Let's turn to another clinical case.
We have a 52-year-old gentleman who's seen in your office for worsening hypertension.
He was diagnosed with hypertension 5 years ago
and he's managed on monotherapy with a thiazide diuretic with pretty good result until recently.
He's vigilant about measuring his blood pressure on a daily basis
and notes that his most recent blood pressures had been in the 160-170 range over 90 mmHg.
He's had no changes in his diet, no new medications, and no family history of early-onset hypertension.
His physical exam is relatively unremarkable. No cardiac murmurs, no abdominal bruits.
On laboratory evaluation, interestingly, his plasma renin activity,
and this was from a morning sample, was quite low at 0.06 ng/mL/h
and his plasma aldosterone concentration was quite high at 29 ng/dL.
Other remarkable labs in this gentleman included a potassium of 3.1 mEq/L
which is low and certainly low compared to his baseline,
and a TCO2 or serum bicarbonate of 29 mEq/L, which is high for him.
So, the question is, what is the most likely etiology
that explains this patient's worsening hypertension and lab abnormalities?
Let's go back through our clinical case and see if we've got some clues.
So, this is a gentleman who was diagnosed with hypertension.
Very well-controlled, very pro-active in his care,
but all of a sudden has precipitation of worsening control.
We also can look at his laboratory data.
He's got a suppressed renin with an elevated plasma aldosterone concentration
along with a low potassium and a metabolic alkalosis.
That's highly suspect for hyperaldosteronism.
So, the likely etiology that explains this patient's worsening hypertension
and lab abnormalities is primary hyperaldosteronism.