Examination of a patient suffering from increased blood pressure begins with collecting their medical history and then performing a physical examination. Before the examination, the patient is asked to measure the blood pressure on their arm at least 3 times a day for 3 days. After that, laboratory tests can be requested, including blood tests and a «Holter» test, measuring blood pressure during 24 to 48 hours.
The results of the initial examination may indicate symptomatic hypertension. When severe hypertension appears suddenly or begins before the patient is 25 years old or after 50 years it is necessary to immediately rule out or confirm renovascular hypertension or the presence of adrenal tumors – pheochromocytoma. The presence of pheochromocytoma can be suspected if a patient complains of severe headaches, heart attacks, panic attacks, sweating, hyperglycemia, or weight loss. With an increase in serum BUN and creatinine and amid proteinuria, in the presence hematuria, renal failure should be excluded. If treatment is ineffective, additional tests are needed. Their list depends on the most likely cause of hypertension.
The easiest and most reliable method to diagnose this tumor is measuring catecholamines and their metabolites in daily urine. It is recommended to collect a urine sample when the patient’s blood pressure is high.
Plasma catecholamine measurement is rarely recommended. It should be noted that only in half of the cases of pheochromocytoma, blood pressure increases suddenly, so ruling out the presence of this tumor is necessary in any case of persistent arterial hypertension.
If this disease is suspected, first of all, cortisol levels in daily urine should be determined or a test with dexamethasone should be performed.
A few years ago, the definition of this pathology began with excretory urography, X-rays that were taken in a short time. In recent years, excretory urography has been replaced by other research methods in many leading clinics:
Subtraction Angiography: this method is more accurate, but also more expensive. It requires intra-arterial contrast instead of intravenous, so it cannot be used as a first-line diagnostic method.
Kidney scintigraphy after taking captopril: the method is based on the dependence of renal vessel tone on angiotensin II levels. With renal artery stenosis, ACE inhibitor (captopril) reduces angiotensin II levels in the affected area, causing a decrease in renal blood flow, isotope accumulation, and slower excretion. In many centers, diagnostics start with this method.
Duplex ultrasound of the renal arteries provides imaging and allows blood flow measurements. It is, theoretically, the best of the non-invasive methods, but its accuracy is highly dependent on staff qualifications.
If renal artery stenosis is suspected, first it’s necessary to prove that it can be treated, resulting in normalization of blood pressure. For this purpose, selective angiography is provided, and renin activity in the corresponding renal vein is measured. Angiography can determine the cause of stenosis (atherosclerosis or fibromuscular dysplasia).
The functional significance of stenosis is assessed using renal vein catheterization with renin activity measurement. When one of the kidneys is ischemic, all of the renin comes from there. If renin activity in one renal vein is 1.5 times higher than in the other, it is considered diagnostically significant.
In blood from a healthy kidney vein, renin activity is usually about the same as in the vena cava in front of the area where the renal veins converge into it.
Stenosis treatment is effective in 80% of cases, but only if renal vein catheterization is performed after proper preparation:
10 days before the catheterization, the patient should not take drugs that reduce renin activity (e.g. β-blockers), 4 days prior, a low salt diet should be instated, and an ACE inhibitor is given less than 24 hours from the procedure.
If angiography determines stenosis not of the renal artery itself, but of its branches as well, blood is taken for examination from the main branches of the renal vein to confirm that the arterial hypertension is caused by stenosis.
In such cases hypokalemia is almost always present, and diagnosis is made due to the ratio of plasma renin activity to the aldosterone level. With primary hyperaldosteronism, aldosterone levels and daily excretion are increased, and renin activity is reduced while sodium in the blood has little effect on these indicators. Then it should be determined whether one or both adrenal glands are affected, because blood pressure can be reduced with surgery only in first case.
The cause of increased blood pressure is rarely diagnosed (only in 5% of cases), but it must be determined. First of all, treating the cause sometimes can help to cure the disease. Secondly, research of symptomatic hypertension gives us new information on its etiology. In the vast majority of cases, the determined cause is associated with either endocrine or renal pathologies.
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