• Causes urinary loss of potassium and hypokalemia, sodium retention and hypertension
  
• Sodium retention causes volume overload, which suppresses the renin-angiotensin system and reduces plasma renin activity; volume overload causes polyuria, polydipsia, nocturia, hypertension, alkalosis and hypernatremia
  
• Primary hyperaldosteronism: due to adrenal pathology (most common are adenoma and cortical hyperplasia), idiopathic and rarely carcinoma; also called Conn’s syndrome
  
• Secondary hyperaldosteronism: due to increased levels of plasma renin from non-adrenal pathology, including congestive heart failure, pregnancy (due to estrogen), decreased renal perfusion (renal arterial stenosis, nephrosclerosis), hypoalbuminemia, ovarian tumor and hyperthyroidism
  
• Tertiary hyperaldosteronism (Bartter’s syndrome): hypertrophy and hyperplasia of renal juxtaglomerular cells, causing elevated plasma renin, angiotensin II and aldosterone, hypokalemic alkalosis but no hypertension; some cases are autosomal recessive; glucocorticoid suppressible hyperaldosteronism - infants or adults, rare and familial; due to mutation which causes developmental derangement of cortical zonation, with hybrid cells between glomerulosa and fasciculata that are under the influence of ACTH, but can be suppressed by dexamethasone
  
• Symptoms: hypokalemia causes weakness, paresthesias, visual disturbances and tetany
  
• Diagnosis: non-suppressible aldosterone excretion with normal cortisol excretion, low plasma renin
  

• Surgery for adenoma
  
• Surgery usually not curative for bilateral adrenal hyperplasia - these patients need spironolactone or other antihypertensive drugs
  

• Adenomas are small, unilateral, solitary and golden-yellow
  

• Thickened glomerulosa layer with tongue-like projections into fasciculata
  
• Spironolactone bodies in patients treated with spironolactone
  
• Variable micronodules of clear cells
  
• Note: adenomas are usually one nodule; nodular hyperplasia is usually bilateral
  

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