NOT a feature of primary hyperaldosteronism is -
" Edema is not seen in primary aldosteronism, even though there is marked sodium and water retention."

Lack of edema is due to the fact that increased atrial natriuretic factor secreted by cardiac tissues limits sodium retention.
When the cause of hyperaldosteronism lies within the adrenal gland itself the condition is known as primary hyperaldosteronism (Conn's syndrome)
The most common cause of primary hyperaldosteronism is unilateral adrenal adenoma.

Clinical features of primary hyperaldosteronism (Conn's syndrome) 

In primary hyperaldosteronism there is excess secretion of mineralocorticoid (aldosterone) by adrenal cortex.
Aldosterone is the major mineralocorticoid secreted by the adrenals. The major physiological effect of aldosterone is

It increases absorption of sodium and simultaneously increases secretion ofpotassium by the renal tubular epithelial cells in the collecting tubules. Therefore aldosterone causes sodium to be conserved in the extracellular fluid while increasing potassium excretion in the urine.
Now,
The effect of excess aldosterone secretion.
Excess aldosterone does not cause significant increase in serum sodium

Excess aldosterone increases extracellular fluid volume and arterial pressure but has only a small effect on plasma sodium concentration.
Although, aldosterone has a potent effect in decreasing the rate of sodium excretion by the kidneys, the concentration of sodium in the extracellular fluid rises only a few milliequivalents. The reason is that when sodium is reabsorbed by the tubules there is simultaneous osmotic absorption of almost equivalents amount of water. Also, small increase in extracellular fluid sodium concentration stimulates thirst and increased water intake, if water is available.
Therefore the extracellular fluid volume increases almost as much as the retained sodium but without much change in sodium concentration.
Therefore even though aldosterone is one of the body's most powerful sodium retaining hormones, only transient sodium retention occurs when excess amounts are secreted.

​Excess aldosterone does not produce edema

Aldosterone mediated increase in extracellular fluid volume lasting more than 1-2 days also leads to increase in arterial pressure.
Increase in extracellular fluid increase the B.P. to 15-20 mm Hg and this elevated B.P. in turn increases kidney excretion of both salt and water called pressure natriuresis and pressure diuresis.
This return to normal of salt and water excretion by the kidneys as a result of pressure natriuresis and diuresis is called aldosterone escape (this mechanism does not allow edema to develop).
Thereafter, the rate of gain of salt and water by the body is zero, and balance is maintained between salt and water intake and output by the kidneys despite continued excess aldosterone.
In the meantime however the person has developed hypertension, which lasts as long as the person remains exposed to high levels of aldosterone.

​Excess aldosterone causes hypokalenzia and muscle weakness

Normally aldosterone increases the secretion of potassium by renal tubular epithelial cells. Excess aldosterone further enhances this process.
Excess aldosterone not only causes loss ofpotassium ions from the extracellular fluid but also stimulates transport of potassium from the extracellular fluid into intracellular fluid.
Therefore, excessive secretion of aldosterone causes serious decrease in plasma potassium concentration.

​Excess aldosterone increases tubular hydrogen ion secretion, with resultant mild alkalosis

Aldosterone not only causes potassium to be secreted into the tubule in exchange for sodium reabsorption in the cells of renal collecting tubules but also causes secretion of hydrogen ions in exchange for sodium in the intercalated cells of the cortical collecting tubules.
The obvious effect of this is to decrease the hydrogen ion concentration in the extracellular fluid. This effect usually causes a mild degree of alkalosis
Pedal edema
Diastolic hypertension
Polyuria
Hypokalemia