What changes are likely to occur in a patient's lab results after starting high-dose fludrocortisone (mineralocorticoid) therapy for orthostatic hypotension?

From the Guidelines

High-dose fludrocortisone therapy for orthostatic hypotension is likely to cause several characteristic laboratory changes, including hypokalemia, mild hypernatremia, metabolic alkalosis, and potential increases in blood glucose. After starting high-dose fludrocortisone therapy, patients with orthostatic hypotension will likely experience these changes due to the mineralocorticoid effects of the medication, which promotes sodium retention and potassium excretion in the kidneys 1. Some key changes to expect in laboratory results include:

• Hypokalemia (low potassium) due to increased potassium excretion
• Mild hypernatremia (high sodium) as the body attempts to maintain sodium homeostasis
• Metabolic alkalosis from increased hydrogen ion excretion and bicarbonate retention
• Potential moderate increases in blood glucose due to the glucocorticoid activity of fludrocortisone at higher doses
• Fluid retention, which may lead to weight gain, edema, and hemodilution, potentially decreasing hemoglobin and hematocrit values Regular monitoring of electrolytes, particularly potassium, is crucial during fludrocortisone therapy, which typically starts at 0.1 mg daily and may be titrated up to 0.2-0.4 mg daily for orthostatic hypotension 1. Supplemental potassium or potassium-sparing diuretics may be necessary to manage hypokalemia in patients on long-term therapy. It's essential to weigh the potential benefits of fludrocortisone against its risks, including supine hypertension, edema, and headache, and to consider alternative treatments, such as midodrine or droxidopa, if necessary 1.

From the FDA Drug Label

Mineralocorticoids act on the distal tubules of the kidney to enhance the reabsorption of sodium ions from the tubular fluid into the plasma; they increase the urinary excretion of both potassium and hydrogen ions In small oral doses, fludrocortisone acetate produces marked sodium retention and increased urinary potassium excretion

The patient's lab results after 5 days of high-dose fludrocortisone therapy are most likely to show:

• Increased sodium levels due to enhanced reabsorption of sodium ions in the kidney
• Decreased potassium levels due to increased urinary excretion of potassium ions These changes are a direct result of the mineralocorticoid effects of fludrocortisone on electrolyte balance 2.

From the Research

Expected Changes in Lab Results

After starting high-dose fludrocortisone therapy for orthostatic hypotension, the following changes are likely to occur in a patient's lab results:

• Increased blood volume and blood pressure due to the mineralocorticoid effects of fludrocortisone 3
• Potential decrease in plasma renin activity and aldosterone concentrations, as fludrocortisone can suppress the renin-angiotensin-aldosterone system 4
• Increased sodium retention, which may lead to increased blood pressure and potential hypertensive effects 5
• Potential development of hypokalemia (low potassium levels) due to increased potassium excretion, although potassium supplementation may ameliorate this effect 4
• Increased atrial natriuretic peptide levels, which can contribute to the mineralocorticoid-induced sodium retention 4

Potential Risks and Considerations

It is essential to monitor the patient's lab results and blood pressure closely, as high-dose fludrocortisone therapy can increase the risk of:

• Hypertension, particularly in the recumbent position 5
• Hypokalemia, which can be ameliorated with potassium supplementation 4
• Congestive heart failure, especially in patients with a history of cardiovascular conditions 6
• All-cause hospitalizations, as compared to midodrine therapy 6