19 y/o woman w/ new onset high BP
normal body weight and no changes in weight
1. Do you suspect primary or secondary HTN? why?
2. What might the abdominal bruit indicate? How does this cause high blood pressure?
3. What lab test can you do to test this hypothesis?
1. secondary HTN is suspected because primary HTN is not likely to occur in a 19 y/o.
2. renal artery stenosis. Renal artery stenosis will cause an increase of renin which increases angiotensin II which causes vasoconstriction (increasing systemic vascular resistance) and an increase in aldosterone which causes sodium and water reabsorption.
3. test plasma renin activity. If it's elevated in the patient, you know that the hypothesis of renal artery stenosis is likely correct.
How do you measure renin levels in a patient?
You typically don't measure renin directly, you measure the activity.
You take normal serum and you add patient serum and you measure how much angiotensin I comes out in a given time period.
Is ultrasound a good way to screen for renal artery stenosis?
How do you confirm a renal artery stenosis?
What drug do you give to someone with renal artery stenosis? What would the purpose of this be?
ACE-I or ARB to address the hypertension.
This is just a temporary fix though. If you let the renal artery stenosis progress, the kidney will get less and less perfusion eventually shrinking in size and becoming uselss. That's why it's important to either perform a bypass surgery or an angioplasty and stent.
What are two causes of primary aldosteronism?
- Aldosterone producing adenoma (typically unilateral)
- Idiopathic adrenal hyperplasia (typically bilateral)
You have a patient with low renin but high aldosterone. How do you get a definitive diagnosis for primary aldosteronism?
Saline injection. If a person does not have primary aldosteronism, a saline injection should bring the renin-angiotensin-aldosterone system values down. If the aldosterone levels remain unchanged, you know it's primary aldosteronism.
You can also test by injecting Fludrocortisone. This drug would cause sodium and water retention which should lower renin-angiotensin-aldosterone values. If you give Fludrocortisone and aldosterone levels are unchanged, you know it's primary aldosteronism.
How do you treat primary aldosteronism?
If it's an aldosterone producing adenoma, you can surgically resect.
If it's idiopathic adrenal hyperplasia, it's typically bilateral and you cannot do any surgical intervention. You must manage medically typically with Spironolactone
How do you determine if primary aldosteronism is from aldosterone producing adenoma or idiopathic adrenal hyperplasia?
You thread a catheter into the adrenal veins to see what's coming out on each side.
If aldosterone is elevated on both sides, it's idiopathic adrenal hyperplasia. If aldosterone is elevated only on one side, it's a unilateral aldosterone producing adenoma.
Primary and secondary aldosteronism often results in hypokalemia and high bicarbonate. Why?
In the principal cells, high aldosterone levels will cause intake of sodium and secretion of K. Secretion of K causes the hypokalemia. When there is sodium intake, it leaves a net negative charge in the lumen which attracts K. However, it also attracts H+ and when H+ enters the lumen, bicarbonate is reclaimed which causes high bicarbonate levels.