60-70% narrowing of the lumen can lead to various diseases: in the case of unilateral stenosis it can lead to renovascular hypertension, in the case of bilateral narrowing (or in a stenotic solitary kidney) also to an often progressive renal insufficiency (ischemic kidney disease) and/or to acute pulmonary edema (pulmonary flash edema). Renal artery stenosis may be treated by revascularization using either percutaneous (balloon angioplasty with or without stenting) or less commonly open surgical procedures, both with excellent primary patency rates of over 90%; however, randomized trials of catheter-based interventions have failed to demonstrate a longer term benefit with respect to blood pressure control and renal function as well as improved overall survival over optimal medicinal management alone. Due to improved clinical outcomes interventional revascularization is justified in cases with critical stenoses and clinical sequelae, such as pulmonary flash edema and progressive renal failure. Careful patient selection is essential to maximize a potential clinical benefit.