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Primary aldosteronism is the most common cause of secondary hypertension, accounting for about 10% of all forms of high blood pressure. Life-time pharmacological therapy is the treatment of choice for primary aldosteronism due to idiopathic adrenal hyperplasia (IHA), while adrenalectomy is effective in curing most patients with an aldosterone producing adenoma (APA). Far from being a benign form of hypertension, primary aldosteronism is characterized by the development of cardiovascular renal and metabolic complications, including left ventricular hypertrophy, myocardial infarction, atrial fibrillation and stroke, microalbuminuria, renal cysts as well as metabolic syndrome, glucose impairment and diabetes mellitus. We review recent clinical experience with the above mentioned complications and long-term outcomes of blood pressure normalization and cardiac, renal and gluco-metabolic complications in patients with primary aldosteronism, after medical treatment with mineralocorticoid receptor antagonists and surgical treatment. We conclude that removal of adrenal adenoma results in normalization of the renin-angiotensin-aldosterone system (RAAS) and of kalaemia and improvement of blood pressure levels in all patients. Complete resolution of hypertension is achieved in nearly half of treated patients. Moreover, unilateral adrenalectomy is the best treatment to have the regression of cardiovascular, renal and metabolic complications in patients with APA. On the other hand, targeted medical treatment with aldosterone antagonists improves blood pressure control and appears able to prevent the progression of cardiac and metabolic complications in patients with IHA.
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PMID:Management of primary aldosteronism: its complications and their outcomes after treatment. 1935 5

The prevalence of obesity, diabetes, hypertension, and cardiovascular and chronic kidney disease is increasing in developed countries. Obesity, insulin resistance, and hypertension commonly cluster with other risk factors for cardiovascular and chronic kidney disease to form the metabolic syndrome. Emerging evidence supports a paradigm shift in our understanding of the renin-angiotensin-aldosterone system and in aldosterone's ability to promote insulin resistance and participate in the pathogenesis of the metabolic syndrome and resistant hypertension. Recent data suggest that excess circulating aldosterone promotes the development of both disorders by impairing insulin metabolic signaling and endothelial function, which in turn leads to insulin resistance and cardiovascular and renal structural and functional abnormalities. Indeed, hyperaldosteronism is associated with impaired pancreatic beta-cell function, skeletal muscle insulin sensitivity, and elevated production of proinflammatory adipokines from adipose tissue, which results in systemic inflammation and impaired glucose tolerance. Accumulating evidence indicates that the cardiovascular and renal abnormalities associated with insulin resistance are mediated in part by aldosterone acting on the mineralocorticoid receptor. Although we have known that mineralocorticoid receptor blockade attenuates cardiovascular and renal injury, only recently have we learned that mineralocorticoid receptor blockade improves pancreatic insulin release, insulin-mediated glucose utilization, and endothelium-dependent vasorelaxation. In summary, aldosterone excess has detrimental metabolic effects that contribute to the metabolic syndrome and endothelial dysfunction, which in turn contribute to the development of resistant hypertension as well as cardiovascular disease and chronic kidney disease.
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PMID:Narrative review: the emerging clinical implications of the role of aldosterone in the metabolic syndrome and resistant hypertension. 1948 12

High blood pressure is often difficult to control. Resistant hypertension is blood pressure above goal despite adherence to a combination of at least three antihypertensive medications of different classes, optimally dosed and usually including a diuretic. The approach to blood pressure that is apparently difficult to control begins with an assessment of the patient's adherence to the management plan, including lifestyle modifications and medications. White-coat hypertension may need to be ruled out. Suboptimal therapy is the most common reason for failure to reach the blood pressure goal. Once-daily fixed-dose combination pills may improve control through the synergism of antihypertensive agents from different classes and improved adherence. Truly drug-resistant hypertension is commonly caused by chronic kidney disease, obstructive sleep apnea, or hyperaldosteronism, all of which can lead to fluid retention. Higher doses of diuretics (or a change to a loop diuretic) are usually needed. Other strategies include adding an alpha blocker, alpha-beta blocker, clonidine, or an aldosterone antagonist (e.g., spironolactone). Particularly in patients with diabetes or renal disease, combining a long-acting nondihydropyridine with a dihydropyridine calcium channel . blocker can also be considered. Obesity, heavy alcohol intake, high levels of dietary sodium, and interfering substances (especially nonsteroidal anti-inflammatory drugs) contribute to hypertension that is resistant or difficult to control.
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PMID:Evaluation and management of the patient with difficult-to-control or resistant hypertension. 2070 61

50 years old female patient, with history of diabetes mellitus and hypertension, receiving metformin (500 mg BID) and atenolol (50 mg BID), presented to the Emergency Room with asthenia and dizziness. The patient was also receiving alternative medication (Dragon Blanco) which contains no licorice. During the emergency workup she developed syncope and three episodes of ventricular fibrillation. She was electrically defibrillated and treated with amiodarone and potassium replacement. The patient was admitted to the Intensive Care Unit. Physical exam: BP: 160/90 mm Hg, RR: 15, Pulse: 83: Cardiovascular: grade II systolic murmur which irradiated to the neck. The rest of the examination was unremarkable. Labs: Na: 138 meg/dl, K: 1.6 meg/dl, Cl: 84 meg/dl, BUN: 17 mg/dl, Creat.: 1.1 mg/dl, Gluc.: 148 mg/dl, Renin: < 0.15 mcgr/ml, Aldosterone: 20.1 mcg%. Aldosterone-Renin ratio: 133. Chest X-Ray: cardiomegaly. EKG: RBBB, long QT segment and prominent broad "u" waves compatible with severe hypokalemia. A CT SCAN of the Abdomen/Pelvis showed a 3.2 cm right adrenal mass, most likely adenomatous. The patient was discharged with the diagnosis of primary aldosteronism. Due to the diagnosis of diabetes mellitus, hypertension and the three episodes of ventricular fibrillation, surgical treatment was postponed until stress tests and eventual coronary angiographic studies were performed. We found in our review of the medical literature 9 reports of fibrillation associated with hyperaldosteronism. Of those, only two were associated with primary aldosteronism, one of them with a fatal outcome. This case is highly unusual and emphasizes the importance of an adequate diagnosis of secondary hypertension.
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PMID:Ventricular fibrillation as the first manifestation of primary hyperaldosteronism. 1961 May 66

Aldosterone excess in the context of primary aldosteronism (PA) has been associated with impaired glucose tolerance and diabetes mellitus. We retrospectively assessed the prevalence of diabetes mellitus in patients from the German Conn's Register and compared the data with those from hypertensive subjects of a population-based survey. In a case-control study, we have compared 638 patients with PA from the German Conn's registry who were treated in 6 German centers with 897 hypertensive control subjects from the population-based F3 survey of the Cooperative Health Research in the Region of Augsburg (KORA). The samples were matched for age, sex, and blood pressure in a 1:1 ratio. Risk factors associated with the presence of diabetes mellitus were calculated in 638 patients with PA and 897 hypertensive controls. In the case control study, the diabetes prevalence was calculated in 338 cases and controls. In patients with primary aldosteronism, age, BMI, and a higher number of antihypertensive drugs (lowest tertile vs. highest tertile) were variables associated with diabetes mellitus. In contrast, serum potassium and plasma aldosterone concentrations were not associated with higher diabetes prevalence, whereas diastolic blood pressure was inversely associated with diabetes mellitus. Diabetes mellitus was more prevalent in patients with PA than in 338 matched controls (23 vs. 10% in controls). Our data for the German population show that diabetes mellitus is more prevalent in patients with primary aldosteronism than in hypertensive controls.
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PMID:Is primary aldosteronism associated with diabetes mellitus? Results of the German Conn's Registry. 2064 12

The prevalence of diabetes, hypertension, and cardiovascular disease (CVD) and chronic kidney disease (CKD) is increasing in concert with obesity. Insulin resistance, metabolic dyslipidemia, central obesity, albuminuria. and hypertension commonly cluster to comprise the cardiometabolic syndrome (CMS). Emerging evidence supports a shift in our understanding of the crucial role of elevated serum aldosterone in promoting insulin resistance and resistant hypertension. Aldosterone enhances tissue generation of oxygen free radicals and systemic inflammation. This increase in oxidative stress and inflammation, in turn, contributes to impaired insulin metabolic signaling, reduced endothelial-mediated vasorelaxation, and associated cardiovascular and renal structural and functional abnormalities. In this context, recent investigation indicates that hyperaldosteronism, which is often associated with obesity, contributes to impaired pancreatic beta-cell function as well as diminished skeletal muscle insulin metabolic signaling. Accumulating evidence indicates that the cardiovascular and renal abnormalities associated with insulin resistance are mediated, in part, by aldosterone's nongenomic as well as genomic signaling through the mineralocorticoid receptor (MR). In the CMS, there are increased circulating levels of glucocorticoids, which can also activate MR signaling in cardiovascular, adipose, skeletal muscle, neuronal, and liver tissue. Furthermore, there is increasing evidence that fat tissue produces a lipid soluble factor that stimulates aldosterone production from the adrenal zona glomerulosa. Recently, we have learned that MR blockade improves pancreatic insulin release, insulin-mediated glucose utilization, and endothelium-dependent vasorelaxation as well as reduces the progression of CVD and CKD. In summary, aldosterone excess exerts detrimental metabolic effects that contribute to the development of the CMS and resistant hypertension as well as CVD and CKD.
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PMID:Aldosterone: role in the cardiometabolic syndrome and resistant hypertension. 2022 58

We describe a diabetic patient successfully treated for an acute mycotic aortic arch pseudoaneurysm with primary aldosteronism. The patient first complained of severe pain in the left upper extremity and left back with high C reactive protein (CRP) and high-grade fever. It was suspected that acute aortic dissection had developed in association with mycotic pseudoaneurysm of the aortic arch because of chest X-ray findings of enlargement of the aortic arch. Computed tomography (CT) of the aortic arch revealed an aortic aneurysm protruding in the superior direction. Staphylococcus aureus was detected in blood culture, suggesting a mycotic aortic aneurysm, and artificial blood vessel replacement of the aortic arch was performed. Intraoperative findings suggested aortic pseudoaneurysm, which consisted of mediastinal rupture of the aorta at the distal arch. Our patient had a 2-year history of type 2 diabetes mellitus and poor blood sugar control, even with twice-daily injection of insulin. Blood pressure was not always well controlled because of primary aldosteronism. Thus, it was speculated that hyperaldosteronism, as well as diabetes-associated atherosclerosis, had persisted for a long time. No reports have described mycotic pseudoaneurysm in the aortic arch in a diabetic patient associated with primary aldosteronism. It is necessary to note that serious vascular complications are possible if aldosteronism is left untreated or is treated insufficiently as essential hypertension.
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PMID:Successful treatment of a mycotic aortic pseudoaneurysm in a patient with type 2 diabetes mellitus while treating primary aldosteronism with spironolactone. 2046 87

A 35-year-old woman was admitted to the Nephrology and Dialysis Unit of Pisa University for hypertension, hypokalaemia, renal impairment, proteinuria and hyperglycaemia. plasma renin activity (PRA) and plasma aldosterone were elevated, but Doppler ultrasound and angio-computed tomography (CT) of renal arteries were normal. Abdomen CT revealed only a left adrenal mass, and measurement of catecholamines suggested the diagnosis of pheochromocytoma. Biochemical findings suggestive of hyperparathyroidism were also detected, but a multiple endocrine disorder was excluded by genetic analysis. Pathology examination confirmed the pheochromocytoma and immunohistochemistry also showed positivity for parathyroid hormone. After surgery, disappearance of the symptoms and normalization of all haemodynamic and humoral parameters was observed. This is a rare case of pheochromocytoma responsible for secondary hyperaldosteronism, hyperparathyroidism, proteinuric renal disease and diabetes mellitus.
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PMID:A case of pheochromocytoma presenting as secondary hyperaldosteronism, hyperparathyroidism, diabetes and proteinuric renal disease. 2121 67

Primary aldosteronism has been considered a rare disease in the past years, affecting 1% of the hypertensive population. Subsequently, growing evidence of its higher prevalence is present in literature, although the estimates of disease range from 5 up to 20%, as in type 2 diabetes and resistant hypertension. The main reasons for these variations are associated with the selection of patients and diagnostic procedures. If we consider that hypertension is present in about 20% of the adult population, primary aldosteronism can no longer be considered a rare disease. Patients with primary aldosteronism have a high incidence of cardiovascular, cerebrovascular and kidney complications. The identification of these patients has therefore a practical value on therapy, and to control morbidities derived from vascular damage. The ability to identify the prevalence of a disease depends on the number of subjects studied and the methods of investigation. Epidemiological studies are affected by these two problems: there is not consensus on patients who need to be investigated, although testing is recommended in subjects with resistant hypertension and diabetes. The question of how to determine aldosterone and renin levels is open, particularly if pharmacological wash-out is difficult to perform because of inadequate blood pressure control.
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PMID:Changes in the perceived epidemiology of primary hyperaldosteronism. 2183 71

Resistant hypertension, defined as failure to achieve target blood pressure despite the use of optimal or maximum doses of at least 3 agents, one of which is a diuretic, or requiring 4 or more medications to achieve blood pressure goal, is likely to affect up to 20% of all patients with hypertension. Apparent resistant hypertension may be caused by medication nonadherence, substances that either interfere with antihypertensive mediations or cause blood pressure elevation, and under- or inappropriate medication treatment. Certain patient characteristics are associated with the presence of resistant hypertension and include chronic kidney disease, diabetes, obesity, and presence of end-organ damage (microalbuminuria, retinopathy, left-ventricular hypertrophy). Secondary causes of resistant hypertension are not uncommon and include obstructive sleep apnea, chronic kidney disease, primary aldosteronism, renal artery stenosis, pheochromocytoma, and Cushing's disease. Initial medication management usually includes adding or increasing the dose of a diuretic, which is effective in lowering the blood pressure of a large number of patients with resistant hypertension. Additional management options include maximizing lifestyle modification, combination therapy of antihypertensive agents depending on individual patient characteristics, adding less-commonly used fourth- or fifth-line antihypertensive agents, and referral to a hypertension specialist.
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PMID:Clinical approach in treatment of resistant hypertension. 2196 29


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