PRIMARY: caused by an aldosterone-secreting tumor, resulting in hypertension, hypokalemia, metabolic alkalosis, and low plasma rennin.
Increased aldosterone secretion from adrenal, which results primary from 2 major subtypes:
1)      Unilateral aldosterone-producing adenoma (APA) or Conn 
2)      Idiopathic hyperaldosteronism (IHA) or bilateral adrenal hyperplasia. Aldosterone increases in response to postural studies. Rarely, patients are hyperplastic (primary adrenal hyperplasia), and the response of aldosterone to standing is similar to rennin-unresponsive APA 
Other subtypes:
3)      Rennin-responsive adenoma
4)      Primary adrenal hyperplasia
5)      Glucocorticoids-remediable aldosteronism.
Aldosterone, by inducing renal distal tubular reabsortion of sodium, enhances secretion of potassium and hydrogen ions, causing hypernatremia, hypokalemia, alkalosis. 
Hypokalemia → fatigue, muscle weakness, cramping, headaches, and palpitations.
                            Polydipsia and polyuria from hypokalemia-induced nephrogeni diabetic insipidus.
Treatment: the goal of treatment is to prevent the morbidity and mortality associated with hypertension and hypokalemia. Appropriate treatment depends on the cause e.g. Conn 
Medication: spironolactone (aldosterone antagonists).
SECUNDARY: Due to: Renal artery stenosis
                                        Chronic renal failure
                                        CHF
                                        Cirrhosis
                                        Nephrotic syndrome
Kidney perception of low intravascular volume results in an overactive rennin-angioitensin system. Associated with high plasma rennin.
 
 
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