Renal · Year 2 · from Renal
Case 3: Primary Hyperaldosteronism
Patient Presentation
A 45-year-old female presents for evaluation of refractory hypertension. She is on four antihypertensive medications but her blood pressure remains poorly controlled. She also reports muscle cramps and weakness.
History of Present Illness
- Hypertension diagnosed at age 38
- Currently on amlodipine, lisinopril, hydrochlorothiazide, and metoprolol at maximum doses
- Frequent headaches
- Muscle cramps, especially at night
- Polyuria and nocturia
- No family history of hypertension
Physical Examination
- Blood pressure: 168/102 mmHg
- Heart rate: 64 bpm
- No edema
- Normal cardiac exam
- Decreased deep tendon reflexes
Workup
Laboratory Studies:
- Serum sodium: 144 mEq/L (high-normal)
- Potassium: 2.8 mEq/L (low)
- Bicarbonate: 32 mEq/L (elevated - metabolic alkalosis)
- Creatinine: 0.9 mg/dL
- Plasma aldosterone: 28 ng/dL (elevated)
- Plasma renin activity: 0.2 ng/mL/hr (suppressed)
- Aldosterone/renin ratio: 140 (elevated, >30 is suggestive)
Confirmatory Test:
- Oral sodium loading test: Aldosterone remains elevated (not suppressed)
Imaging:
- CT adrenals: 1.8 cm left adrenal adenoma
Diagnosis
Primary Hyperaldosteronism (Conn Syndrome) due to Aldosterone-Producing Adenoma
Discussion
This case illustrates aldosterone's role in sodium balance:
- Aldosterone Effects: The lecture describes how aldosterone increases ENaC and Na+/K+-ATPase expression in the collecting duct. This increases sodium reabsorption (causing hypertension and mild hypernatremia) while increasing potassium secretion (causing hypokalemia).
- Suppressed Renin: In primary hyperaldosteronism, the autonomous aldosterone production suppresses renin (negative feedback). This distinguishes it from secondary hyperaldosteronism (like heart failure) where both renin and aldosterone are elevated.
- Metabolic Alkalosis: Aldosterone also stimulates H+-ATPase in intercalated cells, increasing acid secretion and generating metabolic alkalosis.
Treatment
- Spironolactone (mineralocorticoid receptor antagonist) for initial blood pressure control
- Surgical consultation for laparoscopic adrenalectomy (curative for adenoma)
- Potassium supplementation pre-operatively
- Post-operative monitoring for transient hypoaldosteronism
Clinical Pearl
The aldosterone:renin ratio is a screening test for primary hyperaldosteronism. A ratio >30 (with aldosterone >15 ng/dL) should prompt confirmatory testing. Hypokalemia occurs in only 30-40% of cases - most patients have normal potassium.
Image Reference
For visual reference of volume regulation concepts, see:
- Radiopaedia: Hyperaldosteronism - CT images of adrenal adenomas
- Wikimedia Commons: RAAS - Pathway diagrams
- Radiopaedia: Pulmonary edema - Chest X-ray findings in heart failure
Learning Points
- Effective Circulating Volume: In heart failure and cirrhosis, ECV is reduced despite total body volume overload. The kidneys respond as if hypovolemic.
- Urine Sodium Interpretation:
- <20 mEq/L: Volume depletion or reduced ECV (appropriate sodium retention)
- >40 mEq/L: ATN, SIADH, diuretics, or salt-wasting conditions
- Hyponatremia Classification: Always classify by volume status (hypovolemic, euvolemic, hypervolemic) - this determines treatment approach.
- RAAS in Edematous States: Activation of RAAS perpetuates edema formation. RAAS blockers help break this cycle.
- Aldosterone Paradox: Aldosterone causes different effects depending on stimulus - volume depletion causes sodium retention, while hyperkalemia causes potassium excretion, even though aldosterone is elevated in both.