🩺 Mineralocorticoid Replacement (Fludrocortisone) Simulator

Baseline Addison's Disease

No aldosterone means kidneys waste sodium and retain potassium.

• 122: Serum Sodium (mEq/L, low)
• 6.4: Serum Potassium (mEq/L, high)
• 82/54: Blood Pressure (mmHg, hypotensive)
• ~0: Aldosterone (adrenal cortex destroyed)

Adrenal cortex failure

Autoimmune or other destruction eliminates zona glomerulosa aldosterone output.

Sodium wasting

Without aldosterone, distal nephron sodium reabsorption collapses, causing volume loss.

Hyperkalemia risk

Potassium excretion falls, raising serum potassium toward dangerous levels.

Fludrocortisone Initiated

Synthetic mineralocorticoid drug starts binding renal receptors.

• 50–200: Starting Dose (mcg/day typical)
• MR: Receptor Target (mineralocorticoid receptor)
• DCT/CD: Site of Action (distal tubule / collecting duct)
• Hours–days: Onset (to initial effect)

Drug structure

Fludrocortisone is a synthetic steroid with strong mineralocorticoid activity.

Receptor binding

Molecule diffuses into tubule cells and binds cytoplasmic mineralocorticoid receptors.

Gene transcription

Receptor complex enters nucleus, upregulating sodium/potassium transport proteins.

Sodium Reabsorption & Potassium Excretion

New channels drive sodium back into blood, potassium out to urine.

• ↑: ENaC Channels (sodium reabsorption)
• ↑: ROMK Channels (potassium secretion)
• ↑: Na/K-ATPase (basolateral pump activity)
• 1–2: Response Time (weeks to steady state)

ENaC upregulation

Epithelial sodium channels increase, pulling sodium from urine back into blood.

Potassium secretion

ROMK channels open, moving potassium from blood into urine for excretion.

Electrochemical gradient

Sodium reabsorption creates a lumen-negative charge favoring potassium loss.

Dose Titrated to Response

Clinicians adjust dose using BP, sodium, and potassium trends.

• 135–145: Target Sodium (mEq/L)
• 3.5–5.0: Target Potassium (mEq/L)
• 110–130: Target BP (systolic mmHg)
• Q1–3mo: Monitoring (labs + BP checks)

Titration logic

Dose raised if hypotensive/hyponatremic, lowered if hypertensive/hypokalemic.

Postural BP

Orthostatic blood pressure drop signals under-replacement of mineralocorticoid.

Renin feedback

Plasma renin activity helps guide dose adequacy alongside electrolytes.

Balance, Overshoot, or Persistent Deficit

Correct dosing normalizes labs; wrong dosing causes new problems.

• ~125: Optimal Dose (mcg/day (individualized))
• HTN + ↓K: Over-Replacement (hypertension, hypokalemia)
• ↓Na + ↑K: Under-Replacement (hyponatremia, hyperkalemia)
• 118/76: Well-Titrated BP (mmHg, normal)

Properly titrated

Sodium, potassium, and BP settle into normal ranges with stable dosing.

Over-replacement

Excess dose drives hypertension and hypokalemia from too much sodium retention.

Under-replacement

Insufficient dose leaves hyponatremia, hyperkalemia, and hypotension unresolved.