ATLANTA — Clinicians should consider secondary causes when a patient's hypertension does not respond to aggressive treatment, Dr. Angela L. Brown said at a meeting sponsored by the International Society on Hypertension in Blacks.
The first rule, though, is that one must be careful in defining when hypertension is truly refractory, said Dr. Brown of Washington University in St. Louis. Hypertension is considered refractory only if a blood pressure under 140/90 mm/Hg cannot be achieved despite the use of three antihypertensive medications at their maximal doses, one of which must be a diuretic.
Too often, she said, other physicians refer patients with “refractory hypertension” who are on only two antihypertensives or who are at only the starting doses.
There are many secondary causes of hypertension. Renal hypertension and endocrine hypertension are probably the most common, but other causes include aortic coarctation, sleep apnea, and panic disorder.
In addition, there are many exogenous substances that can raise blood pressure. Ethanol and caffeine are probably the most prominent of these, but physicians should carefully question patients about other possible causes, including cocaine, nicotine, sympathomimetics, chlorpromazine, erythropoietin, oral contraceptives, cyclosporine, tricyclic antidepressants, MAO inhibitors, and certain herbal supplements, such as the Chinese stimulant ma huang (ephedrine).
NSAIDs, corticosteroids, and sodium chloride can also interfere with antihypertensive therapy.
Anabolic steroids can also cause hypertension. “Particularly when you see young men who are athletic or buff, ask them about anabolic steroids,” Dr. Brown advised. But she warned that the physician may not get an honest answer unless the young athlete's parents are out of the room.
Dr. Brown suggested a number of screening tests that can uncover some of the secondary causes, particularly the endocrine ones. (See box.)
But she placed a special emphasis on renal function.
“I think it's really important that we know the patient's level of kidney dysfunction,” she said. “We get the serum creatinines, and we often see a creatinine of 1.4 or 1.6 [mg/dL], and we think, 'Oh, that's not too bad.' But it's clear that once the GFR [glomerular filtration rate] diminishes, and particularly around 45% or so, your thiazide diuretic is not going to be as effective.”
Two equations have been developed for estimating GFR based on a patient's serum creatinine, age, and weight, with correction factors for the patient's gender and race (black versus nonblack), and there are Web sites where one can perform the calculations easily (www.medcalc.com/gfr.html
“Some labs have actually started reporting the estimated GFR,” Dr. Brown said. “You actually get a much clearer picture of where the kidney level is. … I think this is one of the most common causes of what is deemed to be resistant hypertension in my patients, and it is inadequate diuretic therapy.”
The meeting was cosponsored by the American Society of Hypertension.
Narrow Down The Possibilities
▸ For hyperthyroidism or hypothyroidism, test TSH, free T4.
▸ For pheochromocytoma, test plasma metanephrines.
▸ For primary aldosteronism, test morning plasma potassium; aldosterone:renin ratio.
▸ For Cushing's syndrome, administer the overnight dexamethasone suppression test.
▸ For hyperparathyroidism, administer a test for albumin-corrected serum calcium; intact parathyroid hormone; serum chloride:phosphate ratio.
▸ For renal artery stenosis, use the renal artery duplex scan; captopril renogram.
Source: Dr. Brown