The hypoaldosteronism is the disorder caused by the lack of the hormone aldosterone, which is produced by the adrenal glands.
Aldosterone is a hormone that plays its role mainly in the kidney which removes sodium and potassium retained, while increasing the volume of fluid circulating in the blood (hypervolemia).
The kidney, as compared to stimuli little blood or blood sodium decreased releases renin, which acts on a blood protein released by the liver, angiotensinogen. By action of renin on angiotensinogen produces angiotensin I is that the effect of ACE (protein found in the pulmonary arteries), produces angiotensin II.Angiotensin II stimulates the production of aldosterone by the adrenal glands.
The causes for which there is a deficit of aldosterone are varied. Some alterations involving adrenal glands themselves, which can be produced by a hereditary disorder which prevents aldosterone synthesis or acquired in patients chronically treated with heparin or derivatives. Others are external causes the adrenal glands, in this case the most common form is usually secondary to kidney disorders such as kidney failure and diabetic neuropathy originating hyporeninemic hypoaldosteronism (with decreased renin levels) can also be observed in cases of removal of an adrenal adenoma.
Most of the symptoms are due to the effect of the deficiency of aldosterone is the regulation of the levels of sodium and potassium. In general, all common manifestation is the inability of the patient to produce adequately in response to aldosterone salt restriction.
As normal levels of aldosterone cause sodium retention and potassium loss in the kidney, in hypoaldosteronism is going to present the opposite effect, causing an increase in potassium levels. This increase in potassium is also accentuated when reducing sodium in the diet eaten by salt restriction.Hyperkalemia manifests as muscular and cardiac: tingling and numbness, muscle weakness and even paralysis, respiratory arrest, and cardiac arrhythmias that can become serious and cause cardiac arrest.
Diagnosis begins by detection of alterations in blood. The occurrence common to all forms of hypoaldosteronism is the inability to adequately increase aldosterone secretion in response to salt restriction.Most patients have potassium lowering is not clear justification and is accentuated by reducing the dietary intake of sodium. In severe cases there is loss of sodium in the urine with normal intake of salt, while milder forms only by excessive loss of urine for sodium salt restriction.
In the analyzes more complex figures find low aldosterone and renin variables as causes.
The treatment is to correct the deficiency of aldosterone and potassium disturbances.
In the low-renin Hypoaldosteronism if excess potassium is mild and asymptomatic rarely needed treatment.In severe forms fludrocortisone occurs. In congenital forms are administered fludrocortisone and salt supplements.
If hyperkalemia is severe are advised diuretics like hydrochlorothiazide and furosemide (to eliminate potassium in the urine).
There are no measures to prevent these disorders. Be suspected in an individual when there is an increase in blood potassium unexplained thereof.
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