The most common causes of endocrine hypertension are excess production of mineralocorticoids (primary
hyperaldosteronism), catecholamines (pheochromocytoma), thyroid hormone, and glucocorticoids (Cushing syndrome) (4).
Both primary and secondary
hyperaldosteronism cause these abnormalities, the former via an appropriate response (renin release) to decreased renal perfusion pressure or decreased sodium concentration in the ultra filtrate, the latter an inappropriate release of aldosterone from the adrenal cortex, often a result of an adrenal adenoma.
Gene mutations in patients with familial
hyperaldosteronism cause changes in the membrane voltage and result in the overproduction of aldosterone, which raises blood pressure.
Leano et al., "Evidence for abnormal left ventricular structure and function in normotensive individuals with familial
hyperaldosteronism type I," The Journal of Clinical Endocrinology & Metabolism, vol.
The various causes of hypoKPP include thyrotoxicosis, use of diuretics, distal RTA (dRTA)(6%), Gitelman syndrome, liquorice consumption, and primary
hyperaldosteronism (2,3).
Primary
hyperaldosteronism (PHA) involves the hypersecretion of the mineralocorticoid aldosterone due to adrenal gland pathology (mostly unilateral adrenal adenoma).
Secondary forms are more common and are the result of acquired hypokalemia such as thyrotoxicosis,
hyperaldosteronism, diabetic ketoacidosis, diarrhea, vomiting, drugs or RTA.
For treatment of ascites in ALD patients, diuretics should be given and in our study, as spironolactone, a potassium sparing diuretic was more commonly prescribed than the loop diuretic furosemide as there will be secondary
hyperaldosteronism in ALD patients and a drug like spironolactone which acts by inhibiting aldosterone receptor will be more effective compared to the other diuretic classes, even better than furosemide.[28]
In fact, OSA was found to have the greatest association with resistant hypertension (64%), even more so than primary
hyperaldosteronism (5.6%) [25].
Fernondez-Celis et al., "Galectin-3 blockade inhibits cardiac inflammation and fibrosis in experimental
hyperaldosteronism and hypertension," Hypertension, vol.
The causes of hypokalemia include decreased distal tubular Na delivery, secondary
hyperaldosteronism, defective H-KATPase, and bicarbonaturia [16].