Adrenal Venous Sampling for Aldosterone
Differential diagnosis of primary hyperaldosteronism, between aldosterone producing adenoma and idiopathic hyperaldosteronism where CT has demonstrated no definite tumour and when the results of selenium cholesterol scanning are ambiguous.
Discuss with radiologist:
Allergy to contrast.
Significant ischaemic heart disease.
Adrenal infarction rarely.
Remember liquorice ingestion and carbenoxolone may mimic hyperaldosteronism.
Spironolactone, oestrogens 6 weeks
Diuretics 4 weeks
ACE Inhibitors and NSAIDs 2 weeks
Calcium antagonists 1 week
Sympathomimetics 1 week
Beta-blockers 1 week
If anti-hypertensive therapy needs to be continued then prazosin, doxazosin or bethanidine may be used.
Patient should be on unrestricted sodium intake before admission.
Consent (risks of bleeding from sheath sites, venous thrombosis).
8 Plain tubes (red top Vacutainers).
Tetracosactrin 250 micrograms (Synacthen).
Arrangements for immediate transfer of samples to laboratory. Two assistants required for this.
Catheter inserted via femoral vein and adrenal veins selectively cannulated under X-ray control. Bolus of Synacthen may be given 20 minutes prior to sampling. Samples taken simultaneously for cortisol, DHEAS, androstenedione and aldosterone.
Normal adrenal vein aldosterone 100-400 ng/dl. In aldosterone producing adenoma the ipsilateral value is 1000-10000 ng/dl. Ratio of >10:1 between sides is considered diagnostic.
Confirm that adrenal veins have been cannulated by comparing cortisol and adrenal androgen levels on the two sides.
SENSITIVITY AND SPECIFICITY
The main problem with this procedure is difficulty in catheterising the right adrenal vein, this is because it enters the inferior vena cava at an acute angle and may be multiple. Even in the best hands cannulation is not possible in 26% of patients.
In patients in whom both adrenal veins are successfully cannulated (as demonstrated by a symmetrical cortisol response to ACTH) this procedure is 90-95% successful in correctly distinguishing between idiopathic hyperaldosteronism and aldosterone producing adenoma by demonstrating a unilateral increase in aldosterone secretion.
Young W.F. Jr., Klee G.G., Endo. Metab. Clin. N. Am., 17,2; 367-395 (1988).
Melby J.C., J. Clin. Endo. Met., 69,4; 697-703 (1989).