Management of Salt Craving in Addison's Disease Without Hyponatremia
Salt craving in Addison's disease without hyponatremia indicates inadequate mineralocorticoid replacement, and you should increase the fludrocortisone dose, typically to 0.2 mg daily, while monitoring plasma renin activity to guide optimal dosing. 1, 2
Understanding the Clinical Picture
Salt craving is a hallmark symptom of mineralocorticoid deficiency in primary adrenal insufficiency, occurring due to aldosterone deficiency causing sodium loss and electrolyte imbalance 1. The absence of hyponatremia does not exclude inadequate mineralocorticoid replacement—patients can be sodium and water depleted with elevated plasma renin activity despite normal serum sodium levels 2.
Key Clinical Assessment Points
When evaluating adequacy of mineralocorticoid replacement, assess for:
- Salt craving itself (the most direct clinical indicator of mineralocorticoid insufficiency) 1
- Postural hypotension (measure blood pressure supine and standing) 3, 1
- Plasma renin activity (the most objective measure of mineralocorticoid adequacy) 2
- 24-hour urinary sodium excretion (to assess sodium balance) 2
- Peripheral edema (indicates over-replacement) 1
The Problem with Standard Dosing
Most patients with Addison's disease are undertreated with the conventional 0.05-0.1 mg daily fludrocortisone dose. 2 A landmark study demonstrated that patients receiving 0.05-0.1 mg fludrocortisone daily with undetectable plasma aldosterone remained sodium and water depleted with persistently elevated plasma renin activity, despite optimized glucocorticoid therapy 2. When fludrocortisone was increased to 0.3 mg daily, all patients retained sodium and water appropriately, with normalization of plasma renin activity 2.
Specific Treatment Algorithm
Step 1: Increase Fludrocortisone Dose
- Increase fludrocortisone from the typical 0.1 mg daily to 0.2 mg daily 3, 2
- The FDA-approved dosing range is 0.1-0.2 mg daily for Addison's disease 4
- Most patients require 0.2 mg to maintain adequate sodium and water balance 2
Step 2: Monitor Response
Assess treatment adequacy at 2-4 weeks by checking:
- Resolution of salt craving (primary clinical endpoint) 1
- Plasma renin activity (should normalize or decrease significantly) 2
- Blood pressure (supine and standing—postural drop should resolve) 3, 1
- Serum potassium and blood urea (should decrease with adequate replacement) 2
- Body weight (modest increase expected with sodium retention) 2
Step 3: Adjust Based on Monitoring
- If salt craving persists with elevated plasma renin activity, further increase fludrocortisone in 0.05 mg increments 2
- If peripheral edema develops or blood pressure becomes elevated, reduce dose to 0.05 mg daily 4
- Continue adjusting according to plasma renin activity in conjunction with 24-hour urinary sodium excretion 2
Critical Management Points
Dietary Sodium
- Allow unrestricted sodium intake and encourage eating salty foods without restriction 1
- This is an essential component of treatment, not just dietary advice 1
- Patients should avoid potassium-containing salt substitutes marketed as "healthy" 1
Substances to Avoid
- Avoid licorice and grapefruit juice, as they potentiate the mineralocorticoid effect of hydrocortisone and can cause apparent over-replacement 1
Common Pitfall
The most common error is accepting persistent salt craving as "normal" for Addison's disease patients on standard 0.1 mg fludrocortisone dosing 2. Salt craving should resolve with adequate mineralocorticoid replacement and serves as an excellent clinical indicator for dose titration 1.
When Hyponatremia is Absent
The absence of hyponatremia does not indicate adequate mineralocorticoid replacement 2. Patients can maintain normal serum sodium through compensatory mechanisms (increased renin-angiotensin system activity, increased salt intake) while remaining in a state of chronic sodium depletion 2. Plasma renin activity is the most reliable objective measure in this scenario 2.