home Diseases Features of diagnosis and treatment of nephrogenic hypertension. Nephrogenic arterial hypertension Nephrogenic hypertension

Features of diagnosis and treatment of nephrogenic hypertension. Nephrogenic arterial hypertension Nephrogenic hypertension

Nephrogenic arterial hypertension - increased blood pressure due to disease of the kidneys and renal vessels.

Etiology and pathogenesis. Activation of the renin-angiotensin system plays a leading role in the pathogenesis of nephrogenic hypertension. Ischemia of the kidney and a decrease in pulse pressure (the difference between systolic and diastolic pressure) leads to ischemia of the juxta-glomerular apparatus. Hyperplasia and hypertrophy of its cells occur and, as a result, the production of the proteolytic enzyme, renin, increases. It combines with a 2 -globulin produced in the liver - angiotensinogen, forming the polypeptide angiotensin I. As a result of the cleavage of two amino acids from angiotensin I, angiotensin II is formed, which, unlike renin and angiotensin I, causes a powerful direct vasopressor effect. Along with this, angiotensin formed in excess stimulates the secretion of aldosterone, which leads to sodium retention in the body. Sodium accumulates in the wall of the renal arteries and arterioles, causing swelling of their walls, narrowing of the lumen, and increases the sensitivity of the vessels to the action of catecholamines.

The medulla of a healthy kidney secretes a proteolytic enzyme, angiotensinase, which destroys angiotensin II and blocks its pressor effect. With pathological changes in the kidneys and renal vessels, the synthesis and activity of angiotensinase decreases.

In the pathogenesis of nephrogenic hypertension, along with the activation of the pressor renin-angiotensin-aldosterone system, a decrease in the production of hypotensive factors by the renal medulla also plays an important role. Prostaglandin E 2 and kinins (bradykinin, kallikrein) create a counterbalance to the renin-angiotensin-aldosterone system in the regulation of intrarenal and systemic hemodynamics and in electrolyte balance. When the renal medulla is damaged, its synthesis is disrupted.

Thus, nephrogenic hypertension develops as a result of an increase in renin synthesis and a decrease in the activity of angiotensinase, prostaglandin and kallikrein-kinin systems.

Classification. Nephrogenic hypertension is divided into three main groups:

1) parenchymal, resulting from unilateral or bilateral damage to the renal parenchyma of a diffuse nature, observed in glomerulo- and pyelonephritis, renal tuberculosis, hydronephrosis, polycystic kidney disease, diabetic glomerulosclerosis, nephropathy of pregnancy, systemic connective tissue diseases, amyloidosis;

2) vasorenal, caused by narrowing of the renal vessels due to atherosclerotic stenosis of the renal artery, fibromuscular dysplasia of the renal artery, thrombosis, embolism and aneurysm of the renal artery, anomalies of the development of the renal vessels and aorta;

3) mixed - a consequence of damage to the renal parenchyma and changes in the renal vessels with nephroptosis, tumors, renal cysts, combinations of anomalies of the kidneys and their vessels.

Symptoms and clinical course. The clinical picture of nephrogenic arterial hypertension consists of symptoms characteristic of hypertension and symptoms of kidney damage.

Nephrogenic hypertension can have a slow-flowing (benign) and fast-flowing (malignant) form.

With benign hypertension, blood pressure is usually stable and does not tend to decrease. Both diastolic and systolic pressure are increased, but diastolic pressure is more significant. Patients complain of periodic headaches, dizziness, weakness, fatigue, palpitations, shortness of breath, discomfort in the heart area.

The malignant form of hypertension is characterized by an increase in diastolic pressure above 120 mmHg. Art., sudden and rapidly progressive visual impairment due to the development of retinopathy, patients complain of constant headaches, often in the back of the head, dizziness, nausea, vomiting.

With nephrogenic hypertension, in contrast to hypertension, low back pain often occurs, both due to circulatory disorders in the kidney and as a result of the underlying urological disease.

Diagnostics. It is very important to carefully collect anamnesis, based on the data of which one can suspect the symptomatic nature of hypertension. Nephrogenic hypertension is characterized by:

Sudden onset;

The appearance of hypertension after acute lower back pain, previous diseases and kidney injury, kidney surgery;

The emergence and rapid progression of hypertension in young people;

Malignant course of the disease;

Ineffectiveness of standard antihypertensive therapy;

Absence of hereditary predisposition to hypertension.

When examining patients, high blood pressure is determined, much higher than with hypertension. Diastolic blood pressure increases, due to which pulse pressure (the difference between systolic and diastolic pressure) decreases. During tonometry, blood pressure should be measured in the right and left arms. A significant difference in blood pressure values in the arms, as well as a sharp weakening of the pulse and unequal pulsation of the carotid and peripheral arteries are characteristic of nonspecific aortoarteritis (Takayasu disease).

One of the characteristic signs of renovascular hypertension is a systolic or diastolic murmur in the epigastric region above the navel, extending to the lateral parts of the abdomen and to the costovertebral angle. Renal artery stenosis is accompanied by a systolic murmur, which occurs under the influence of accelerated blood flow through the narrowed area. With an aneurysm of the renal arteries, turbulent blood flow occurs, which causes a systolic-diastolic murmur.

With diffuse atherosclerotic changes in the aorta and its large branches, noise also occurs in the epigastric region, but it spreads along the iliac and femoral arteries.

In patients with nephrogenic hypertension, fundus examination is of great importance. In this case, narrowing of the central retinal artery, uneven diameter of vessels, arteriolospasm, neuroretinopathy with foci of ischemia and exudation, hemorrhages, circulatory disorders in the vessels supplying the optic nerve, edema of the retina and optic discs and venous congestion are determined. As a result of these changes in the fundus, patients with nephrogenic hypertension often experience a rapid decrease in acuity and loss of visual fields. Changes in the fundus in hypertension are observed much less frequently compared to nephrogenic hypertension.

Ultrasound of the kidneys can obtain reliable data on their size and structure, diagnose anomalies, tumors, and detect signs of pyelonephritis and glomerulonephritis.

Doppler ultrasound angiography in patients with nephrogenic hypertension is an important diagnostic procedure that allows one to assess blood flow in the vessels of the kidney, determine the size, thickness and structure of the renal artery wall. Excess body weight of the patient and flatulence make it difficult to perform the study and correctly interpret the results.

An important method of examining patients with nephrogenic hypertension is excretory urography. To diagnose nephroptosis, it is necessary to take photographs in a vertical position. With nephroptosis in a vertical position, the kidney will be displaced by more than one lumbar vertebra. In the renovascular form of nephrogenic hypertension, a slow contrast of the collecting system is determined in the initial stages of the study (1-5 minutes) and an increase in its contrast in the later stages (at 15, 25, 45 and 60 minutes), a decrease in size kidneys by 1 cm or more on the affected side compared to the contralateral kidney.

Patients with nephrogenic hypertension should undergo dynamic and static renography to assess separate renal function.

The condition of the renal vessels can be assessed by dynamic scintigraphy with indirect radioisotope angiography (with intravenous administration of a radiopharmaceutical). With renal artery stenosis, there is a decrease in the rate at which the radiopharmaceutical reaches the kidney. It should be remembered that the method of radioisotope angiography cannot determine the nature and localization of the pathological process in the renal vessels.

One of the important methods for diagnosing the renovascular form of nephrogenic hypertension is renal angiography with a radiocontrast agent, which allows one to determine the nature, localization and extent of damage to the renal arteries. When performing the study, the femoral artery is punctured according to Seldinger, a catheter is inserted into the aorta and moved above the mouth of the renal arteries. The study begins with aortography and renal non-selective angiography to assess the condition of the aorta and its visceral branches, and diagnose additional branches of the renal artery. For a more thorough examination of the distal renal artery, selective renal angiography is performed.

This study allows you to determine the location and degree of narrowing of the lumen of the renal artery, vascular collaterals around the kidneys. On the affected side, there is a delay in the parenchymal phase, a decrease in the intensity of accumulation of the radiopaque substance, and a decrease in the size of the kidney. In case of an aneurysm of the renal vessels or aorta, the radiopaque substance remains in the aneurysm cavity for a long time. Signs of renal artery stenosis can be observed when the renal artery is lengthened due to severe nephroptosis. In this case, tension and bending of the renal artery and a significant disturbance of renal hemodynamics are observed. In the vertical position of the patient, the renal artery is stretched and departs from the aorta at an acute angle.

With angiography, a renin test is possible - determining the level of renin in the peripheral blood and blood flowing from the kidneys, which makes it possible to prove the dependence of hypertension on the detected stenosis of the renal artery.

Currently, MRI and spiral CT are increasingly used to assess the condition of renal vessels. Based on their results, it is possible to reliably and informatively assess the condition of the renal arteries and veins, intrarenal angioarchitecture, and visualize the aorta.

Kidney biopsy allows us to determine the condition of the juxtaglomerular apparatus, interstitial cells, tubules, intrarenal arterioles, the nature and extent of kidney damage and predict the results of treatment.

Differential diagnosis nephrogenic hypertension should be carried out with other symptomatic hypertension due to thyrotoxicosis, pheochromocytoma, tumors of the medulla and cortical layers of the adrenal glands, hypertension.

Paroxysmal atrial fibrillation and increased levels of thyroid hormones indicate thyrotoxicosis.

Frequent hypertensive crises (especially with decreased visual acuity), increased levels of catecholamines in the blood and urine, and mass formation of the adrenal glands indicate the presence of pheochromocytoma.

With tumors of the adrenal cortex (primary aldosteronism, Conn's syndrome), general weakness, transient paresis and paralysis, constant thirst, polyuria, and increased concentrations of aldosterone in the urine and blood are observed.

Hypertension (essential hypertension) is characterized by the appearance of symptoms of kidney damage after an increase in blood pressure.

rial pressure, hereditary predisposition to hypertension, left ventricular hypertrophy, benign hypertension, increased blood pressure due to systolic.

Treatment. Nephrogenic arterial hypertension, as a rule, has a severe and malignant course with rapid secondary damage to the brain, heart, and kidneys. In this regard, treatment should be carried out as soon as possible from the onset of the disease and determined by the cause of hypertension.

The modern method of treating renovascular hypertension consists of intravascular dilatation of stenotic areas of the renal arteries using a balloon catheter (balloon angioplasty). Indications for balloon angioplasty are fibromuscular dysplasia and atherosclerosis of the renal artery; contraindications - damage to the mouth of the renal artery or its occlusion.

Dilatation is combined with stenting of the renal artery (installation of a vascular stent in it - a special elastic metal tube) to avoid re-stenosis.

Open operations in patients with renovascular hypertension are performed for occlusion of the renal artery with preserved renal function, damage to the ostium of the renal artery, complex stenosis and ineffectiveness of balloon angioplasty. The main goal of the operation is to normalize blood flow and preserve kidney function. Depending on the type of vascular damage, reconstructive plastic surgery on the renal vessels is performed, if indicated, in combination with autologous or alloplasty of the renal artery. Surgical treatment is indicated in the absence of malformations, parenchymal disease, a pronounced decrease in the function and size of the kidney on the affected side, and disorders of cerebral and coronary circulation.

In case of atherosclerotic stenosis of the renal arteries, a transaortic endarterectomy is performed - the affected inner lining of the artery with the atherosclerotic plaque is removed through the lumen of the aorta to eliminate the stenosis and normalize blood flow in the kidney.

Treatment of parenchymal nephrogenic hypertension includes both a specific effect on the underlying kidney disease and the administration of antihypertensive drugs.

Specific, including surgical, treatment of parenchymal hypertension due to chronic pyelo-, glomerulo-nephritis, diabetic glomerulosclerosis is aimed at reducing

activity of the inflammatory process, restoration of urine outflow, normalization of the blood coagulation system and immune status.

For nephrogenic hypertension due to nephroptosis, nephropexy is the treatment of choice.

For the treatment of nephrogenic hypertension, drug therapy with angiotensin-converting enzyme inhibitors (captopril, enalapril, ramipril, etc.) and β-blockers that suppress the activity of cells of the juxtaglomerular apparatus (pindolol, propranolol) is also used (mainly as an additional treatment method).

In some cases, mainly in the absence of parenchyma and kidney function on the affected side, as well as in the impossibility of reconstructive vascular operations and balloon dilatation of the renal artery, with unilateral severe parenchymal lesions of the kidney, nephrectomy has to be performed to treat nephrogenic hypertension.

Forecast. In nephrogenic arterial hypertension, the prognosis largely depends on the duration of the disease and the timing of the start of etiotropic and pathogenetically based surgical treatment. If the surgical intervention turned out to be effective (led to a decrease in blood pressure) and was performed before the development of arteriolosclerosis in the opposite kidney, then the prognosis is favorable. With bilateral kidney damage, the prognosis is unfavorable. Complications of hypertension such as cardiovascular failure, stroke, myocardial infarction and progressive chronic renal failure, in the absence of adequate treatment, including surgery, relatively quickly lead to death.

Treatment of nephrogenic hypertension is as follows: improved well-being, adequate control of blood pressure, slowed progression of chronic renal failure, increased life expectancy, including without dialysis.

Indications for hospitalization for nephrogenic hypertension

Newly diagnosed nephrogenic hypertension or suspicion of it is an indication for hospitalization to clarify the causal nature of the disease.

In an outpatient setting, preoperative preparation for surgery for vasorenal hypertension is possible, as well as management of patients in whom the parenchymal form of the disease is detected or, due to the severity of the condition, surgical treatment for vasorenal hypertension is contraindicated.

Non-drug treatment of nephrogenic hypertension

The role of non-drug treatment is small. Patients with nephrogenic hypertension usually limit their salt intake and fluid intake, although the effect of these recommendations is questionable. They are rather needed to prevent hypervolemia, which is possible with excessive consumption of salt and liquid.

The need for active treatment tactics for patients with lesions of the renal arteries is generally recognized, since surgical treatment is aimed not only at eliminating the hypertensive syndrome, but also at preserving renal function. The life expectancy of patients with renovascular hypertension who have undergone surgery is significantly longer than that of patients who, for one reason or another, have not undergone surgery. During the period of preparation for surgery, if it is insufficiently effective or if it is impossible to perform it, patients with renovascular hypertension must be treated with medication.

Physician tactics in drug treatment of renovascular hypertension

Surgical treatment of patients with renovascular hypertension does not always lead to a decrease or normalization of blood pressure. Moreover, in many patients with renal artery stenosis, especially of atherosclerotic origin, increased blood pressure is due to hypertension. That is why the final diagnosis of renovascular hypertension relatively often has to be established ex juvantibui, focusing on the results of surgical treatment.

The more severe arterial hypertension is in patients with atherosclerosis or fibromuscular dysplasia, the greater the likelihood of its renovascular genesis. Surgical treatment gives good results in young patients with fibromuscular dysplasia of the renal arteries. The effectiveness of surgery on the renal arteries is lower in patients with atherosclerotic stenosis, since many of these patients are elderly and suffer from hypertension.

Possible variants of the course of the disease that determine the choice of treatment tactics:

true renovascular hypertension, in which renal artery stenosis is the only cause of arterial hypertension; hypertension, in which atherosclerotic or fibromuscular damage to the renal arteries is not involved in the genesis of arterial hypertension; hypertension, which is “layered” with renovascular hypertension.

The goal of drug treatment for such patients is to constantly keep blood pressure under control, take measures to minimize target organ damage, and strive to avoid unwanted side effects of the medications used. Modern antihypertensive drugs make it possible to control the blood pressure of a patient with renovascular hypertension during the period of preparation for surgery.

Indications for drug therapy in patients with nephrogenic (renal) arterial hypertension, including renovascular hypertension:

advanced age, severe atherosclerosis; questionable angiographic signs of hemodynamically significant stenosis of the renal arteries; high risk of surgery; impossibility of surgical treatment due to technical difficulties; patient's refusal of invasive treatment methods.

Drug treatment of nephrogenic hypertension

Drug antihypertensive therapy for nephrogenic hypertension should be carried out more aggressively, achieving tight control of blood pressure at the target level, although this is difficult to achieve. However, treatment should not rapidly reduce blood pressure, especially in renovascular hypertension, regardless of the prescribed drug or combination of drugs, as this leads to a decrease in GFR on the affected side.

Typically, for the treatment of nephrogenic hypertension, and primarily its parenchymal form, various combinations of the following groups of drugs are used: beta-blockers, calcium antagonists, ACE inhibitors, diuretics, peripheral vasodilators.

In patients with tachycardia, which is not typical for vasorenal hypertension, beta blockers are prescribed: nebivolol, betaxolol, bisoprolol, labetalol, propranolol, pindolol, atenolol, which require strict control in chronic renal failure.

In patients with bradycardia or with a normal heart rate, beta blockers are not indicated and the first-line drugs are calcium antagonists: amlodipine, felodipine (long-acting forms), felodipine, verapamil, diltiazem, long-acting dosage forms of nifedipine.

ACE inhibitors play the role of second-line drugs, and sometimes first-line drugs: trandolapril, ramipril, perindopril, fosinopril. It is quite possible to prescribe enalapril, but the dose of the drug is likely to be close to the maximum.

In case of renovascular genesis of hypertension, which in the vast majority of cases is high-renin, the prescription of ACE inhibitors has its own characteristics. It is impossible to sharply reduce blood pressure, as this can lead to a pronounced filtration deficiency in the affected kidney, including due to a decrease in the tone of the efferent arterioles, which increases the filtration deficiency by reducing the filtration pressure gradient. Therefore, due to the risk of acute renal failure or exacerbation of chronic renal failure, ACE inhibitors are contraindicated in cases of bilateral damage to the renal arteries or in cases of damage to the artery of a single kidney.

When conducting a pharmacological test, the strength of the bond with the enzyme is not important; You need a drug with the shortest action and fastest onset of effect. Captopril has these properties among ACE inhibitors.

Centrally acting drugs in the treatment of patients with nephrogenic hypertension are deep reserve drugs, but sometimes, due to the peculiarities of their action, they become the drugs of choice. The main feature of these drugs is the possibility of prescribing them for high hypertension without concomitant tachycardia. They also do not reduce renal blood flow while reducing systemic blood pressure and enhance the effect of other antihypertensive drugs. Clonidine is not suitable for continuous use, as it has a withdrawal syndrome and causes tachyphylaxis, but it is the drug of choice when it is necessary to quickly and safely lower blood pressure.

Among commercially available imidazoline receptor agonists, rilmenidine has some advantage due to its longer half-life.

If secondary hyperaldosteronism is detected, spironolactone should be prescribed.

Diuretics for renovascular hypertension are deep reserve drugs.

This is due to the fact that the cause of renovascular hypertension is not fluid retention, and prescribing diuretics for their diuretic effect does not make much sense. In addition, the hypotensive effect of diuretics due to increased sodium excretion in renovascular hypertension is questionable, since an increase in sodium excretion by a conditionally healthy kidney leads to increased renin release.

Angiotensin II receptor antagonists are very similar in their effects to ACE inhibitors, but there are differences in the mechanisms of action that determine the indications for their use. In this regard, if the effect of ACE inhibitors is insufficient, it is necessary to resort to the prescription of angiotensin II receptor antagonists: telmisartan, candesartan, irbesartan, valsartan. The second indication for angiotensin II receptor antagonists is determined by the tendency of ACE inhibitors to provoke cough. In these situations, it is advisable to change the ACE inhibitor to an angiotensin II receptor antagonist. Due to the fact that all drugs in this group, compared to ACE inhibitors, have less effect on the tone of the blood-carrying arterioles and thereby reduce the filtration pressure gradient less, they can be prescribed for bilateral damage to the renal arteries and for damage to the artery of a single kidney under the control of creatinine and potassium levels in blood.

Alpha blockers are not usually prescribed for nephrogenic hypertension, but an elderly man with nephrogenic hypertension due to atherosclerosis and concomitant prostate adenoma may be additionally prescribed a long-acting alpha blocker to the main regimen.

In extreme cases, hydralazine (a peripheral vasodilator), nitrates (peripheral vasodilators) and ganglion blockers can be prescribed. Nitrates and ganglion blockers can only be used in a hospital to reduce blood pressure.

It is necessary to take into account that when considering drugs, only the fact of nephrogenic hypertension was taken into account, however, in conditions of chronic renal failure or cardiac complications, the treatment regimen changes significantly.

The effectiveness of beta-adrenergic receptor blockers and especially ACE inhibitors is explained by their specific effect on the renin-angiotensin-aldosterone system. playing a leading role in the pathogenesis of nephrogenic hypertension. Blockade of beta-adrenergic receptors, suppressing the release of renin, consistently inhibits the synthesis of angiotensin I and angiotensin II, the main substances that cause vasoconstriction. In addition, beta-blockers help lower blood pressure by reducing cardiac output and depressing the central nervous system. reducing peripheral vascular resistance and increasing the sensitivity threshold of baroreceptors to the effects of catecholamines and stress. Slow calcium channel blockers are quite effective in treating patients with a high probability of nephrogenic hypertension. They have a direct vasodilatory effect on peripheral arterioles. The advantage of drugs in this group for the treatment of renovascular hypertension is their more favorable effect on the functional state of the kidneys than that of ACE inhibitors.

Complications and side effects of drug treatment for renovascular hypertension

In the treatment of renovascular hypertension, a number of inherent undesirable functional and organic disorders are important, such as hypo- and hyperkalemia, acute renal failure. decreased renal perfusion, acute pulmonary edema and ischemic shrinkage of the kidney on the side of renal artery stenosis.

The patient's advanced age, diabetes mellitus and azotemia are often accompanied by hyperkalemia, which can reach a dangerous degree when treated with slow calcium channel blockers and ACE inhibitors. Acute renal failure is often observed when treating patients with bilateral renal artery stenosis or severe stenosis of a solitary kidney with ACE inhibitors. Attacks of pulmonary edema have been described in patients with unilateral or bilateral renal artery stenosis.

Surgical treatment of renovascular hypertension

Surgical treatment for renovascular hypertension is reduced to the correction of vascular lesions that underlie it. There are two approaches to solving this problem:

various methods of expanding a stenotic artery using devices mounted at the end of a catheter inserted into it (balloon, hydraulic nozzle, laser waveguide, etc.); different options for operations on the open vessels of the kidney, performed in situ or extracorporeally.

The first option, available not only to surgeons, but also to specialists in the field of angiography, is called in our country x-ray endovascular dilatation or percutaneous transluminal angioplasty. The term “radioendovascular dilatation” is more consistent with the content of the intervention, which includes not only angioplasty, but also other types of radiosurgical dilatation of the renal arteries: transluminal, mechanical, laser or hydraulic atherectomy. The same area of surgical treatment of renovascular hypertension includes X-ray endovascular occlusion of the afferent artery of arteriovenous fistulas or the fistulas themselves.

X-ray endovascular balloon dilatation

For the first time, X-ray endovascular dilatation in renal artery stenosis was described by A. Grntzig et al. (1978). Subsequently, C.J. Tegtmeyer and T.A. Sos simplified and improved the technique of this procedure. The essence of the method is to insert a double-lumen catheter into the artery, at the distal end of which an elastic but difficult-to-extend balloon of a certain diameter is attached. The balloon is inserted through the artery into the stenotic area, after which fluid is injected into it under high pressure. In this case, the balloon is straightened several times, reaching the set diameter, and the artery is expanded, crushing the plaque or other formation that narrows the artery.

Technical failures include the immediate development of restenosis after successful dilatation of the renal artery. This may be due to the presence of a flap of tissue that functions as a valve, or the entry into the renal artery of atheromatous debris from a plaque located in the aorta in close proximity to the origin of the renal artery.

If it is not possible to perform X-ray endovascular dilatation due to technical difficulties, drug therapy, stent installation, renal artery bypass, atherectomy, including the use of laser energy, are used. Sometimes, if the contralateral kidney has good function, nephrectomy or arterial embolization is performed.

Serious complications of X-ray endovascular dilatation:

perforation of the renal artery with a conductor or catheter, complicated by bleeding: intimal detachment; formation of intramural or retroperitoneal hematoma; artery thrombosis; microembolism of the distal parts of the vascular bed of the kidney with detritus from a damaged plaque; a sharp drop in blood pressure due to inhibition of renin production in combination with the abolition of preoperative antihypertensive therapy: exacerbation of chronic renal failure.

Percutaneous transluminal angioplasty is effective for fibromuscular hyperplasia in 90% of patients and for atherosclerotic renovascular hypertension in 35% of patients.

Superselective embolization of the segmental renal artery for arteriovenous fistula of the renal vessels

In the absence of effective drug treatment for arterial hypertension, it is necessary to resort to operations that previously amounted to kidney resection or even nephrectomy. Advances achieved in the field of endovascular surgery, and, in particular, the method of endovascular hemostasis, make it possible to reduce local blood flow using endovascular occlusion, thereby relieving the patient of hematuria and arterial hypertension.

X-ray endovascular occlusion of a cavernous sinus fistula was first performed in 1931 by Jahren. In the last two decades, interest in the method of x-ray endovascular occlusion has been increasing, which is due to the improvement of angiographic equipment and instruments, and the creation of new embolic materials and devices. The only method for diagnosing intrarenal arteriovenous fistulas is angiography using selective and superselective methods.

Indications for X-ray endovascular occlusion of the afferent artery are arteriovenous fistulas complicated by hematuria, arterial hypertension, resulting from:

traumatic kidney injury; congenital vascular anomalies; iatrogenic complications: percutaneous puncture kidney biopsy or endoscopic percutaneous kidney surgery.

Contraindications to X-ray endovascular dilatation are only in the extremely severe condition of the patient or intolerance to RCV.

Open surgical interventions for nephrogenic hypertension

The main indication for surgical treatment of renovascular hypertension is high blood pressure.

The functional state of the kidneys is usually considered from the point of view of the risk of intervention, since in the majority of patients with renovascular hypertension, the total renal function does not exceed the physiological norm. Violation of total renal function is most often observed in patients with bilateral damage to the renal arteries, as well as with severe stenosis or occlusion of one of the arteries and dysfunction of the contralateral kidney.

The first successful reconstructive operations on the renal arteries for the treatment of renovascular hypertension were performed in the 50s of the last century. Direct reconstructive operations (transaortic endarterectomy, renal artery resection with reimplantation into the aorta or end-to-end anastomosis, splenorenal arterial anastomosis and operations using grafts) have become widespread.

For aortorenal anastomosis, a piece of vena saphena or a synthetic prosthesis is used. An anastomosis is performed between the infrarenal aorta and the renal artery distal to the stenosis. This operation is applicable to a greater extent in patients with fibromuscular hyperplasia, but can also be effective in patients with atherosclerotic plaques.

Thromboendarterectomy is performed by arteriotomy. To prevent narrowing of the artery, a patch of vein graft is usually applied at the site of opening.

In case of severe atherosclerosis of the aorta, surgeons use an alternative surgical technique. For example, creating a splenorenal anastomosis during surgery on the vessels of the left kidney. Sometimes they are forced to perform autotransplantation of the kidney.

Nephrectomy remains one of the methods for correcting renovascular hypertension. Surgery can relieve hypertension in 50% of patients and reduce the dosage of antihypertensive drugs used in the remaining 40% of patients. Increasing life expectancy, effective control of arterial hypertension, and protection of renal function support aggressive treatment of patients with renovascular hypertension.

Further management of nephrogenic hypertension

Regardless of whether surgical treatment was performed or not, further management of the patient comes down to maintaining blood pressure levels.

If the patient has undergone reconstructive surgical treatment on the renal vessels, in order to prevent thrombosis of the renal artery, acetylsalicylic acid must be included in the treatment regimen. Side effects on the gastrointestinal tract are usually preventable by prescribing special dosage forms - effervescent tablets, buffer tablets, etc.

Blockers of platelet ADP receptors—ticlopidine and clopidogrel—have a more pronounced antiaggregation effect. Clopidogrel has advantages due to its dose-dependent and irreversible action, the possibility of use in monotherapy (due to the additional effect on thrombin and collagen), and the rapid achievement of effect. Ticlopidine must be used in combination with acetylsalicylic acid, since its antiplatelet effect is achieved after about 7 days. Unfortunately, the widespread use of modern highly effective antiplatelet agents is hampered by their high cost.

Patient Information

It is necessary to train the patient to independently monitor blood pressure levels. It is good when the patient takes medications meaningfully, and not mechanically. In this situation, he is quite capable of independently making minor adjustments to the therapy regimen.

Prognosis for nephrogenic hypertension

The survival rate of patients directly depends on how much blood pressure can be adjusted. When the cause of hypertension is promptly eliminated, the prognosis is significantly better. The hypotensive effect of reconstructive operations for renovascular hypertension is about 99%, but only 35% of patients can be completely removed from antihypertensive drugs. In 20% of operated patients, there is a significant positive change in the functional parameters of the affected kidney. The likelihood of a radical resolution of the situation with conservative treatment is impossible, however, full-fledged antihypertensive therapy with modern drugs leads to a decrease in blood pressure in 95% of patients (without taking into account the degree of correction, durability of the effect, cost of treatment, etc.). Among untreated patients with a full-blown clinical picture of malignant renovascular hypertension, the annual survival rate does not exceed 20%.

Symptoms of renal pressure and diagnosis of nephrogenic arterial hypertension

In this review, we will consider in more detail the features of the clinical manifestations of nephrogenic arterial hypertension, as well as methods for diagnosing renal pressure.

Symptoms of nephrogenic arterial hypertension

First of all, it is worth noting that there are no typical complaints with nephrogenic hypertension. As urologists note. Nephrogenic hypertension is characterized by an early (at a young age) onset of arterial hypertension, a stable course of its course, a high level of diastolic pressure, and the ineffectiveness of antihypertensive therapy. Renal hypertension most often occurs before the age of 50 years. Atherosclerotic lesions of the renal artery occur at the age of over 40 years. Sometimes there is pain in the lower back, which can be combined with pain in the kidneys.

It is mandatory to measure arterial blood pressure in both arms in vertical and horizontal body positions after physical activity. Orthostatic hypertension is observed in 80 - 90% of patients with nephroptosis. This test can be performed by a nurse.

In the parenchymal form of aerogenic hypertension, a clinical picture of the diseases that led to it is observed.

Diagnosis of nephrogenic arterial hypertension, or how to diagnose renal pressure?

To confirm the renal origin of arterial hypertension, a complex examination is necessary. An important sign of renovascular hypertension is the asymmetry of blood pressure and pulse in the upper and lower extremities. This symptom occurs with aortoarteritis. With fibromuscular stenosis of the renal artery, a diastolic murmur is heard during auscultation of the epigastric area; with aneurysm of the renal artery, a systolic murmur is heard. In some patients due to renal artery stenosis, high levels of red blood cells and hemoglobin may occur due to stimulation of the secretion of erythropoietin by the UGK.

Ultrasound examination allows us to evaluate the following parameters: the size of the kidney, the condition of the calyceal-pelvic system, the thickness of the parenchyma, the size and condition of the adrenal glands and adjacent organs, the nature of blood flow in the renal vessels (using Doppler ultrasound). Such a study is mandatory for all patients with suspected nephrogenic hypertension.

With the help of excretory urography and isotope renography, renal dysfunction is detected; with renal arteriography, Dopplerography of renal vessels, renal anomalies or vascular diseases are detected. Indications for renal angiography include appropriate medical history and detection of changes in the above-mentioned examinations and persistent malignant arterial hypertension in the absence of effect from conservative treatment. Renal angiography is the only method for diagnosing lesions of the renal artery, allowing one to determine the nature of the lesion, its location and extent.

In our other publications, read the continuation of this review, as well as the specifics of the treatment of arterial hypertension of a nephrogenic nature.

Renal hypertension. symptoms, treatment.

Renal hypertension- This is secondary arterial hypertension caused by organic kidney diseases. A distinction is made between renal hypertension associated with diffuse kidney damage and renovascular hypertension.

Renal hypertension associated with diffuse kidney damage often develops with chronic pyelonephritis, chronic and acute glomerulonephritis, kidney damage with systemic vasculitis, with diabetic nephropathy, polycystic kidney disease, less often with interstitial lesions and amyloidosis; may first appear as a sign of chronic renal failure. Renal hypertension develops due to sodium and water retention, activation of pressor systems (reninangiotensin in 20% of cases and sympathetic-adrenal systems), with a decrease in the function of the renal depressor system (renal prostaglandins). Vasorenal hypertension is caused by narrowing of the renal arteries, it accounts for 2-5% of all forms of arterial hypertension, narrowing of the renal artery by atherosclerotic plaque or fibromuscular hyperplasia of the artery, less commonly aortoarteritis, renal artery aneurysm.

Symptoms of renal hypertension

Signs of arterial hypertension in kidney disease are determined by the degree of increase in blood pressure, the severity of damage to the heart and blood vessels and the initial condition of the kidneys. The severity of hypertensive syndrome ranges from mild labile hypertension to malignant hypertensive syndrome. Complaints of patients: fatigue, irritability, palpitations, less often - headache. With malignant hypertensive syndrome, persistent high blood pressure, severe retinopathy with foci of hemorrhage, papilledema, plasmorrhagia, sometimes with decreased vision to the point of blindness, hypertensive encephalopathy, heart failure (initially left ventricular, then with stagnation of blood in the systemic circulation) are noted. In chronic heart failure, the development of heart failure is facilitated by anemia. Hypertensive crises in kidney diseases are relatively rare and are manifested by severe headache, nausea, vomiting, and blurred vision. Compared with hypertension, complications of hypertension (stroke, mycardial infarction) with nephropathies are less common. The development of hypertensive syndrome worsens the prognosis of kidney disease.

Arterial hypertension can be a leading sign of nephropathy (hypertensive variant of chronic glomerulonephritis); the combination of hypertension with severe nephrotic syndrome is characteristic of rapidly progressing subacute glomerulonephritis. In patients with chronic pyelonephritis, hypertensive syndrome occurs against the background of severe hypokalemia, and bacteriuria is often detected. Malignant hypertension most often occurs in patients with systemic diseases - periarteritis nodosa and systemic scleroderma.

In the differential diagnosis of nephrogenic hypertension and essential hypertension, it is taken into account that in patients with renal hypertension, changes in urine are detected before an increase in blood pressure is detected, edema syndrome often develops, vegetative-neurotic disorders are less pronounced, the course of hypertension is less often complicated by hypertensive crises, myocardial infarction, and stroke. When diagnosing vasorenal hypertension, instrumental studies, studying the activity of renin in the peripheral veins and renal veins, and listening to the systolic murmur in the projection of the renal arteries are of great importance.

Treatment of renal hypertension

Drug therapy for hypertensive syndrome should be carried out by limiting the intake of table salt to 3-4 g per day; Taking any drug starts with small doses; therapy should be combined; Therapy should be prescribed with one drug, adding others sequentially; if renal hypertensive syndrome exists for more than 2 years, treatment should be continuous; in case of severe renal failure, diastolic blood pressure should not be reduced below 90 mmHg. Art.

When carrying out antihypertensive therapy, the severity of renal failure should be assessed; the drugs of choice are drugs that improve renal function; in case of end-stage renal failure (glomerular filtration less than 15 ml/min), blood pressure is corrected using chronic dialysis; if hypertension is refractory to therapy, kidney removal followed by transplantation is indicated.

An increase in blood pressure can signal not only pathology of the heart and blood vessels, but also other pathological changes in the body. Most changes in renal tissue radically change the functioning of internal organs, including the functioning of blood vessels and the heart.

Nephrogenic arterial hypertension

Nephrogenic arterial hypertension (secondary hypertension) is a disease in which the level of blood pressure increases as a result of damage to the parenchymal tissue of the kidneys or their vascular system.

Disease classification:

Vasorenal form (pathology of the renal vessels);
Parenchymal form (various types, chronic inflammatory interstitial processes);
Mixed form.

In the international classification ICD-10, nephrogenic arterial hypertension has code I 12

In the video about what arterial hypertension is:

Causes and types

Causes of secondary nephrogenic hypertension:

Vascular factors include thickening of the fibromuscular layer of the renal arteries, the formation of atherosclerotic plaques on their inner layer, as well as aneurysms (pathological areas of thinning). Pathologies such as coarctation of the aorta, arteriovenous fistulas (fistulas), displacement of the renal artery during kidney prolapse contribute to the development of an increased level of blood pressure in the patient’s vascular bed.

The cause of increased blood pressure is renal ischemia. When the blood supply to the renal parenchyma is impaired, the production of renin increases, which promotes the transformation of angiotensinogen into angiotensin. Angiotensin 1 is transformed into angiotensin 2, which significantly increases renal vascular tone and vascular resistance in the periphery. The production of aldosterone increases, which retains fluid in the human body.

The mechanism of development of arterial hypertension

If the patient suffers from inflammatory kidney diseases or one of the types of nephropathy, then atrophy of the kidney tissue develops. As a result, the volume of blood in the vascular bed increases due to an increase in the concentration of sodium from the body.

There are the following types of nephropathies:

. Due to increased blood glucose levels, biochemical and metabolic disturbances in metabolic processes are observed, which affect the elasticity and strength of the vascular wall and renal parenchyma;
In gout, uric acid crystallizes in the kidney tissue, which reduces the number of normal functional units (nephrons);
With autoimmune processes and taking certain medications, membranous nephropathy may occur, the development mechanism of which is the fixation of immune complexes in the cells of the renal tissue;
, arising under the influence of toxic substances;
Dysmetabolic nephropathy is caused by the deposition of crystals of various substances in the interstitium of the kidneys against the background of metabolic disorders.

Signs and symptoms

Arterial hypertension of renal origin most often develops gradually, differs from primary hypertension by a higher level of blood pressure during the relaxation phase of the heart. Blood pressure is resistant to antihypertensive therapy. Patients complain of headaches, most often localized in the back of the head, thirst, constant fatigue, loss of appetite, which is typical for hypertension. In the morning, swelling often appears (mainly on the face - of renal origin), which decreases in the evening; with a certain pathology, a laboratory test reveals a certain amount of protein in the urine that exceeds the norm.

Diagnostic methods

Nephrogenic arterial hypertension syndrome is diagnosed after the following studies:

MRI and MRI are widely used to diagnose the state of the renal vascular system and their interstitial tissue.

Treatment

Arterial hypertension of renal origin has a malignant course in most cases. In order to prevent the occurrence of severe consequences, therapy should be prescribed in the early stages of the disease.

The renovascular form of arterial hypertension is subject to treatment through invasive interventions. If the lumen of the renal artery is narrowed, the blood supply to the parenchyma is disrupted. By placing a balloon catheter or a special stent inside the artery at the site of stenosis, normal blood flow can be restored.

Open operations are also used to reconstruct the artery: resection of the narrowed section with anastomosis, endarterectomy, installation of an arterial prosthesis.

For nephroptosis, interventions are used to perform nephropexy (fixation). Lack of functional activity of the kidney is an indication for kidney removal.

Treatment of the parenchymal form of arterial hypertension should be aimed at eliminating the cause and primary pathological process in the human body.

There are the following drug treatments for various forms of nephropathies:

If the cause of the development of hypertensive syndrome is chronic pyelonephritis, then the goal of therapy is to eliminate the bacterial factor and restore the free flow of urine. Depending on the causative agent of the disease, a specific antibacterial drug is prescribed (penicillin antibiotics, cephalosporins, carbapenems, monobactams, aminoglycosides, tetracyclines). Nonsteroidal anti-inflammatory drugs are also used.

To improve the elasticity of red blood cells, trental (pentoxifylline) is prescribed. This drug reduces the aggregation ability of platelets, thereby improving blood flow in the vascular bed. For the same purpose, Venoruton (troxevasin) is prescribed for 3-4 weeks.

In the case of the formation of arterial hypertension against the background of various nephropathies, the cause of their development should be eliminated: for diabetic or dysmetabolic nephropathy, it is recommended to follow a low-protein diet and normalize the balance of lipids in the body. ACE inhibitors are prescribed (lisinopril, captopril, berlipril, Prestarium).
Gouty nephropathy is treated by prescribing allopurinol, which helps dissolve uric acid crystals and reduce their formation. Patients should adhere to a low-purine dietary regimen.
In order to reduce high blood pressure, angiotensin 2 receptor blockers (valsartan, losartan).
To improve the immunological properties of the body, various adaptogens are prescribed (schisandra chinensis, ginseng), methyluracil 4 g per day for several weeks.
Levamisole, thymalin, and T-activin are used as immunomodulators for long-term inflammatory processes of an autoimmune nature. They reduce the response of the body's immune system.

Traditional recipes that are used to lower blood pressure are quite effective, but their disadvantage is that only the symptoms of the disease are eliminated, but the cause remains. Therefore, traditional methods of therapy should be combined in parallel with drug treatment.

Traditional recipes for lowering blood pressure:

Use crushed flax seeds internally before eating;
A mixture of crushed cranberries with honey, take every day;
Pine cones, pre-washed with water, are filled with 40% alcohol and infused in a dark place for 3-4 weeks.

Prognosis and complications

The prognosis for the life and ability to work of a patient suffering from hypertension of renal origin is quite favorable if the primary disease was identified in the early stages of development and certain therapeutic measures were prescribed in a timely manner.

Positive dynamics are observed in patients who underwent surgery. If both kidneys are affected, the prognosis is poor.

Possible complications: heart and vascular failure, myocardial hypoxia and ischemia, strokes, development of renal failure.

Arterial hypertension (AH) is a symptom of many diseases, but 35-40% of patients who have “hypertension” are patients with kidney damage. This type of increase in blood pressure is called nephrogenic (renal) arterial hypertension. It is separated into a separate group of hypertension that does not belong to idiopathic arterial hypertension - hypertension.

Hypertension is quite often observed in acute diffuse kidney diseases (acute glomerulonephritis, nephrotic syndrome of any origin, especially in the initial stage). In such cases, hypertension is accompanied by edema and disappears after the edema subsides and proteinuria and hematuria significantly decrease. It is caused by overflow of blood vessels (hypervolemia) and is a consequence of sodium and water retention in the body. Over time, hypertension can manifest itself as a complication of some chronic kidney disease, in particular glomerulonephritis, pyelonephritis, urolithiasis, tuberculosis, and the like.

Nephrogenic arterial hypertension is observed in almost all diseases and anomalies of the kidneys - hydronephrosis, tuberculosis, cysts, tumors, urolithiasis, radiation injury, etc. But most often it is caused by pyelonephritis - primary or secondary (developed against the background of other diseases).

Distinguish renorenal(renovascular) and parenchymal(renoparenchymal, nephrosclerotic) nephrogenic arterial hypertension.

With vasorenal hypertension, the kidney does not receive the required amount of blood due to a decrease in the caliber of the renal artery and its main branches; with parenchymal hypertension, the intraorgan network of vessels, for various reasons, is not able to accommodate a sufficient amount of blood. The share of vasorenal hypertension accounts for 30%, parenchymal hypertension - 70%.

The development of nephrogenic arterial hypertension is based on humoral mechanisms. Venous blood flowing from an ischemic kidney, like hemogenate from such a kidney, has pressor properties, and the carrier of this property is a renintermolabile substance. Renin is produced in the juxtaglomerular complex (JGC) of the renal cortex, where granules are formed. With renal ischemia, the number of these granules increases or their disorganization occurs, as a result of which in both cases hyperproduction of renin begins. Excessive amounts of renin in the blood are not enough to cause hypertension. Renin combines with the alpha2-globulin fraction of blood plasma, angiotensinogen, to form a polypeptide, angiotensin II. Over time, amino acids are included in the process and an antipeptide is formed - angiotensin II, which has a vasopressive effect and is therefore called hypertensin.

The medulla of a healthy kidney produces the enzyme angiotensinase, which destroys hypertensin or inhibits the manifestation of its pressor effect. Under pathological conditions, the production of angiotensinase is reduced or its activity is not high enough.

Thus, nephrogenic arterial hypertension develops according to one of the following options: a) hyperproduction of renin-angiotensin; b) decreased production of angiotensinase; c) inactivation of angiotensinase under the influence of another blood component. A combination of several of these factors is possible.

There are various theories of the occurrence of nephrogenic arterial hypertension. According to the renopressor theory, it is a consequence of hyperproduction of renin, and according to the renoprivile theory, it is due to increased inactivation of angiotensinase.

Arterial hypertension is both a symptom of kidney disease and an independent nosological entity (nephrogenic hypertension).

Vasorenal (renovascular) arterial hypertension

The cause of renovascular (renovascular) hypertension can be both congenital anomalies and acquired diseases of the kidneys (renal) arteries.

Congenital anomalies include hypoplasia of the main trunk of the renal artery, fibromuscular hyperplasia of its walls, which leads to narrowing of the lumen, aneurysm of the renal artery, coarctation of the aorta. Among acquired diseases in adults, the first place is occupied by atherosclerosis of the renal artery, in children - post-traumatic sclerosing paranephritis, aneurysm of the renal artery, panarteritis, thrombosis or embolism of the renal artery, that is, renal infarction, stenosis of the renal artery with nephroptosis - functional or organic, compression of the renal artery from the outside . This also includes iatrogenic etiological factors: resection of the kidney, intersection of an (additional) blood vessel, damage to the artery supplying the part of the kidney that remains after heminephrectomy, etc.

Fibromuscular hyperplasia of the renal artery is sometimes expressed in a small segment and has a circular character. In some cases, diffuse or multiple wall thickening is noted. Histological examination reveals thickening of the muscular and connective layers of both the main trunk of the renal artery and its branches. Hypertension is quite often observed with kidney tumors and cysts. It is likely that in these cases it is caused by the pressure of the tumor or cyst on the renal vessels. After nephrectomy or cyst removal, blood pressure usually normalizes.

With renovascular hypertension, the course of the disease depends on the degree of narrowing of the renal artery. If the narrowing is moderate, then hypertension has a benign course and kidney function is preserved. With significant narrowing of the renal artery, hypertension has a malignant course and kidney function is significantly reduced. With congenital anomalies, a characteristic sign of renovascular hypertension in 95% of cases is the absence of patient complaints until the disease is accidentally detected.

In children, the objective symptoms of renovascular hypertension are systolic murmur in the umbilical region, and in some cases, absence of pulsation in both legs (or low blood pressure), and ribs.

In most cases, no pathological changes are observed in the urine, although even if they are present, hypertension may be of vascular origin, and pyelonephritis may follow later.

In the peripheral blood, there is an increased level of renin (normally 0.0066-0.0078 mg/l), an impaired ratio of sodium and creatinine excretion by the kidneys.

An informative research method is radionuclide renography. A decrease in the vascular segment of the renogram indicates a lesion. This method is especially effective in case of unilateral damage to the renal artery, when there is asymmetry of renograms on both sides.

X-ray examination is usually performed after renography, when it is already known which side is affected. On excretory urograms with narrowing of the renal artery, a slowdown in the appearance of a radiopaque substance in the pyelocaliceal system or a decrease in the kidney due to its atrophy, an early and persistent nephrogram, are observed. Urography often reveals a “silent” kidney or a sharp depression of its function.

Dynamic scintigraphy plays an important role in the diagnosis of renovascular hypertension, allowing not only to identify the functional significance of narrowing (stenosis) of the renal artery, but also to quantify functional changes in the renal parenchyma.

The final diagnosis is made using angiography, which reveals the presence of narrowing or other changes in the lumen of the renal artery, and depletion of the vascular pattern. In addition, this research method is crucial when choosing a treatment method.

In the case of atherosclerotic stenosis, the atherosclerotic plaque is usually located in the proximal third of the renal artery, closer to the aorta. The process is often one-sided. Narrowing (stenosis) of the renal artery due to its fibromuscular hyperplasia in most cases develops on both sides. It is localized in the middle and distal thirds of the main renal artery, spreading to its branches, and often to the intrarenal vessels. Angiographically it appears as a necklace.

A renal artery aneurysm appears as a sac-like vessel on the aortogram; thrombosis or embolism of the renal artery - amputated end of the vascular trunk.

In case of nephroptosis, the study is performed in the vertical and horizontal positions of the patient. On an aortogram taken in a vertical position, the artery is sharply elongated, often rotated, and its diameter is small.

Differential diagnosis of vasorenal arterial hypertension is carried out with hypertension, parenchymal nephrogenic and symptomatic hypertension of various types.

Treatment. To treat patients with vasorenal hypertension, drug therapy and surgery are used. Drug therapy is widely used during preparation for surgery and in the postoperative period. Its main goal is to constantly keep blood pressure under control, take measures to minimize target organ damage and try to avoid unwanted side effects of drugs. In case of ineffectiveness or unacceptable side effects of therapy, the question of surgical treatment is raised. A number of plastic organ-preserving interventions have been proposed, the purpose of which is to restore the main blood circulation in the kidney. The nature of the operation depends on the type, location, degree of narrowing of the renal arteries, the spread of the process (unilateral or bilateral), the quantity and quality of the preserved parenchyma in the affected and opposite kidneys (transaortic endarterectomy, removal of the narrowing site, replacement with a Dacron graft, autovenous, splenic-renal arterial anastomosis, kidney removal, etc.). When vascular pathology is localized (narrowing of an aneurysm, etc.) deep in the renal parenchyma, the operation is performed extracorporeally.

The results of the operation depend on the duration of the disease (up to 5 years), the type of damage to the artery - the best for fibromuscular dysplasia of the renal artery. Moreover, the effectiveness of surgical treatment does not depend on the level of blood pressure before surgery.

Nephrectomy is contraindicated in cases of bilateral renal artery stenosis or atherosclerosis of the opposite kidney. In such cases, to select a treatment method, a puncture percutaneous biopsy of the opposite kidney is performed.

The prognosis for vasorenal arterial hypertension without surgery is unfavorable. Hypertension progresses and in most cases becomes malignant. Therefore, the shorter the duration of hypertension before the intervention, the better the postoperative result. With timely surgery, the prognosis is favorable, but patients should be under medical supervision.

Parenchymatous nephrogenicarterialhigh blood pressureI

The most common cause of the development of nephrogenic arterial hypertension in a therapeutic clinic is glomerulonephritis, in a urological clinic it is pyelonephritis. All diseases of the kidneys and urinary tract, except glomerulonephritis, can cause hypertension only when complicated by pyelonephritis. The only exceptions are some kidney anomalies (hypoplasia, duplication, some cysts), which can cause hypertension without pyelonephritis. Hypertension is observed in chronic pyelonephritis with a latent course, sometimes with an erased clinical picture (hypertensive form). It can be primary or develop against the background of various diseases (secondary). As for glomerulonephritis, hypertension develops mainly in the proliferative sclerotic form, less often in the membranous form of the disease. Hypertension can be caused by renal amyloidosis, nephrotic syndrome, collagenous nephropathy, etc.

The frequency of hypertension in bilateral chronic pyelonephritis reaches 58-65%, in unilateral - 20-45%. At a certain stage of development, nephrogenic arterial hypertension may be the only manifestation of pyelonephritis, but it is often considered essential.

A significant proportion of patients with pyelonephritis see a doctor only after the development of nephrogenic arterial hypertension. In 70-78% of patients with chronic pyelonephritis, hypertension is detected before the age of 40, while patients with hypertension are predominantly (in 75% of cases) people over 40 years of age.

The relationship between pyelonephritis and hypertension is confirmed by the fact that in patients with unilateral pyelonephritis, blood pressure normalizes after nephrectomy. In 12% of patients with chronic pyelonephritis over 40 years of age, blood pressure normalizes after long-term pathogenetic treatment.

In arterial hypertension caused by chronic pyelonephritis, both diastolic (to a greater extent) and systolic pressure are increased. Pulse blood pressure remains low. As the disease progresses, systolic pressure increases more rapidly than diastolic pressure. In 15-20% of cases, hypertension, which is caused by pyelonephritis, is accompanied by high diastolic pressure, that is, it has a malignant course. This is mainly observed with long-term illness and severe renal impairment.

It is not always possible to trace the connection between the degree and nature of hypertension in pyelonephritis and impaired renal function. Often patients have impaired renal function with normal blood pressure. In urolithiasis, arterial hypertension is caused by its complication, mainly chronic calculous pyelonephritis. Its frequency in this group of patients ranges from 12-64%.

In chronic pyelonephritis, hypertension can be receding, transient, appearing only during the period of exacerbation of the process due to increased inflammatory edema of the kidney tissue and deterioration of its blood supply. However, most often it is stable, with a tendency to increase blood pressure. The development of parenchymal neurogenic hypertension is based on humoral mechanisms. It has been proven that arterial hypertension in chronic pyelonephritis is associated with renal ischemia due to sclerotic changes in the interstitial tissue, accompanied by vascular sclerosis and a resulting disturbance of intrarenal hemodynamics.

The main hemodynamic mechanism for increasing blood pressure in pyelonephritis is an increase in intrarenal vascular pressure, which is especially pronounced in a bilateral process, the syndrome of malignant hypertension.

The main mechanism in the formation of arterial hypertension in patients with pyelonephritis is renoprival, i.e. caused by loss of depressor function. Consequently, hypertension in patients with pyelonephritis is caused primarily by damage to the renal medulla, then production is suppressed. The activity of kinins affects the content of depressor prostaglandins in the kidneys. Together, they create the functional opposite of the renin-angiotensin-aldosterone system in regulating both intrarenal systemic hemodynamics and electrolyte balance.

It has been established that not only the renin-angiotensin-aldosterone system, but also many other biologically active substances (products of lipoxygenase and epoxygenase activity, cytochrome P450 endothelial relaxing factor, etc.) are involved in the genesis of nephrogenic arterial hypertension. And a number of physiological mechanisms (the size of perfusion pressure, the volume of circulating blood, the activity of the beta-adrenergic system, etc.).

Thus, the occurrence of nephrogenic arterial hypertension is a complex process. In some cases, it develops due to hyperproduction of renin, in others - increased inactivation of angiotensinase. As pyelonephritis develops, other factors that are not yet fully understood are included in the pathogenesis.

Clinical picture . The symptoms of arterial hypertension in chronic pyelonephritis differ in many ways from those in hypertension and consist of symptoms of pyelonephritis and increased blood pressure. With nephrogenic hypertension, the pressure is usually stable, but tends to increase and progresses steadily. Moreover, both diastolic and systolic pressure are increased, but to a greater extent - diastolic. The transient nature of hypertension does not exclude its renal origin.

Parenchymal renal hypertension is more often observed in women (mostly young), and hypertension is observed in middle-aged and elderly people. Arterial hypertension in pyelonephritis is poorly responsive to antihypertensive drugs.

Almost 30% of patients with chronic pyelonephritis exhibit only hypertension, which is discovered by chance in 6% of patients during routine examinations. About 7% of patients consult a doctor about the following manifestations of arterial hypertension: pain in the forehead or back of the head, pulsations in the temples, dizziness, decreased visual acuity, etc. Some complain of lower back pain, hematuria, low-grade body temperature, dry mouth, thirst, polyuria.

In the clinical course of chronic pyelonephritis, two types of arterial hypertension are distinguished.

In the first of these, pyelonephritis as a source of hypertension should be considered in the following cases: a) if in a patient over 60-70 years of age, systolic hypertension turns into systolic-diastolic; b) if there is a relationship between exacerbation of pyelonephritis and an increase in diastolic pressure, which decreases during the period of remission; c) if hypertension progresses along with renal failure.

The second variant of hypertension caused by pyelonephritis remains unrecognized for a long time. Blood pressure is unstable. It ranges from high to normal and even low. The benign nature of hypertension is disorienting, sometimes the complete absence of changes in the urine. In such cases, you need to pay attention to the fact that blood pressure increases in parallel with a decrease in diuresis, swelling of the eyelids, numbness of the fingers, and a feeling of chills at normal body temperature. It should also be taken into account that nephrogenic arterial hypertension most often occurs in young people. Diastolic blood pressure increases predominantly; there are no signs of autonomic neurosis. The disease is not complicated by hypertensive crises, disturbances of cerebral and coronary blood flow. There is a connection between the exacerbation of the process and the disease with sore throat and acute viral infections.

The diagnosis is based on identifying arterial hypertension, pyelonephritis and establishing an etiological connection between them. With hypertension that has developed against the background of unilateral pyelonephritis with a latent course, pathological changes are minimal or absent. This is due to the fact that a small number of nephrons function in the affected kidney and diuresis is reduced. In such cases, it is necessary to examine not only the total function of both kidneys, but also each of them separately, especially when determining the content of creatinine and sodium in the urine.

During the diagnosis of nephrogenic hypertension, two tasks are solved: a) determine the nature of the kidney pathology, the degree of their damage and functional ability; b) establish the sequence of development of nephrogenic hypertension and hypertension. If the patient has long suffered from arterial hypertension, and symptoms of kidney damage appeared later and there is a family history of hypertension, one can suspect hypertension, which has caused secondary changes in the kidney. The parenchymal form of nephrogenic arterial hypertension is characterized by: a history of previous kidney diseases or injuries (or the appearance of changes in the urine, edema), the absence of a family history of hypertension, a sudden onset, often a malignant course of the disease, the absence or short-term effect of conservative treatment, decreased function of one or both kidneys, increased renin activity in the peripheral blood, hypokalemia, decreased sodium and creatinine concentrations in the urine, decreased blood pressure during the treatment of a patient with pyelonephritis.

The results of a puncture biopsy of the kidneys, the Howard-Rappoport test, determination of the level of aldosterone and catecholamines in the urine, and aortography are of diagnostic value.

Differential diagnosis carried out with hypertension, chronic glomerulonephritis and various types of symptomatic arterial hypertension. For the differential diagnosis of hypertension and pyelonephritis, the results of comparing the function of the right and left kidneys are important. In such cases, when the inflammatory process affects both kidneys, one of them is more affected than the other.

In hypertension, the main task is to clarify the nature of symptomatic hypertension and ensure that the patient does not have kidney pathology.

Treatment treatment of patients with chronic pyelonephritis with arterial hypertension should be comprehensive and aimed at eliminating the underlying disease that caused these disorders. In the case of unilateral pyelonephritis, the only treatment option is nephrectomy. However, sustained normalization of blood pressure after surgery occurs only in 50-65% of patients. This is explained by the fact that at the time of the operation, the process of wrinkling occurs not only in the kidney that is removed, but also in the one that remains. Irreversible secondary changes are observed in the heart and blood vessels.

Nephrectomy is effective in the initial stages of the disease (75-80%). With bilateral chronic pyelonephritis, the process of wrinkling in one kidney occurs more intensely. Therefore, in case of malignant arterial hypertension, nephrectomy is also advisable if the second kidney can provide homeostasis. In advanced forms, a bilateral nephrectomy followed by a donor kidney transplant is required.

Many patients with pyelonephritis have a decrease in blood pressure after conservative therapy. The simultaneous use of corticosteroids, antibacterial and antihypertensive drugs for chronic pyelonephritis not only helps to inactivate the inflammatory process, but also reduces the likelihood of developing hypertension. The use of diuretics is promising. These drugs block intracellular aldosterone receptors. One of the main places in complex treatment is occupied by beta-adrenergic receptor blockers. They suppress the activity of JGC cells, especially when the renin-angiotensin-aldosterone system is involved in the pathogenesis of blood pressure support.

In case of arterial hypertension caused by calculous pyelonephritis, early stone removal followed by systematic comprehensive treatment for the inflammatory process and hypertension is advisable. Patients require active clinical observation.

Early diagnosis of acute and chronic pyelonephritis can provide effective and rational treatment, and therefore the prevention of hypertension.

Forecast. After nephrectomy, performed before the development of irreversible changes in the opposite kidney, as well as with unilateral chronic pyelonephritis causing hypertension, the prognosis is favorable. In case of bilateral kidney damage, the prognosis is unfavorable.

The disease has various forms and is classified as dangerous to humans. Nephrogenic arterial hypertension is characterized by an increase in blood pressure due to pathologies associated with the kidneys. The disease can only be eliminated through drug therapy. It involves regular use of prescribed medications over a long period of time. It is impossible to cure the disorder without pharmaceutical drugs.

The disease occurs only against the background of damage to the kidneys or renal arteries. It can appear at any age and is diagnosed in 30% of cases with arterial hypertension. In medicine, pathology is defined as renal hypertension, accompanied by impaired circulation in the kidneys, vasoconstriction, and persistently high blood pressure.

Nephrogenic arterial hypertension is high levels of lower blood pressure

In the international classification of diseases, nephrogenic hypertension was coded I12, which includes two types of disorders - with or without renal failure. In addition, the disease is divided into three forms:

Vasorenal - pathologies developing in the renal arteries.
Parenchymal - inflammatory processes in the kidneys.
Mixed - a combination of inflammatory processes with pathological changes in the blood vessels of the organ.

Nephrogenic hypertension is one of the forms of the disease that develops quite rapidly, and as it progresses, it affects various “target organs”.

Note. Any form is dangerous and requires immediate treatment. Without the correct doctor's prescription, the disease progresses, acquires more severe stages and leads to the development of dangerous complications.

Causes

Each of the forms is a consequence of various internal and/or external factors:

Form	Cause of occurrence
Vasorenal	Most often it is diagnosed due to a genetic predisposition, but it can occur against the background of acquired pathologies of the kidneys and their arteries - atherosclerotic lesions, aneurysm, thrombosis, etc.
Parenchymatous	Appears due to renal failure, lupus erythematosus, impaired blood supply to the kidneys, inflammatory pathologies (pyelonephritis and others), atrophy of the kidney tissue, kidney cysts.
Mixed	It can arise either due to a genetic predisposition or become a consequence of various serious diseases.

Clinical picture of the pathology

The main signs of nephrogenic arterial hypertension are malfunctions of the kidneys and adrenal glands. In addition, the disease is accompanied by other symptoms - regular headaches, general weakness, increased irritability and heart rhythm disturbances.

Frequent urination, false urges, increased or decreased urine output - all these are manifestations of kidney failure

Most often, with this disease, an increased heart rate (tachycardia) is observed; a low heart rate (bradycardia) is observed much less frequently. As the pathology develops, blood pressure tends to rise to critical levels, which often becomes the cause of a hypertensive attack.

In the final stages of the disease, body temperature may rise, hearing and vision may deteriorate, and unbearable symptoms may appear. Many patients experience swelling throughout the body and pain in the heart area. If left untreated, the disease progresses and leads to stroke or myocardial infarction.

Diagnostic methods

To make an accurate diagnosis, the doctor collects complete information about the patient (age, living conditions, past illnesses, etc.).

Urine and blood tests to determine the level of white blood cells, which show whether there are inflammatory processes.
Measurement of blood pressure at rest and after minor physical activity.
Consultation with an ophthalmologist and examination of the fundus to determine the extent of damage to the visual apparatus.
Ultrasound of the kidneys with Doppler sonography. This diagnostic measure helps determine the condition of the kidneys, adrenal glands and renal arteries.
Excretory urography, which helps to study the excretory functions of the kidneys.

If it is impossible to make a diagnosis, the doctor may prescribe radioisotope renography of the kidneys (detection of pathologies), consultation with specialists, for example, a nephrologist, and other specific examinations.

Principles of treatment

Treatment of nephrogenic arterial hypertension depends on the severity of the disease, as well as the extent of damage to the kidneys and renal arteries. With the renovascular form, as a rule, surgical intervention is required to expand the lumen of the blood vessels. To do this, an open operation is performed or a special dilating catheter is installed inside the vessel. This will help restore blood flow and kidney function.

Parenchymal and mixed forms are treated with medications of various groups. These include:

Beta blockers;
Calcium antagonists;
Diuretics;
ACE inhibitors.

If the cause of the development of the pathology is inflammatory kidney disease, the doctor may prescribe antibiotics of the penicillin or cephalosporin group. To improve blood flow, Pentoxifeline or Venoruton is used.

To boost the immune system, medications from the adaptogen group are prescribed, for example, Methyluracil. In addition, antispasmodics and other drugs that eliminate associated symptoms can be used.

Important! Therapeutic measures are selected by the doctor, and for each patient individually. Self-medication does not bring a positive effect and most often leads to complications of the disease.

Rehabilitation after illness

The rehabilitation period includes physical therapy, diet therapy and other health-improving activities. During this period, it is important to follow a diet, eat healthy foods and not overexert yourself. Walking in the fresh air and regular breathing exercises help a lot.

The best way to quickly improve your health is sanatorium treatment. In addition, doctors often recommend physiotherapeutic measures and the use of decoctions prepared at home, based on flax seeds, cranberries and pine cones.

Treatment prognosis

The prognosis will be favorable only if treatment is started on time. After surgical interventions, as a rule, positive dynamics are also observed. However, in the case of damage to both kidneys, the outcome is not always positive, and rehabilitation will be long. Doctors say that the sooner therapeutic measures are taken, the more beneficial the result will be. Lack of necessary treatment leads to the development of acute heart failure, stroke, myocardial infarction, and in severe cases to sudden death.