| Confirmatory test . | Procedure . | Interpretation . | Concerns . |
|---|---|---|---|
| Oral sodium loading test | Patients should increase their sodium intake to >200 mmol/d (∼6 g/d) for 3 d, verified by 24-h urine sodium content. Patients should receive adequate slow-release potassium chloride supplementation to maintain plasma potassium in the normal range. Urinary aldosterone is measured in the 24-h urine collection from the morning of d 3 to the morning of d 4. | PA is unlikely if urinary aldosterone is lower than 10 μg/24 h (27.7 nmol/d) in the absence of renal disease where PA may coexist with lower measured urinary aldosterone levels. Elevated urinary aldosterone excretion [>12 μg/24 h (>33.3 nmol/d) at the Mayo Clinic, >14 μg/24 h (38.8 nmol/d) at the Cleveland Clinic] makes PA highly likely. | This test should not be performed in patients with severe uncontrolled hypertension, renal insufficiency, cardiac insufficiency, cardiac arrhythmia, or severe hypokalemia. The 24-h urine collection may be inconvenient. Laboratory-specific poor performance of the RIA for urinary aldosterone (aldosterone 18-oxo-glucuronide or acid-labile metabolite) may blunt diagnostic accuracy, a problem obviated by the currently available HPLC-tandem mass spectrometry methodology (52). Aldosterone 18-oxo-glucuronide is a renal metabolite, and its excretion may not rise in patients with renal disease. |
| SIT | Patients stay in the recumbent position for at least 1 h before and during the infusion of 2 liters of 0.9% saline iv over 4 h, starting at 0800–0930 h. Blood samples for renin, aldosterone, cortisol, and plasma potassium are drawn at time zero and after 4 h, with blood pressure and heart rate monitored throughout the test. | Postinfusion plasma aldosterone levels <5 ng/dl make the diagnosis of PA unlikely, and levels >10 ng/dl are a very probable sign of PA. Values between 5 and 10 ng/dl are indeterminate (57–60). | This test should not be performed in patients with severe uncontrolled hypertension, renal insufficiency, cardiac insufficiency, cardiac arrhythmia, or severe hypokalemia. |
| FST | Patients receive 0.1 mg oral fludrocortisone every 6 h for 4 d, together with slow-release KCl supplements (every 6 h at doses sufficient to keep plasma K+, measured four times a day, close to 4.0 mmol/liter), slow-release NaCl supplements (30 mmol three times daily with meals) and sufficient dietary salt to maintain a urinary sodium excretion rate of at least 3 mmol/kg body weight. On d 4, plasma aldosterone and PRA are measured at 1000 h with the patient in the seated posture, and plasma cortisol is measured at 0700 and 1000 h. | Upright plasma aldosterone >6 ng/dl on d 4 at 1000 h confirms PA, provided PRA is < 1 ng/ml·h and plasma cortisol concentration is lower than the value obtained at 0700 h (to exclude a confounding ACTH effect) (42, 43, 56, 61–63). | Although some centers (10, 16) conduct this test in the outpatient setting (provided that patients are able to attend frequently to monitor their potassium), in other centers, several days of hospitalization are customary. |
| Most of the data available come from the Brisbane group (42, 43, 56, 61–63) who have established, on the basis of a very large series of patients, a cutoff of a plasma aldosterone concentration of 6 ng/dl at 1000 h in an ambulatory patient on d 4. | |||
| Proponents of the FST argue that 1) it is the most sensitive for confirming PA, 2) it is a less intrusive method of sodium loading than SIT and therefore less likely to provoke non-renin-dependent alterations of aldosterone levels, 3) it allows for the potentially confounding effects of potassium to be controlled and for ACTH (via cortisol) to be monitored and detected, and 4) it is safe when performed by experienced hands. | |||
| Captopril challenge test | Patients receive 25–50 mg captopril orally after sitting or standing for at least 1 h. Blood samples are drawn for measurement of PRA, plasma aldosterone, and cortisol at time zero and at 1 or 2 h after challenge, with the patient remaining seated during this period. | Plasma aldosterone is normally suppressed by captopril (>30%). In patients with PA, it remains elevated and PRA remains suppressed. Differences may be seen between patients with APA and those with IHA, in that some decrease of aldosterone levels is occasionally seen in IHA (23, 64–66). | There are reports of a substantial number of false-negative or equivocal results (67, 68). |
| Confirmatory test . | Procedure . | Interpretation . | Concerns . |
|---|---|---|---|
| Oral sodium loading test | Patients should increase their sodium intake to >200 mmol/d (∼6 g/d) for 3 d, verified by 24-h urine sodium content. Patients should receive adequate slow-release potassium chloride supplementation to maintain plasma potassium in the normal range. Urinary aldosterone is measured in the 24-h urine collection from the morning of d 3 to the morning of d 4. | PA is unlikely if urinary aldosterone is lower than 10 μg/24 h (27.7 nmol/d) in the absence of renal disease where PA may coexist with lower measured urinary aldosterone levels. Elevated urinary aldosterone excretion [>12 μg/24 h (>33.3 nmol/d) at the Mayo Clinic, >14 μg/24 h (38.8 nmol/d) at the Cleveland Clinic] makes PA highly likely. | This test should not be performed in patients with severe uncontrolled hypertension, renal insufficiency, cardiac insufficiency, cardiac arrhythmia, or severe hypokalemia. The 24-h urine collection may be inconvenient. Laboratory-specific poor performance of the RIA for urinary aldosterone (aldosterone 18-oxo-glucuronide or acid-labile metabolite) may blunt diagnostic accuracy, a problem obviated by the currently available HPLC-tandem mass spectrometry methodology (52). Aldosterone 18-oxo-glucuronide is a renal metabolite, and its excretion may not rise in patients with renal disease. |
| SIT | Patients stay in the recumbent position for at least 1 h before and during the infusion of 2 liters of 0.9% saline iv over 4 h, starting at 0800–0930 h. Blood samples for renin, aldosterone, cortisol, and plasma potassium are drawn at time zero and after 4 h, with blood pressure and heart rate monitored throughout the test. | Postinfusion plasma aldosterone levels <5 ng/dl make the diagnosis of PA unlikely, and levels >10 ng/dl are a very probable sign of PA. Values between 5 and 10 ng/dl are indeterminate (57–60). | This test should not be performed in patients with severe uncontrolled hypertension, renal insufficiency, cardiac insufficiency, cardiac arrhythmia, or severe hypokalemia. |
| FST | Patients receive 0.1 mg oral fludrocortisone every 6 h for 4 d, together with slow-release KCl supplements (every 6 h at doses sufficient to keep plasma K+, measured four times a day, close to 4.0 mmol/liter), slow-release NaCl supplements (30 mmol three times daily with meals) and sufficient dietary salt to maintain a urinary sodium excretion rate of at least 3 mmol/kg body weight. On d 4, plasma aldosterone and PRA are measured at 1000 h with the patient in the seated posture, and plasma cortisol is measured at 0700 and 1000 h. | Upright plasma aldosterone >6 ng/dl on d 4 at 1000 h confirms PA, provided PRA is < 1 ng/ml·h and plasma cortisol concentration is lower than the value obtained at 0700 h (to exclude a confounding ACTH effect) (42, 43, 56, 61–63). | Although some centers (10, 16) conduct this test in the outpatient setting (provided that patients are able to attend frequently to monitor their potassium), in other centers, several days of hospitalization are customary. |
| Most of the data available come from the Brisbane group (42, 43, 56, 61–63) who have established, on the basis of a very large series of patients, a cutoff of a plasma aldosterone concentration of 6 ng/dl at 1000 h in an ambulatory patient on d 4. | |||
| Proponents of the FST argue that 1) it is the most sensitive for confirming PA, 2) it is a less intrusive method of sodium loading than SIT and therefore less likely to provoke non-renin-dependent alterations of aldosterone levels, 3) it allows for the potentially confounding effects of potassium to be controlled and for ACTH (via cortisol) to be monitored and detected, and 4) it is safe when performed by experienced hands. | |||
| Captopril challenge test | Patients receive 25–50 mg captopril orally after sitting or standing for at least 1 h. Blood samples are drawn for measurement of PRA, plasma aldosterone, and cortisol at time zero and at 1 or 2 h after challenge, with the patient remaining seated during this period. | Plasma aldosterone is normally suppressed by captopril (>30%). In patients with PA, it remains elevated and PRA remains suppressed. Differences may be seen between patients with APA and those with IHA, in that some decrease of aldosterone levels is occasionally seen in IHA (23, 64–66). | There are reports of a substantial number of false-negative or equivocal results (67, 68). |
| Confirmatory test . | Procedure . | Interpretation . | Concerns . |
|---|---|---|---|
| Oral sodium loading test | Patients should increase their sodium intake to >200 mmol/d (∼6 g/d) for 3 d, verified by 24-h urine sodium content. Patients should receive adequate slow-release potassium chloride supplementation to maintain plasma potassium in the normal range. Urinary aldosterone is measured in the 24-h urine collection from the morning of d 3 to the morning of d 4. | PA is unlikely if urinary aldosterone is lower than 10 μg/24 h (27.7 nmol/d) in the absence of renal disease where PA may coexist with lower measured urinary aldosterone levels. Elevated urinary aldosterone excretion [>12 μg/24 h (>33.3 nmol/d) at the Mayo Clinic, >14 μg/24 h (38.8 nmol/d) at the Cleveland Clinic] makes PA highly likely. | This test should not be performed in patients with severe uncontrolled hypertension, renal insufficiency, cardiac insufficiency, cardiac arrhythmia, or severe hypokalemia. The 24-h urine collection may be inconvenient. Laboratory-specific poor performance of the RIA for urinary aldosterone (aldosterone 18-oxo-glucuronide or acid-labile metabolite) may blunt diagnostic accuracy, a problem obviated by the currently available HPLC-tandem mass spectrometry methodology (52). Aldosterone 18-oxo-glucuronide is a renal metabolite, and its excretion may not rise in patients with renal disease. |
| SIT | Patients stay in the recumbent position for at least 1 h before and during the infusion of 2 liters of 0.9% saline iv over 4 h, starting at 0800–0930 h. Blood samples for renin, aldosterone, cortisol, and plasma potassium are drawn at time zero and after 4 h, with blood pressure and heart rate monitored throughout the test. | Postinfusion plasma aldosterone levels <5 ng/dl make the diagnosis of PA unlikely, and levels >10 ng/dl are a very probable sign of PA. Values between 5 and 10 ng/dl are indeterminate (57–60). | This test should not be performed in patients with severe uncontrolled hypertension, renal insufficiency, cardiac insufficiency, cardiac arrhythmia, or severe hypokalemia. |
| FST | Patients receive 0.1 mg oral fludrocortisone every 6 h for 4 d, together with slow-release KCl supplements (every 6 h at doses sufficient to keep plasma K+, measured four times a day, close to 4.0 mmol/liter), slow-release NaCl supplements (30 mmol three times daily with meals) and sufficient dietary salt to maintain a urinary sodium excretion rate of at least 3 mmol/kg body weight. On d 4, plasma aldosterone and PRA are measured at 1000 h with the patient in the seated posture, and plasma cortisol is measured at 0700 and 1000 h. | Upright plasma aldosterone >6 ng/dl on d 4 at 1000 h confirms PA, provided PRA is < 1 ng/ml·h and plasma cortisol concentration is lower than the value obtained at 0700 h (to exclude a confounding ACTH effect) (42, 43, 56, 61–63). | Although some centers (10, 16) conduct this test in the outpatient setting (provided that patients are able to attend frequently to monitor their potassium), in other centers, several days of hospitalization are customary. |
| Most of the data available come from the Brisbane group (42, 43, 56, 61–63) who have established, on the basis of a very large series of patients, a cutoff of a plasma aldosterone concentration of 6 ng/dl at 1000 h in an ambulatory patient on d 4. | |||
| Proponents of the FST argue that 1) it is the most sensitive for confirming PA, 2) it is a less intrusive method of sodium loading than SIT and therefore less likely to provoke non-renin-dependent alterations of aldosterone levels, 3) it allows for the potentially confounding effects of potassium to be controlled and for ACTH (via cortisol) to be monitored and detected, and 4) it is safe when performed by experienced hands. | |||
| Captopril challenge test | Patients receive 25–50 mg captopril orally after sitting or standing for at least 1 h. Blood samples are drawn for measurement of PRA, plasma aldosterone, and cortisol at time zero and at 1 or 2 h after challenge, with the patient remaining seated during this period. | Plasma aldosterone is normally suppressed by captopril (>30%). In patients with PA, it remains elevated and PRA remains suppressed. Differences may be seen between patients with APA and those with IHA, in that some decrease of aldosterone levels is occasionally seen in IHA (23, 64–66). | There are reports of a substantial number of false-negative or equivocal results (67, 68). |
| Confirmatory test . | Procedure . | Interpretation . | Concerns . |
|---|---|---|---|
| Oral sodium loading test | Patients should increase their sodium intake to >200 mmol/d (∼6 g/d) for 3 d, verified by 24-h urine sodium content. Patients should receive adequate slow-release potassium chloride supplementation to maintain plasma potassium in the normal range. Urinary aldosterone is measured in the 24-h urine collection from the morning of d 3 to the morning of d 4. | PA is unlikely if urinary aldosterone is lower than 10 μg/24 h (27.7 nmol/d) in the absence of renal disease where PA may coexist with lower measured urinary aldosterone levels. Elevated urinary aldosterone excretion [>12 μg/24 h (>33.3 nmol/d) at the Mayo Clinic, >14 μg/24 h (38.8 nmol/d) at the Cleveland Clinic] makes PA highly likely. | This test should not be performed in patients with severe uncontrolled hypertension, renal insufficiency, cardiac insufficiency, cardiac arrhythmia, or severe hypokalemia. The 24-h urine collection may be inconvenient. Laboratory-specific poor performance of the RIA for urinary aldosterone (aldosterone 18-oxo-glucuronide or acid-labile metabolite) may blunt diagnostic accuracy, a problem obviated by the currently available HPLC-tandem mass spectrometry methodology (52). Aldosterone 18-oxo-glucuronide is a renal metabolite, and its excretion may not rise in patients with renal disease. |
| SIT | Patients stay in the recumbent position for at least 1 h before and during the infusion of 2 liters of 0.9% saline iv over 4 h, starting at 0800–0930 h. Blood samples for renin, aldosterone, cortisol, and plasma potassium are drawn at time zero and after 4 h, with blood pressure and heart rate monitored throughout the test. | Postinfusion plasma aldosterone levels <5 ng/dl make the diagnosis of PA unlikely, and levels >10 ng/dl are a very probable sign of PA. Values between 5 and 10 ng/dl are indeterminate (57–60). | This test should not be performed in patients with severe uncontrolled hypertension, renal insufficiency, cardiac insufficiency, cardiac arrhythmia, or severe hypokalemia. |
| FST | Patients receive 0.1 mg oral fludrocortisone every 6 h for 4 d, together with slow-release KCl supplements (every 6 h at doses sufficient to keep plasma K+, measured four times a day, close to 4.0 mmol/liter), slow-release NaCl supplements (30 mmol three times daily with meals) and sufficient dietary salt to maintain a urinary sodium excretion rate of at least 3 mmol/kg body weight. On d 4, plasma aldosterone and PRA are measured at 1000 h with the patient in the seated posture, and plasma cortisol is measured at 0700 and 1000 h. | Upright plasma aldosterone >6 ng/dl on d 4 at 1000 h confirms PA, provided PRA is < 1 ng/ml·h and plasma cortisol concentration is lower than the value obtained at 0700 h (to exclude a confounding ACTH effect) (42, 43, 56, 61–63). | Although some centers (10, 16) conduct this test in the outpatient setting (provided that patients are able to attend frequently to monitor their potassium), in other centers, several days of hospitalization are customary. |
| Most of the data available come from the Brisbane group (42, 43, 56, 61–63) who have established, on the basis of a very large series of patients, a cutoff of a plasma aldosterone concentration of 6 ng/dl at 1000 h in an ambulatory patient on d 4. | |||
| Proponents of the FST argue that 1) it is the most sensitive for confirming PA, 2) it is a less intrusive method of sodium loading than SIT and therefore less likely to provoke non-renin-dependent alterations of aldosterone levels, 3) it allows for the potentially confounding effects of potassium to be controlled and for ACTH (via cortisol) to be monitored and detected, and 4) it is safe when performed by experienced hands. | |||
| Captopril challenge test | Patients receive 25–50 mg captopril orally after sitting or standing for at least 1 h. Blood samples are drawn for measurement of PRA, plasma aldosterone, and cortisol at time zero and at 1 or 2 h after challenge, with the patient remaining seated during this period. | Plasma aldosterone is normally suppressed by captopril (>30%). In patients with PA, it remains elevated and PRA remains suppressed. Differences may be seen between patients with APA and those with IHA, in that some decrease of aldosterone levels is occasionally seen in IHA (23, 64–66). | There are reports of a substantial number of false-negative or equivocal results (67, 68). |
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