About 40 causes of the development of arterial hypertension are known, which are divided into congenital and acquired.
• fibro-muscular dysplasia of the renal arteries;
• renal artery and kidney hypoplasia;
• extravasal compression of the renal artery;
• renal artery aneurysms;
• arteriovenous fistula.
• nonspecific aortoarteritis;
• kidney infarction;
• stratified aortic aneurysm.
Atherosclerosis is the main cause of vasorenal hypertension in people over 40 years of age; it accounts for 60–85% of cases. Atherosclerotic plaques are localized mainly at the mouth or in the proximal third of the renal artery.
In the vast majority of cases, unilateral lesion is observed, while bilateral occurs in about 1/3 of cases and leads to a more severe course of CVH. The right and left renal arteries are affected equally often. In 10% of cases, atherosclerosis of the renal arteries can be complicated by thrombosis. The disease is more common (2-3 times) in men.
Musculoskeletal dysplasia (FMD) as the cause of vasorenal hypertension is second only to atherosclerosis. It occurs mainly in young and even childhood (from 12 to 44 years old), the average age is 28-29 years. In women, PMD is detected 4-5 times more often than in men.
Morphologically, this pathological condition manifests itself in the form of dystrophic and sclerosing changes, capturing mainly the inner and middle membranes of the renal arteries and their branches. In this case, hyperplasia of the muscle elements of the wall can be combined with the formation of microaneurysms.
As a result, there is an alternation of sections of narrowing and expansion (aneurysms), which gives the arteries a peculiar shape – in the form of pearls or beads. The pathological process, although it is widespread, but in 2/3 of the cases it is one-sided.
Nonspecific aortoarteritis is the third most common cause of ADH (up to 10%). It is characterized by a primary lesion of the middle membrane of the vessel. Inflammatory infiltration of the media with the transition to adventitia and intima ends with sclerosis and destruction of the elastic frame of the renal artery, which leads to stenosis of its lumen.
The pathological process is mainly limited to the proximal segment of the vessel and almost never spreads to its internal organ branches. In contrast to fibromuscular dysplasia with nonspecific aortoarteritis, there is always a varying degree of severity of aortic damage.
Vasorenal hypertension can develop as a result of extravasal compression of the renal artery, as a result of thrombosis or embolism of the renal artery, the formation of aneurysm, hypoplasia of the main renal arteries, nephroptosis, tumors, cysts, abnormalities in the development of the kidneys, etc.
Narrowing the width of the lumen of the renal vessels leads to a decrease in perfusion pressure and a decrease in the blood supply to the renal glomerulus. Sensitive to the smallest fluctuations in hemodynamics, juxtaglomerular secretory cells, having undergone ischemia, begin to produce an increased amount of the renin hormone. As a result of the action of excess renin, the angiotensinogen is converted into angiotensin 1, a transforming angiotensin 2.
Narrowing or occlusion of the renal artery leads to a decrease in renal blood flow and a decrease in perfusion pressure. This, in turn, causes insufficient stretching of the leading arterioles of the Malpighian glomerulus.
Its granular cells of the juxtatomerular apparatus (SOA) located in the medial layer, which are a kind of volume-receptor apparatus, respond very subtly to any changes in renal hemodynamics and excrete renal incretrenin into the blood. The development of renal tissue ischemia leads to hyperplasia of Juga cells, resulting in hypersecretion of renin.
Renin itself is an enzyme that converts angiotensinogen I coming from the liver into angiotensin I, which, under the influence of the angiotensin converting enzyme, passes into angiotensin II. The latter is one of the strongest vasoconstrictors, which, directly acting on systemic arterioles, causes their spasm, which sharply increases peripheral resistance.
In addition, angiotensin II stimulates the production of aldosterone by the adrenal cortex, which leads to the development of secondary hyperaldosteronism with a delay in sodium and water in the body (increasing bcc) and in the wall of arterioles, causing their edema and an even greater increase in peripheral resistance.
Peripheral angiospasm, hypernatremia and hypervolemia lead to aggravation of arterial hypertension. This is the essence of the generally accepted “renopressor” theory of pathogenesis of ADH, the founder of which is Goldblatt.
In contrast, the Grenlman’s “renal” theory suggests that the body’s hypertensive response to impaired normal blood circulation is caused not by increased production of pressor substances, but rather by insufficient production of depressant substances by the kidney.
According to this theory, “any decrease in the amount of renal tissue in the body, violating to one degree or another the metabolic function of the kidneys, will create the prerequisite for the development of arterial hypertension.”
The experiment really proved that the complete removal of both kidneys, as a rule, leads to the development of malignant hypertension. A.A. Spiridonov believed that this theory is imperfect for the following reasons: firstly, stenosis of the renal artery does not always lead to a decrease in the size of the kidneys and the amount of renal parenchyma;
At the same time, the existence of depressant substances secreted by the kidney is generally recognized. The main one is prostaglandin F2, which has a pronounced hypotensive effect due to the direct expansion of the lumen of small arterioles.
The natural course of atherosclerotic VRH is characterized by a progressive decrease in renal blood flow, which ultimately leads to a complete loss of renal function (“ischemic nephropathy”).
This disease manifests itself in middle or old age. In contrast, fibromuscular dysplasia usually occurs at a young age, is more common in women, does not have a progressive course, and rarely leads to ischemic nephropathy.
How is it manifested?
There is no specific symptomatology characteristic only of renovascular arterial hypertension, except for high numbers of blood pressure. The defeat of the glomerular system leads to persistent vascular hypertension, which is manifested by a small difference between the high numbers of systolic and diastolic pressure. Patient complaints in each case are individual and depend on the presence of kidney disease.
An experienced doctor will suspect vasorenal hypertension if antihypertensive drugs do not have the desired effect or there is a history of inflammatory processes, injuries and vascular pathological processes. Heredity does not play a significant role in the occurrence of renal hypertension. In laboratory studies, there are signs of renal failure.
There are no pathognomonic symptoms of vasorenal hypertension characteristic of some forms of hypertension (Conn syndrome, Itsenko-Cushing syndrome, pheochromocytoma).
• characteristic of cerebral hypertension – headaches, a feeling of heaviness in the head, tinnitus, pain in the eyeballs, memory loss, poor sleep;
• associated with overload of the left heart and coronary insufficiency – pain in the heart, palpitations, feeling of heaviness behind the sternum;
• a feeling of heaviness in the lumbar region, non-intense pain, hematuria in case of kidney infarction;
• due to ischemia of other organs, the main arteries of which are affected simultaneously with the renal vessels;
• characteristic of the syndrome of a systemic inflammatory reaction (with nonspecific aortoarteritis);
• characteristic of secondary hyperaldosteronism – muscle weakness, paresthesias, attacks of tetany, isohypostenuria, polyuria, polydipsia, nocturia.
However, it should be noted that in about 25% of patients, vasorenal hypertension is asymptomatic.
How is vasorenal hypertension diagnosed?
Diagnostic procedures for suspected renal hypertension are usually carried out in three stages to avoid unnecessary interventions, reduce the time of diagnosis and significantly reduce the costs of the patient and the hospital. At the first stage, a detailed history is taken taking into account the individual characteristics of the course of the disease (taking into account the patient’s age, frequency of hypertensive crises, the presence of symptoms of encephalopathy or chronic cerebrovascular insufficiency). Of the examinations, the following are prescribed as standard:
- Urinalysis (in the results – the appearance of protein, red blood cells).
- Biochemical renal tests (in the analysis there are increased indicators of creatinine, urea, rest-nitrogen and electrolyte balance is disturbed).
- Fundus studies (persistent increase in blood pressure leads to changes in the structure of the retina).
- ECG (presence of left ventricular hypertrophy with chronically high blood pressure).
At the second stage, more detailed differential diagnostics using medical equipment occurs. An ultrasound of the kidneys is prescribed by the doctor with a dopplerographic examination of the renal vessels (renal asymmetric deviations and the presence of vascular pathology are detected). Radioisotope renal scintigraphy (functional imaging by introducing radioactive isotopes into the body).
The first step in the diagnosis of vasorenal hypertension is the clinical diagnosis and selection of patients with an average and high probability of this pathology according to clinical criteria. Non-invasive screening tests provide targeted screening of patients with high likelihood of renal artery stenosis who should undergo an x-ray.
Spiral CT can provide excellent visualization of the renal vessels (Fig. 1), but requires a large amount of contrast. Currently, magnetic resonance angiography provides a good image of the renal vessels without risk to the patient.
But, with its higher cost and lower availability, it should be reserved for patients with uncertain functional image results, but high clinical suspicion of VRH, and patients who have a contraindication to standard angiography: renal failure or allergy to iodine drugs.
Fig. 1. CT angiography. Right renal artery stenosis (indicated by arrow)
Nephrogenic hypertension is a dangerous disease and, in terms of prognosis, is not very favorable. Drug therapy loses significantly before surgical treatments. In most cases, with timely surgical intervention, the quality of life of patients improves. Diagnosis and treatment is best trusted by specialized nephrology centers.
The prognosis for infectious endocarditis remains serious. If with infectious endocarditis of the right heart of drug addicts caused by Staphylococcus aureus, with the timely start of treatment, more than 85% of patients can recover, then with fungal endocarditis, mortality reaches 80%. On average, nosocomial mortality is about 20-25%.
- infectious endocarditis caused by Staphylococcus aureus or streptococci, not belonging to the group of verdant;
- thromboembolic or neurological complications;
- heart failure;
- lack of surgical intervention in the presence of indications for it.
- progressive heart failure;
- septic shock, multiple organ failure;
- renal insufficiency.
In patients who have had infectious endocarditis, there remains a risk of embolic complications and relapse of the disease even in the long term, and heart failure may progress.
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