Hypertension and Hypokalemia: Suspected Hyperaldosteronism
Review renin-angiotensin-aldosterone physiology
- Renin is released by the kidneys (macula densa cells in the juxtaglomeral apparatus) in response to decreased renal artery persion, decreased Na delivery to distal tubules, and sympathetic nerve stimulation (Beta-1 receptors).
- Renin acts on circulating angiotensinogen and cleaves it into angiotensin I, which is coverted by ACE (which is presented in vascular endothelium) to Angiotensin II.
- Angiotensin II – causes vasoconstriction , especially of the efferent arteriole of the glomerulus. It also acts on the adrenals to release aldosterone, and stimulates ADH release from the pituitary.
- Aldosterone – causes Na reabsorption and K excretion in the kidneys, with the purpose of raising blood volume and blood pressure.
Primary Hyperaldosteronism - means that aldosterone secretion is exogenous, independent of the renin-angiotensin pathway - expect high aldosterone levels and suppresssed renin levels.
Causes:
- Aldosterone-producing Adrenal Adenoma (aka Conn’s Syndrome)
- Bilateral adrenal hyperplasia
- Aldosterone-producing adrenal carcinoma - rare
- Screening test is with a morning plasma aldosterone: renin ratio: if > 20, this is positive and warrants more workup.
Confirmatory test is a Salt Suppression test, whereby a patient either ingests a high Na diet x 3 days, or a IV normal saline load over several hours, then measuring the urine aldosterone level. If high, this confirms primary hyperaldosteronism. Next steps would then be to obtain imaging of the adrenals via an Adrenal CT scan or MRI.
Secondary Hyperaldosteronism - means that aldosterone secretion is secondary to increased renin levels --> angiotensin I and II --> aldosterone
Causes:
- Renin-secreting tumor
- Renovascular disease - decreased GFR stimulates renin release
- Low flow states - CHF, nephrosis, cirrhosis - decreased GFR
Workup in this case involves evaluation for the above causes, with renal ultrasound/doppler, and possibly MRI/MRA.
(Chanu Rhee MD, 10/22/10)