Mineralocorticoid Replacement Therapy
From the desk of Lewis S. Blevins Jr., M.D. – Treatment of partial and complete aldosterone deficiency seems to be an arena where inexperienced physicians miss the mark more often than not. In this brief summary, I will address mineralocorticoid deficiency as it applies to most patients with aldosterone deficiency whether it be primary or secondary. I will share my experiences in the form of statements that I believe apply to most affected patients. Several of the following statements pertain to specific conditions.
Patients with hypopituitarism do not develop aldosterone deficiency.
Patients who have been treated with excessive doses of glucocorticoid hormones and have a suppressed pituitary-adrenal axis do not require mineralocorticoid replacement.
Patients with POTS and other sympathetic dystrophies may or may or may not have hyporeninemic hypoaldosteronism but might still respond to mineralocorticoid replacement.
Patients with cerebral or renal salt wasting often require mineralocorticoid therapy to help them conserve sodium.
Patients with primary adrenal insufficiency and those with salt wasting 21-hydroxylase deficiency have the most severe form of aldosterone deficiency.
Patients with hyporeninemic hypoaldosteronism often require mineralocorticoid replacement unless they have the syndrome of apparent mineralocorticoid excess or clear cut evidence of volume overload accounting for the suppression of renin and aldosterone. Treating physicians should always make a careful assessment of these patients and refer to an endocrinologist or nephrologist if unable to decide if a patient needs mineralocorticoid replacement. I would say the most common error in this arena is failure to treat people who need it.
Some people with primary adrenal insufficiency and mild forms of CAH can avoid mineralocorticoid replacement therapy if they maintain an aggressive sodium intake. I do not advise this approach. I’ve seen too many patients develop hyponatremia and hyperkalemia attempting to manage with oral sodium alone. Prevention of catastrophe is key here.
Florinef, also known as fludrocortisone, is the typical replacement for aldosterone deficiency. This drug binds to the mineralocorticoid receptor in the kidneys. It’s function is to conserve sodium and water and it will waste potassium by doing so. Too little leads to volume depletion with hyponatremia due to salt losses and hyperkalemia as potassium is not secreted by the kidney. The plasma renin is usually high. Too much results in salt and water excesses and potassium wasting leading to hypokalemia. Sodium levels are usually normal. Patients often have edema (swelling) in the ankles and legs. The plasma renin is usually low.
Plasma renin and electrolytes are essential in the evaluation and management of the adequacy of dose. I aim for mid- to high-normal plasma renin levels and normal electrolytes. Sometimes I advise increasing or decreasing salt intake rather than a fludrocortisone dose adjustment. Patients who have pitting edema of the ankles or lower legs may be taking too much fludrocortisone or salt. They may have some other condition leading to the edema, but the doses certainly may need to be adjusted.
Patients treated with high or stress doses of hydrocortisone, for example in the hospital setting for illness or operation, do not usually require mineralocorticoid replacement. For example, hydrocortisone doses over 75 mg daily usually provide sufficient mineralocorticoid activity. The fludrocortisone can be discontinued during stress dose hydrocortisone therapy unless there is hyperkalemia or evidence for volume depletion. Florinef does do not usually require doubling or tripling during medical stress or procedures.
Children usually require higher doses of fludrocortisone: on average 0.3 mg daily.
Most adults require 0.1 to 0.2 mg fludrocortisone daily.
Older adults often only require 0.05 mg daily.
Liberalize sodium intake if you have aldosterone deficiency. This is especially important in summer months. Salt and water need to be moving through the urinary space of the kidney for the drug to have an effect. If you don’t take in an adequate amount of salt you will likely get dehydrated or hyperkalemic even on replacement therapy.
Mineralocorticoid deficiency is usually the culprit in patients with severe adrenal crisis. The deficiency causes the hyponatremia and hypokalemia with profound volume depletion. Hyponatremia can develop due to cortisol deficiency and compound the matter.
Children with salt-wasting 21-hydroxylase deficiency tend to grow better if their plasma renin levels are controlled.
Medic-Alert tags, bracelets, and other forms of identification that relate an underlying condition should list the condition and necessary treatments. For example:
Addisons Disease
Steroid and Florinef Dependent
Learn more about fludrocortisone by visiting these sites/
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