The relationship between aldosteronism and hypertension

  The prevalence of hypertension in China has increased rapidly in recent years, reaching 160 million patients, the highest in the world, but its awareness rate, treatment rate and control rate is very low, only 27%. Primary aldosteronism (referred to as proaldosterone) is a secondary hypertension characterized by hypertension, low or normal blood potassium, low plasma renin, and high plasma aldosterone levels due to excessive secretion of aldosterone by adrenal cortical tumors or hyperplasia, with the peak age of onset being 30-50 years old and more female patients than male. The prevalence of primary aldehyde in the hypertensive population is about 5% to 13%.  1, the characteristics of hypertension in patients with aldosteronism protanal hypertension more long course, for the slow development of hypertension; blood pressure is mostly moderate increase, but there are a few patients show malignant hypertension, and the application of general antihypertensive drugs often no significant effect. As the disease progresses, heart, brain and kidney damage of hypertension may occur, but its fundus changes often do not parallel the degree of hypertension.  2, aldosteronism hypertension concomitant symptoms: patients with proaldosteronism may have spontaneous hypokalemia (2.0-3.5 mmol / L) due to excessive renal tubular K+ discharge, but about half of the patients have normal blood K+, and hypokalemia is induced by a high sodium diet or taking antihypertensive drugs containing diuretics. Prolonged hypokalemia can lead to renal tubular vacuolar degeneration, impaired urinary concentration, increased nocturnal urine output, and in severe cases, renal function impairment. Hypokalemia can also inhibit insulin secretion, so long-term hypokalemia can lead to low glucose tolerance or even diabetes in half of the patients.  Screening of hypertensive patients: (1) Spontaneous hypokalemia (serum K+ <3.5 mmol/L); (2) Moderate or severe hypokalemia (serum K+ <3.O mmol/L); (3) Severe hypokalemia induced by taking regular doses of thiazide (3) Severe hypokalemia induced by taking regular doses of thiazide diuretics and difficult to correct with large amounts of potassium salt supplementation; (4) Serum K+ does not return to normal within 4 weeks after stopping diuretics; (5) Refractory hypertension due to other secondary causes are excluded.  4. Tests related to proaldosteronism hypertension: plasma renin activity (PRA) low PRA levels and no spikes due to low sodium, dehydration or standing position 5. Treatment of proaldosteronism hypertension Surgical treatment of patients with proaldosteronism should be preferred to surgical removal of adrenal tumors. Patients with secondary aldosteronism can be treated satisfactorily with unilateral, subtotal or bilateral adrenalectomy. Laparoscopic adrenalectomy is an ideal surgical procedure with the advantages of short hospital stay and low long-term mortality. In order to reduce the risk of surgery, patients should be given Antiseptic before surgery to correct hypokalemia. Postoperative hypoaldosteronism is likely to occur and a high sodium diet is required for several weeks to prevent hyperkalemia due to hypoaldosteronism. Even after total bilateral adrenalectomy, it is still difficult to control hypertension in patients with special aldehydes. Therefore, patients with tertiary aldehyde tend to be treated medically.