Orthostatic Hypotension with Fludrocortisone Treatment: Expected Laboratory Changes
This elderly man has neurogenic orthostatic hypotension (likely from autonomic failure), and after 5 days of high-dose fludrocortisone treatment, you should expect serum potassium to be LOW, plasma renin to be SUPPRESSED, and urine potassium to be ELEVATED. 1, 2
Diagnosis: Neurogenic Orthostatic Hypotension
The clinical presentation confirms classical orthostatic hypotension with:
- Sustained BP drop of 36/21 mmHg (from 130/85 supine to 94/64 standing), which exceeds diagnostic criteria of ≥20 mmHg systolic or ≥10 mmHg diastolic drop within 3 minutes 1, 3
- 8-month chronic history with lightheadedness on standing, suggesting progressive autonomic dysfunction rather than acute volume depletion 1
- Likely blunted heart rate response (though not explicitly stated), which is characteristic of neurogenic OH where HR increase is typically <10 bpm due to impaired autonomic control 1, 3
The elderly population is particularly susceptible, with OH prevalence of 10-30% in this age group, often related to aging-associated autonomic dysfunction, diabetes, or Parkinson's disease 4, 5.
Mechanism of Fludrocortisone Action
Fludrocortisone is a mineralocorticoid that acts on renal mineralocorticoid receptors to:
- Increase sodium reabsorption in the distal tubule and collecting duct 6, 4
- Expand plasma volume through sodium and water retention 6, 5
- Increase blood pressure via volume expansion 2, 4
This medication is recommended as first- or second-line pharmacological therapy for neurogenic orthostatic hypotension by multiple guidelines 1, 2, 6.
Expected Laboratory Changes After 5 Days of High-Dose Fludrocortisone
Serum Potassium: DECREASED (Hypokalemia)
- Mineralocorticoid activity promotes potassium excretion in exchange for sodium reabsorption in the distal nephron 1, 2
- High-dose fludrocortisone significantly increases urinary potassium losses 1
- Hypokalemia is a recognized adverse effect that requires monitoring, particularly in patients with left ventricular hypertrophy or cardiac disease where it increases arrhythmia risk 1
Plasma Renin: SUPPRESSED (Low)
- Volume expansion from sodium retention suppresses the renin-angiotensin-aldosterone system 4, 5
- The increased plasma volume signals the kidneys to reduce renin secretion 7
- This represents appropriate negative feedback to the volume-expanded state 7
Urine Potassium: ELEVATED (Increased)
- Direct consequence of mineralocorticoid action on the distal tubule, where sodium reabsorption is coupled with potassium secretion 1
- High-dose fludrocortisone amplifies this effect, leading to substantial urinary potassium losses 1, 2
- This kaliuresis contributes to the development of hypokalemia 1
Clinical Monitoring Considerations
Avoid hypokalemia and QT-prolonging drugs as a priority in patients receiving fludrocortisone, especially those with cardiac disease or left ventricular hypertrophy 1. The combination of:
- Volume expansion (average weight gain 1.6 kg) 7
- Sodium retention (decreased nocturnal sodium excretion from 8.0 to 5.9 mmol/h) 7
- Potassium wasting 1
creates a metabolic profile requiring careful electrolyte monitoring.
Supine hypertension is a common complication of fludrocortisone therapy in neurogenic OH, as it is impossible to normalize standing BP without generating excessive supine hypertension 4. The practical goal is symptom improvement and increased standing time for activities of daily living, not BP normalization 4, 5.
Treatment Efficacy Timeline
Combined treatment with fludrocortisone and non-pharmacologic measures (high salt diet 150-200 mmol Na+/day, head-up tilt sleeping position):