Wallach's Interpretation of Diagnostic Tests: Pathways to Arriving at a Clinical Diagnosis (1124 page)

   Renin-producing tumors of the kidney

   Reduced plasma volume due to low-sodium diet, diuretics, hemorrhage, Addison disease

   Some edematous normotensive states (e.g., cirrhosis, nephrosis, congestive heart failure)

   Sodium or potassium loss due to GI disease or in 10% of patients with chronic renal failure

   Normal pregnancy

   Pheochromocytoma

   Last half of menstrual cycle (twofold increase)

   Erect posture for 4 hours (twofold increase)

   Ambulatory patients compared to bed patients

   Bartter syndrome

   Various drugs (diuretics, ACE inhibitors, vasodilators; sometimes by calcium antagonists and alpha-blockers, e.g., diazoxide, estrogens, furosemide, guanethidine, hydralazine, minoxidil, spironolactone, thiazides)

TABLE 16–66. Differentiation of Primary and Secondary Aldosteronism Based on Blood Tests and Clinical Symptoms

↑, increased; ↓, decreased; N, normal.

Decreased In

   Ninety-eight percent of cases of primary aldosteronism. Usually absent or low and can be increased less or not at all by sodium depletion and ambulation in contrast to secondary aldosteronism. PRA may not always be suppressed in primary aldosteronism; repeated testing may be necessary to establish the diagnosis. Normal PRA does not preclude this diagnosis; it is not a reliable screening test.