Renal hypertension: causes, symptoms, treatment, prognosis, prevention. Renal hypertension disease: causes, symptoms and treatment In what cases is a tolerant salt regime allowed?

Hypertension is one of the most common diseases today. Doctors also note the fact that from year to year the disease is becoming younger and younger, that is, it affects not only people of mature and old age, but also young people. Doctors have not yet figured out what explains this fact. Among the many assumptions one can note genetic predisposition, environmental pollution, abuse of alcohol and energy drinks, smoking. Some experts suggest that the reason for the development of hypertension at an early age is the abnormally hot summer, which has been observed for several years in a row.

The term used by ordinary people to denote an increase or decrease in blood pressure - hypertension - does not mean a disease - but a condition of the muscles of blood vessels or arterioles. And to indicate instability blood pressure use terms arterial hypertension or hypertension.

But the worst thing, probably, for the majority of people with arterial hypertension is that it practically does not manifest itself in any way, and therefore many find out about it only when complications of the disease occur in the form of a stroke or heart attack. This asymptomatic course of the disease can last for quite a long time, up to several years.

But if symptoms of hypertension appear, then doctors consider this a good sign. After all, they mean that the patient can start treatment on time.

Main symptom hypertension Constantly high blood pressure is considered. Doctors consider the remaining symptoms mainly in accordance with the stages of hypertension. There are three degrees of hypertension: mild, moderate and severe. In accordance with the degrees of hypertension, it has the following symptoms:

Hypertension of the second and third degrees can sometimes have such a “symptom” as a hypertensive crisis. It occurs only in one case, when the patient feels relief from his condition and therefore independently decides to stop taking medications.

With kidney damage, renal hypertension develops. She has her own symptoms. For example, increased diastolic pressure is considered a symptom of renal hypertension. The pulse pressure is low.

Very important symptom with renal hypertension there is such a clinical sign as systolic and diastolic murmur. It is usually heard in the area of ​​​​the projection of the renal arteries. This noise is better heard in patients with atherosclerosis of the renal arteries in the epigastric region above the navel. And if a patient has fibromuscular hyperplasia, the noise can be heard above the navel. Sometimes it can be heard from the back.

True, some doctors do not consider systolic murmur to be an absolute sign of renal hypertension. Sometimes the same sign is present in patients without renal artery stenosis.

The second obvious symptom of hypertension in kidney damage is the asymmetry of blood pressure in the patient’s extremities.

In one third of patients with hypertension, the disease can develop into a malignant form. Symptoms of malignant hypertension are frequent attacks of angina. Functional kidney failure is also recognized as a symptom of hypertension. Other symptoms in the malignant form: increased blood levels of indican, residual nitrogen, oliguria and azotomic uremia.

At the same time, high blood pressure is practically not reduced by medications. In addition, all this is very often complicated by strokes, heart attacks, and hypertensive crises. And often all this can end in the death of the patient.

Therefore, almost all people need to especially carefully monitor their blood pressure and consult a doctor if it constantly increases.

Conservative treatment of hypertension in kidney diseases

To resolve the issue of the feasibility and methods of treating hypertension in kidney diseases, fundamental ideas about whether the rise in blood pressure is compensatory in nature and whether its decrease will have a positive or negative effect on kidney function and the course of the underlying disease are of utmost importance. In this regard, Page (1965) points out that until the early 1930s, “most doctors thought that a decrease in blood pressure would necessarily lead to a drop in renal blood flow and ultimately to uremia.” If this opinion prevailed in relation to lowering blood pressure in essential hypertension, then in relation to renal patients, where filtration and blood flow are often reduced before treatment, it seemed even more justified. However, studies conducted in 1931 by Van Slyke and Page showed that a decrease in blood pressure (of course, within certain limits) did not in itself lead to a noticeable decrease in urea clearance or renal blood flow. It was further found that a prolonged increase in blood pressure (especially diastolic) leads to a deterioration in the blood supply to the kidneys and the progression of their arteriolosclerosis. Long-term observations by Abrahams (1957), Wilson (1960), N.A. Ratner (1965), Dollery (1966, 1967) allowed them to come to the conclusion that the malignant type of hypertension is observed much more often in chronic kidney diseases than with essential hypertension; according to Wilson, in almost half of the cases - with kidney disease and in a ratio of 1.1000 cases - with essential hypertension; the corresponding ratios, according to N.A. Ratner (1965), are 8:1. In 1966, the question of the effect of treatment of hypertension on renal function was again studied in a review by Moyer et al. They found a direct connection between the height of blood pressure and damage to renal hemodynamics. Untreated malignant hypertension within a year led to 100% death due to a progressive decline in filtration and blood flow. Mortality among 12 similar patients who received adequate antihypertensive therapy for 29 months was 17%; however, renal function deteriorated slightly. Similar observations were made by Dustan et al. (1959). When treating moderate hypertension, the authors did not find any significant difference in the nature of renal functions depending on the treatment. Reubi (1960) noted that with severe hypertension in untreated patients, glomerular filtration decreases by 18% and renal blood flow by 27% per year, and with treatment, respectively, by 2.4 and 7.4% per year.

Most researchers (Abrahams, 1957; Goldberg, 1957; S.K. Kiseleva, 1958; Wilson, 1960; N.A. Ratner, 1965; special conclusion Ciba Medical Documentation, 1963; Smyth, 1965; Page, 1965; symposium on Hypertension, 1968) believe (we subscribe to this point of view) that renal hypertension, like hypertension, must be treated immediately after its detection, for a long time and vigorously. However, for specific clinical recommendations it is necessary to study a number of issues:

1) how does a decrease in blood pressure affect kidney function during kidney disease (depending on the initial values ​​and the degree of impairment);

2) what are the features of the action of various antihypertensive drugs, given that for some of them the kidneys are one of the main points of application;

3) what is the course of the disease and changes in kidney function and urine composition during long-term (months and years) antihypertensive therapy due to the fact that in kidney diseases, hypertension is, although important, but not the only symptom that determines the course and prognosis;

4) are the principles of treatment of renal hypertension the same during periods of sufficient and insufficient renal function;

5) what is the effect on blood pressure in chronic renal failure such methods of extrarenal cleansing as vivodialysis, including peritoneal dialysis.

For the treatment of renal hypertension, the same complex of drugs and techniques is usually used as for hypertension, i.e. a diet limited to 1.5-3 g (in some cases up to 500 mg per day) of sodium and medication (most often combined ) therapy.

The medications used can be grouped as follows: a) Rauwolfia serpentina preparations; b) saluretics; c) ganglion blockers; d) α - adrenergic blockers of sympathetic nerves (guanethidine and its analogs - ismelin, isobarine, sanotensin, octadin), betanidine, α-Methyl Dopa (al-domet, dopegit); e) β-adrenergic blocking agents (propranolol); f) hydrazinophthalazine preparations; g) aldosterone antagonists (including spironolactone); h) monoamine oxidase inhibitors; i) various combination drugs (used most often).

Thus, we have a range of drugs suitable for the treatment of both moderate (Rauwolfia serpentina saluretics) and high and persistent (guanethidine) hypertension. Prescribing patients a diet with food restriction of table salt to 1.5-3 g per day and protein to 50-60 g (i.e. 0.7-0.8 g/kg body weight) caused a decrease in blood pressure to normal levels within 10 days from the start of treatment in 25% of patients with hypertension dependent on nephritis and pyelonephritis, in the absence of renal failure (from total number 250 patients, Fig. 61), as shown by studies conducted in our clinic by N. T. Savchenkova and E. M. Kuznetsova. From Fig. 61 shows, however, that a decrease in blood pressure, accompanied by an improvement in well-being, is observed in patients with low systolic pressure values, although the initial diastolic pressure was relatively high (102.3 mm Hg).

The composition of urine did not change significantly. At the same time, in 3/4 of renal patients, the use of drug therapy is necessary. In this case, therapy for renal hypertension should be long-term (sometimes many years).

Rice. 61. The effect of a diet limiting salt to 1.5-3 g and protein to 0.7-0.8 g/kg body weight on renal hypertension.

The shaded sector is effective; without shading - ineffective

Causes and symptoms of renal hypertension

Renal hypertension is a disease in which blood pressure increases due to kidney disease. Renal pathology is characterized by stenosis. With stenosis, the main and internal renal arteries and their branches narrow.

In 10% of patients with high blood pressure, renal arterial hypertension is diagnosed. It is characteristic of nephrosclerosis, pyelonephritis, glomerulonephritis, and other kidney diseases. It most often affects men aged 30 to 50 years.

What are the features of the disease?

Renal hypertension is secondary arterial hypertension that occurs as a manifestation of other diseases. The causes of the disease are explained by disruption of the kidneys and their participation in hematopoiesis. With such a health disorder, it is necessary to treat the underlying disease; with successful therapy, the pressure returns to normal.

The cause of renal arterial hypertension is damage to the kidney tissue, while the renal arteries narrow. Due to impaired kidney function, the volume of circulating blood increases and water is retained in the body. This causes an increase in blood pressure. There is an increased sodium content in the body due to a failure in its excretion.

Special sensitive formations in the kidneys that perceive irritations and transmit them to the nervous system, receptors that respond to various changes in the movement of blood through the vessels (hemodynamics), are irritated. The hormone renin is released, it activates substances that can increase the peripheral resistance of blood vessels. This causes abundant release of hormones from the adrenal cortex, and sodium and water retention occurs. The tone of the renal vessels increases, their sclerosis occurs: soft deposits accumulate in the form of gruel, from which plaques are formed that limit the lumen and affect the patency of blood to the heart. There is a circulatory disorder. The kidney receptors are irritated again. Renal hypertension may be accompanied by hypertrophy (excessive enlargement) of the left cardiac ventricle. The disease mainly affects older people; it can occur in young men, because they, compared to women, have more body weight, and therefore a larger vascular bed in which blood circulates.

What is the danger of kidney hypertension and how can it be determined?

Kidney hypertension is dangerous due to complications. They may be:

• hemorrhage in the retina with decreased vision up to blindness;
• heart or kidney failure;
• serious damage to the arteries;
• changes in blood properties;
• vascular atherosclerosis;
• lipid metabolism disorder;
• cerebrovascular disorders.

Such disorders often become causes of decreased ability to work, disability, and death.

Clinical signs of the disease that may appear in patients:

• systolic or diastolic murmurs heard in the area of ​​the renal arteries;
• heartbeat;
• headache;
• violation of nitrogen excretory function;
• a small amount of protein in the urine;
• decreased specific gravity of urine;
• asymmetry of blood pressure in the extremities.

Renal hypertension, the symptoms of which are stable hypertensive syndrome with predominantly elevated diastolic pressure, can be malignant in 30% of cases. Arterial hypertension may be the main symptom of nephropathy. The combination of hypertension with severe nephrotic syndrome is typical for the development of subacute glomerulonephritis. Malignant hypertension affects patients suffering from periarteritis nodosa, and symptoms of impaired renal function are combined with clinical signs other diseases. In most cases, renal pathology is expressed by vasculitis of intrarenal arteries of medium caliber, and renal ischemia and infarction develop.

With hypertension of renal origin, patients complain of fatigue and irritability. Damage to the retina of the eyeball (retinopathy) with foci of hemorrhage, swelling of the optic disc, and impaired vascular permeability (plasmorrhagia) are observed. To make an accurate diagnosis, instrumental and laboratory diagnostics, studies of the heart, lungs, kidneys, urinary tract, aorta, renal arteries, adrenal glands. Patients are tested for the presence of adrenaline, norepinephrine, sodium, and potassium in the blood and urine. An important role belongs to radioisotropic and x-ray methods. If damage to the renal arteries is suspected, angiography is performed, which establishes the nature of the pathology that caused arterial stenosis.

How to treat renal hypertension?

Kidney disease is a common cause of high blood pressure. Treatment of hypertension of renal origin is carried out by cardiologists and nephrologists. Preservation of kidney function is the main goal of therapy. Adequate blood pressure control is carried out, therapeutic measures are aimed at slowing the development of chronic renal failure and increasing life expectancy. If nephrogenic hypertension is detected or this diagnosis is suspected, patients are sent to the hospital to clarify the diagnosis and treatment. In an outpatient clinic, preoperative preparation is carried out according to the doctor’s indications.

Treatment of renal hypertension combines conservative and surgical methods, antihypertensive and pathogenetic therapy of the underlying disease. The most widely used conservative approach is drugs that affect the pathogenetic mechanisms of the development of arterial hypertension, reducing the risk of disease progression, do not reduce renal blood supply, do not inhibit renal function, do not disrupt metabolism, and develop minimal side effects.

A progressive method is often used - renal phonation. Treatment is carried out using a vibroacoustic device, microvibrations audio frequencies, applying vibraphones to the body. Sound microvibrations are natural for the human body and have a beneficial effect on the functions of systems and individual organs. This technique can restore kidney function, increase the amount uric acid secreted by the kidneys, normalize blood pressure.

During therapy, a diet is prescribed; its features are determined by the nature of the kidney damage. General recommendations include limiting salt and liquid intake. Smoked meats, hot sauce, cheese, strong broth, alcohol, and coffee are excluded from the diet. In some cases, surgical intervention is performed vital signs. One of the methods for correcting nephrogenic hypertension is nephrectomy (removal of the kidney). With the help of surgery, the majority of patients get rid of nephrogenic hypertension; in 40% of patients, the dosage of antihypertensive drugs used is reduced. Increasing life expectancy, controlling arterial hypertension, and protecting kidney function are important results of surgical intervention.

Timely effective therapy renal hypertension is the key to rapid and successful remission.

Nephropathy in pregnant women. Nephropathies of pregnancy, which pathogenetically do not represent a single group (Lanz and Hochuli), but clinically can give all the signs of renal hypertension, present almost no differential diagnostic difficulties if kidney damage develops during pregnancy.

Glomerulosclerosis(Kimmelstiel - Wilson) is often the cause of hypertension in diabetic patients.

Hypertension with gout. Glomerulosclerotic changes as a cause of hypertension have also been found in gout (Zollinger and Koller).

Periarteritis nodosa. Hypertension, observed in half of all cases of nodule new periarteritis (Kussmaul - Maier), is mostly of renal origin, i.e., it becomes pronounced only with more severe damage to the renal vessels. The disease is rare and even less often correctly diagnosed during the patient’s lifetime (according to larger statistics - only 20%). Symptoms: febrile course, leukocytosis with eosinophilia; with damage to the mesenteric vessels in the foreground, sharp paroxysmal pain in the abdomen; polyneuritis and polymyositis are common, and etiologically unclear polyneuritis with simultaneous fever (which usually responds quickly to cortisone drugs) and vascular changes (heart) can become the leading symptom; as a rule, polyneuritis is limited lower limbs, paralytic phenomena on the legs and arms are also common; an early symptom may be hemorrhagic testicular infarction (clinically, swelling of the testicles with or without pain). Only in in some cases nodules are palpated along the arteries. Changes in urinary sediment may be diagnostically valuable. According to Crurr, erythrocytes, leukocytes, fatty and waxy cylinders, oval fatty bodies and especially wide cylinders are found simultaneously in the same sediment. In renal diseases of other etiologies, it is unlikely that all the mentioned cellular elements can be found simultaneously. Such simultaneous presence of them indicates pathological changes in both glomeruli and tubules. Pulmonary vessels may also be involved, leading to a remarkable but typical pulmonary pattern (nodule formation).

If with differential diagnostics When the question arises about periarteritis nodosa, we must always remember that its symptomatology can be very varied, variable, changing depending on which vessels of which organs are especially affected by the process. Symptoms from the abdomen, nerves, testicles, skin, heart and, above all, the kidneys (prolonged jaundice is also occasionally observed) come to the fore along with general symptoms - fever, leukocytosis, eosinophilia and “chlorotic” marasmus. The diagnosis is sometimes determined by muscle biopsy. The duration of the disease ranges from several months to many years.

Unilateral kidney damage. With every unclear hypertension, you must also always remember that renal hypertension also occurs when only one kidney is affected. The mechanism here corresponds to the same as in experimental studies Goldblatt. If the blood supply to the kidney is impaired, whether due to vascular abnormalities or kinks or intrarenal lesions (tuberculous purulent-caseous nephrosis, hydronephrosis and, above all, pyelonephritic wrinkled kidney), substances that increase blood pressure can enter the blood. Since pyelonephritis occurs more often in women, it is clear that hypertension as a result of unilateral kidney damage is observed mainly in women. Among Zollinger's 24 patients there was only one man.

Thus, in unclear cases, especially in young patients hypertension. A urological examination should always be carried out, and this is especially important because after removal of the diseased kidney, a complete recovery can occur. An intravenous pyelogram usually reveals a dwarf kidney (with the cranial end of the kidney changing the most). Urine may not be changed. Such cases are very rare.

From more rare kidney damage. which sometimes occur with high blood pressure, and hypertension is not at all an obligatory symptom, let us mention cystic kidneys and amyloid wrinkled kidney. Hypertension in advanced cases of lead poisoning is apparently also caused by kidney damage.

Renal hypertension - Arterial hypertension - differential diagnosis

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Symptomatic hypertension, both benign and malignant, most often has a renal origin. The appendix lists kidney diseases that occur with increased blood pressure. The experience accumulated by the clinic gives reason to believe that arterial hypertension appears only when the listed diseases have led to such kidney damage that is detected modern methods research. In the initial stages, these diseases usually occur without arterial hypertension. Consequently, if we are talking about the renal origin of arterial hypertension, then in each case we must detect functional and morphological signs of clearly defined kidney damage.

Arterial hypertension of renal origin is most often a consequence of pyelonephritis or chronic glomerulonephritis. Both diseases can occur with both benign and malignant hypertension. Differential diagnosis with the corresponding forms of hypertension can be very difficult and often requires large number special research.

Chronic pyelonephritis is one of the most common kidney diseases in all age groups. According to A. Ya. Pytel (1972), arterial hypertension occurs in approximately 3.2% of patients with unilateral chronic pyelonephritis. Its true frequency probably exceeds the indicated figure. Because of poverty clinical symptoms this pyelonephritic arterial hypertension is often mistaken for essential. The number of diagnostic errors of this kind can be significantly reduced by asking the patient in detail about urological diseases in his relatives, about the urological diseases he has suffered and related diagnostic studies.

Chronic pyelonephritis is especially often the cause of arterial hypertension in young women. Its exacerbations often occur atypically with short-term dysuria and are mistaken for a vaginal infection, for example, defloration cystitis. Some authors associate not only nephropathy in pregnancy with asymptomatic urinary tract infection, but even any decrease in the concentration function of the kidneys during pregnancy.

Asymptomatic urinary tract infection occurs in 3-7% of pregnant women (Kass, 1966). The prescription of antibiotics is sometimes accompanied by a marked improvement in the concentrating ability of the kidneys. The diagnostic value of this test, to our knowledge, has not yet been systematically tested.

Arterial hypertension is rarely the only sign of pyelonephritis. In many cases of this disease, simultaneously with an increase in blood pressure, it is possible to note complaints of dysuria, thirst, polyuria, pain or discomfort in the lower back, increased fatigue, short-term increases in body temperature. The listed phenomena can be explained by the inflammatory process in the kidneys, difficulties in the outflow of urine from the upper urinary tract, selective damage to the functions of the tubular epithelium, and the existence of latent or mildly expressed renal failure.

Arterial hypertension is usually only one of the elements of this constellation of symptoms and signs of pyelonephritis. High blood pressure in most cases of mild hypertension is (in contrast to pyelonephritis) not only its main, but also its only symptom. The existence of monosymptomatic pyelonephritis does not refute this differential diagnostic position, since monosymptomatic pyelonephritis, as well as glomerulonephritis, occurs relatively infrequently and only at one of the stages of their development. In addition, in many cases of arterial hypertension, which initially seemed monosymptomatic, with targeted questioning we were able to identify a constellation of symptoms and signs characteristic of symptomatic hypertension.

Objective signs of chronic pyelonephritis in the early and late stages of the disease can differ markedly and even dramatically from each other. In the early stage of the disease, bacteria, casts, leukocytes, a small amount of protein, and sometimes red blood cells are usually found in the urine. As the disease progresses, the severity of urinary syndrome decreases. Hematuria and leukocyturia gradually disappear, and sometimes only traces of protein can be detected in the urine. The main syndrome of the disease becomes arterial hypertension, which is joined at a later stage by anemia and azotemia.

At a certain stage of development of pyelonephritis, arterial hypertension may be its leading, and sometimes the only clinical syndrome. Differentiation of such cases of chronic pyelonephritis from hypertension is carried out according to the results of renography, kidney scanning, pyelography and urinary sediment analysis.

In the urine of patients with a benign form of arterial hypertension, as in the urine of healthy people, bacteria are found in approximately 6% of cases, but their number is insignificant. Bacteriuria precedes pyelonephritis and naturally occurs in its early stages. You should think about pyelonephritis when 1 ml of urine taken by catheter contains more than 100,000 bacteria. The number of bacteria is counted using bacterioscopic, bacteriological or indirect methods.

The bacterioscopic method for determining bacteriuria is applicable only to freshly released urine, since when storing urine it is difficult to prevent its contamination or rapid growth of bacteria already contained in it. The severity of bacteriuria is determined by the number of bacteria either in the field of view or in one or two squares of the counting chamber. One may think of pyelonephritis if more than two bacteria are found in one large square of the counting chamber.

Culture of urine on solid media allows a more accurate assessment of the degree of bacteriuria, obtaining a pure culture of the pathogen and determining its sensitivity to antibiotics. The main advantage of the bacteriological method is the ability to solve diagnostic and therapeutic issues in one study.

In practical work, indirect methods for determining the intensity of bacteriuria are often used by adding sulfanilic acid and alpha-naphthylamine or triphenyltetrazolium chloride to the urine. The formation of a red precipitate indicates that 1 ml of test urine contains more than 100,000 microbial bodies. The differential diagnostic value of these tests is small. A positive response is observed in approximately 80% of cases of pyelonephritis.

Much attention was paid to clarifying the differential diagnostic value of the formed elements of urine: erythrocytes, leukocytes, cylinders. In the daily urine of patients benign hypertension, as in daily urine healthy person, studied using the Kakovsky-Addis method, up to 2,000,000 erythrocytes, up to 4,000,000 leukocytes and up to 100,000 cylinders are detected. Pyelonephritis and bacterial infections urinary tract leaks from increased secretion leukocytes in urine. The number of leukocytes in daily urine with active pyelonephritis increases sharply and in typical cases significantly exceeds the number of erythrocytes. The contents of the cylinders remain unchanged.

In the urine of patients with pyelonephritis and other inflammatory diseases of the urinary tract, “active” leukocytes are often found, which differ from ordinary (“inactive”) leukocytes by the characteristic mobility of the cytoplasm. In isosthenuric or hyposthenuric urine, active leukocytes swell sharply and become almost twice as large as normal. A water-alcohol mixture of safronin and gentian violet colors the cytoplasm of these large leukocytes pale blue. According to N.A. Ratner (1974), pale leukocytes (Sternheimer-Malbin cells) are found in approximately 40% of cases of pyelonephritis with hypertension.

They tried to increase the importance of examining urinary sediment for the diagnosis of pyelonephritis by simultaneously determining the number of “active” and normal leukocytes in the urine, the ratio of “active” and “inactive” leukocytes, as well as through the use of so-called provocative tests. It is assumed that prescribing certain drugs to a patient, for example, prednisolone, leads to an exacerbation of pyelonephritis, as a result of which the number of leukocytes and bacteria in the urine increases, and “active” leukocytes often appear.

Many authors (Glezer G. A. 1973; Pytel A. Ya. 1972) point to the great diagnostic value of provocative tests. It is believed that intravenous administration 40 mg of prednisolone is accompanied by the release of “active” leukocytes from the source of inflammation in the kidneys and their passage into the urine. G. Manjrakov (1976) also speaks positively about this test. Compared to the authors mentioned above, our experience is relatively small, but it does not give grounds to classify the prednisolone test as one of the tests that can significantly improve differential diagnosis between pyelonephritis and benign hypertension.

Differential diagnostic value in various ways Urine counts and provocative tests are often overestimated. The content of formed elements in the urinary sediment, as well as the results of provocative tests in different stages of pyelonephritis, may be different. Active leukocytes are often found in acute pyelonephritis. As the disease progresses, proteinuria gradually decreases, and urinary sediment gradually becomes more scanty. In chronic pyelonephritis with some degree of inflammatory process activity remaining, Sternheimer-Malbin cells can be detected only in some cases. With a pyelonephritis-shrinked kidney, sometimes only traces of protein are found in the urine, and it may not contain any formed elements at all.

Hypertension is most easily distinguished from symptomatic hypertension in pyelonephritis by comparing the functional state of the right and left kidneys. In cases where inflammatory process covers both kidneys, one of them, as a rule, is affected noticeably more than the other. The function of one of the kidneys is always more impaired than the function of the other. The functions of the right and left kidneys are affected, as a rule, to the same extent in hypertension. Reliable and safe methods for comparative assessment of the functional state of the right and left kidneys include: isotope renography, infusion urography and kidney scanning.

Isotope renography is usually performed using 1311-hippuran. Renograms of the right and left kidneys in patients with uncomplicated essential hypertension (as in healthy people) are symmetrical. After intravenous injection of 1311-hippuran, maximum radioactivity over the kidney in a healthy person occurs after 3-4 minutes. The half-life of hippuran from the blood is 8-10 minutes (Kramer A. A. 1972). Differences in the time of maximum rise of renograms do not exceed 1 minute, and differences in the half-life of the isotope - 2 minutes.

Renograms of the right and left kidneys with pyelonephritis differ from each other in the height of the rise and the time of its onset. Functional asymmetry of the kidneys is best detected in the excretory phase of the renogram. Functional asymmetry of the kidneys in pyelonephritis and some features of their morphological structure can be detected by scanning. On scanograms you can see a decrease in the size of the affected kidney, reduced and uneven accumulation of the isotope in it. At the same time, the degree of vicarious hyperfunction of the unaffected kidney can be assessed. Kidney scans for benign hypertension do not differ from scans for a healthy kidney.

Comparative data on the functional state of the kidneys and upper urinary tract can be obtained through excretory urography, which is best performed by infusion. In cases of benign hypertension, contrasting of both kidneys begins and ends simultaneously. The main symptom of pyelonephritis (as well as other predominantly unilateral kidney diseases) is contrast enhancement asymmetry. On the affected side or on the side of the more affected kidney, the contrast agent appears later than on the healthy or less affected side. The concentration ability of the affected kidney is also impaired, which is judged by the time of maximum contrast. Particularly characteristic is the slow release of radiopaque contrast agent from the more affected kidney.

Violation of the muscle tone of the urinary tract is manifested by spasms of the pelvicaliceal system, changes in the shape of the cups and pelvis. As the disease progresses, the spastic phase is replaced by an atonic phase, which leads to expansion of the calyces and pelvis. Primary departments The calyxes become rounded, their necks narrow, and the edges take on a mushroom shape. In the later stages of the disease, the affected kidney shrinks. Its size is decreasing. The small calyxes move closer to each other. Structure collecting system is best detected on a retrograde pyelogram, which is usually used when the results of infusion renography are not clear enough.

Renal angiography reveals deformation of the arterial bed. Due to the uneven development of scar processes, the symmetry of the branching of the renal artery is disrupted. Due to the obliteration of small vessels of the cortical layer of the pyelonephritic kidney, its angiographic picture takes on the characteristic appearance of a charred tree. Renal angiography is used to distinguish late stages of pyelonephritis from occlusive renal hypertension and renal hypoplasia. The use of the above methods makes it possible to make a correct diagnosis in approximately 80% of cases of pyelonephritis.

The diagnosis of pyelonephritis as one of the causes of arterial hypertension has improved markedly after the introduction of puncture kidney biopsy into clinical practice. The focal nature of kidney damage in pyelonephritis has given rise to some clinicians to question the diagnostic value of a puncture biopsy. Data from N.A. Ratner (1974) indicate the decisive importance of puncture biopsy in the diagnosis of all doubtful cases of pyelonephritis.

A renal biopsy for pyelonephritis reveals interstitial sclerosis in combination with tubular atrophy and lymphohistiocytic infiltrates, periglomerular sclerosis, deformation of the arteries with arteritis and perivascular sclerosis, thyroidization of the tubules, alternating areas of significantly altered and almost normal kidney tissue. In hypertension, only hyalinosis of single glomeruli, changes in small arteries and arterioles are detected (Petrov I.I. 1974).

Pyelonephritis can be associated with other kidney diseases. Especially often it complicates diabetes mellitus and obstructive uropathy that develop in connection with dysfunction of the urinary tract or with their structural abnormalities. Unilateral or bilateral obstructive uropathy is naturally observed when the lumen of the ureter is blocked by a stone, with inflammatory strictures of the urethra and ureters, with vesicoureteral reflux, compression of the urinary tract by tumors, cysts, scarring connective tissue and other diseases listed in the appendix. Each of these diseases can lead to the development of pyelonephritis, which becomes one of the causes of arterial hypertension.

Everyday clinical practice indicates that the longer the history of urolithiasis, the more often it is combined with arterial hypertension. Chronic calculous pyelonephritis is considered by most authors main reason development of hypertension in patients with urolithiasis. The diagnosis of this form of symptomatic hypertension in most cases is not difficult due to a fairly clearly defined clinical picture of the underlying disease.

Polycystic disease and others congenital anomalies kidney Polycystic disease is one of the less common kidney diseases. It occurs in 0.35% of all autopsies. Arterial hypertension is observed in approximately half of the cases of this disease (Javat-Zade M.D. 1964). Its causes are either pyelonephritis or renal ischemia, which occurs due to mechanical compression of the renal vessels by individual cysts or due to obstruction of the outflow of urine from the upper urinary tract. The inclusion of these same mechanisms explains hypertension in solitary renal cysts and echinococcus of the kidneys.

Polycystic kidney disease is often complicated by pyelonephritis, less often by suppuration of individual cysts, and the formation of kidney stones. These complications are usually one-sided. For a long time, the disease can be asymptomatic. The first complaints appear most often at the age of 35-45 years.

Arterial hypertension in polycystic kidney disease is initially transient in nature and clinical course resembles benign hypertension. The patients' ability to work is not impaired, but they often complain of dull pain in the lower back, usually on one side. Later, arterial hypertension of a permanent type develops with changes in the fundus and hypertrophy of the left ventricle of the heart. Repeated renal bleeding is often observed.

Careful palpation of organs abdominal cavity often, and X-ray examination They always find enlargement of the kidneys characteristic of this disease, which is often combined with enlargement of the liver. Even minor deviations in urine analysis should be assessed as an indication for a more detailed study of the anatomical and functional state of the kidneys. In combination with a detailed and targeted questioning of the patient, these small signs facilitate timely identification of the true cause of arterial hypertension.

The addition of pyelonephritis explains the development of arterial hypertension in some other congenital anomalies of kidney development (duplication, agenesis, dystopia, hypoplasia, fusion of the poles), in diseases of the ureters and lower urinary tract that occur with impaired urine outflow. The real reason Hypertension in these conditions is in most cases determined by a urologist rather than a physician.

Diabetic glomerulosclerosis. Arterial hypertension in diabetes mellitus most often occurs due to the addition of intercapillary glomerulosclerosis (Kimmelstiel-Wilson syndrome). The development of diabetic glomerulosclerosis is associated with metabolic disorders accompanying diabetes, which are more pronounced the longer and more severe the underlying disease. Proteinuria, inconsistent and usually mildly expressed, is the first and sometimes the only sign of this complication diabetes mellitus. Intermittent proteinuria may continue for 6-8 years. Blood pressure may remain normal at this time, but sometimes it increases.

In more late dates disease, proteinuria becomes constant, and the patient develops edema. Blood pressure often increases in this stage of diabetic glomerulosclerosis. Clinical picture suffering resembles a picture of a mixed form of chronic glomerulonephritis, and not hypertension. Further development of glomerulosclerosis leads to a diabetically shriveled kidney. High hypertension and chronic renal failure appear.

Arterial hypertension in diabetic glomerulosclerosis usually appears for the first time in middle and old age and is often mistaken for hypertension. When making a differential diagnosis between these diseases, one should pay attention to Special attention the following provisions: 1) proteinuria in benign hypertension, if it occurs, is only during severe hypertensive crises and in the first 1-2 days after their end. Proteinuria in diabetic glomerulosclerosis exists independently of hypertensive crises; 2) glomerulosclerosis appears in the late stages of diabetes, when most patients already have characteristic signs of diabetic microangiopathy. It is especially clearly expressed in the vessels of the retina. Such changes are never observed in hypertension; 3) arterial hypertension in a diabetic patient may be a consequence of associated pyelonephritis or stenosing atherosclerosis of the renal artery. Diabetic glomerulosclerosis is a diffuse disease. It affects both kidneys equally. Pyelonephritis in most cases is unilateral. With bilateral pyelonephritis, one of the kidneys is usually more affected than the other. Urological examination makes it possible to distinguish these forms from each other. In diagnostically difficult cases, it is recommended to resort to puncture biopsy of the kidneys. The diagnosis of renal artery stenosis is made based on the results of aortography.

Chronic glomerulonephritis. The acute onset of diffuse glomerulonephritis in our time is the exception rather than the rule. According to I.I. Petrov (1974), only 14.8% of the patients he observed remembered having suffered acute nephritis in the past. In other cases, chronic glomerulonephritis began unnoticed. About 45% of patients with chronic nephritis came under medical supervision due to arterial hypertension discovered in them.

When collecting anamnesis, it is important to find out in each case of arterial hypertension its temporary connection with urinary syndrome.

Proteinuria and microhematuria in patients with chronic glomerulonephritis can be detected long (sometimes several years) before the onset of arterial hypertension. Urinary syndrome is never detected in the initial period of hypertension. Proteinuria and microhematuria first appear only during hypertensive crises, that is, usually several years after the establishment of more or less stable hypertension.

An increase in blood pressure during pregnancy can be considered as an indirect indication of nephritis or pyelonephritis suffered in the past, since the mentioned diseases are the most common reasons nephropathy in pregnant women. Unfortunately, even this anamnestic indication can be identified in no more than 1/3 of patients with chronic glomerulonephritis. From the above it follows that negative data from the anamnesis in no way exclude a possible connection between arterial hypertension and chronic nephritis, and positive data allow us to consider this connection to be very probable.

Arterial hypertension in chronic nephritis, as in hypertension, is initially transient and later becomes permanent. Diastolic pressure usually does not exceed 110 mmHg. Art. In the morning, arterial hypertension is noticeably lower than in the evening. Despite high blood pressure, patients, especially young ones, remain fully functional. A decrease in kidney function is sometimes detected only 15-20 years after the onset of arterial hypertension. Changes in blood pressure in the hypertensive form of chronic glomerulonephritis before the appearance of signs of renal failure can completely imitate changes in benign hypertension.

The compared diseases still differ from each other in the severity of changes in the vessels of the heart and brain. Hypertrophy of the left ventricle of the heart, clinical and electrocardiographic signs of coronary insufficiency in hypertension are usually more pronounced than in chronic glomerulonephritis. A similar pattern is observed in changes in the fundus. The reason for these differences in the severity of changes in the heart and brain is usually explained by the unequal height of blood pressure and the unequal severity of metabolic disorders. Changes in the fundus are caused mainly by the height and duration of hypertension. Their lesser severity in chronic glomerulonephritis is explained by the fact that in most cases it occurs with a lower level of blood pressure.

Hypertension is so naturally complicated by atherosclerosis that A. L. Myasnikov even proposed to distinguish its stages according to the severity of atherosclerosis in the aorta, large vessels of the brain and heart. The appearance and progressive increase in the frequency and severity of angina attacks and electrocardiographic signs of coronary insufficiency are as characteristic of essential hypertension as the appearance and gradual increase of signs of renal failure for chronic nephritis. Identification of signs of atherosclerosis of the aorta and coronary arteries in benign arterial hypertension has long been assessed as an indication of hypertension, and a decrease in glomerular filtration rate as an indication of chronic glomerulonephritis.

The further from the onset of the disease, the more clearly the differences in the nature of complications of the compared diseases become apparent. Patients with benign hypertension die, as a rule, from stroke, myocardial infarction, or from heart failure that develops as a result of post-infarction cardiosclerosis. Renal failure usually does not develop in these patients. Chronic nephritis and especially its hypertensive form are not an absolute guarantee against myocardial infarction or stroke, but the longer the period has passed from the onset of the disease, the more clearly the threat of death from renal failure and its complications hangs over the patient.

IN early period hypertension, the signs of atherosclerosis of the aorta and coronary arteries are not yet clearly expressed, and arterial hypertension in its course is no different from arterial hypertension in chronic glomerulonephritis. Meanwhile, elucidating the causes of arterial hypertension in such cases is of enormous practical importance, since the results of this work determine the volume and nature of therapeutic and preventive measures. Greater diagnostic help in such cases of recent hypertension can be provided by identifying humoral or morphological signs of an autoimmune process in the body and the results of repeated urine tests.

The differential diagnostic value of urinary syndrome depends on its severity and the consistency with which it is detected during repeated urine tests. Proteinuria more than 1 g per day can be considered as an indirect indication of the connection between arterial hypertension and primary kidney damage. This assumption becomes even more likely if erythrocyturia and leukocyturia are detected simultaneously with proteinuria. Proteinuria and erythrocyturia do not occur in cases of mild hypertension. In cases of more severe hypertension, the amount of protein in daily urine still does not exceed 1 g.

The differential diagnostic value of urinary syndrome also depends on the systematicity of urine tests. A small amount of protein and single red blood cells in benign hypertension are detected only in the first 1-2 days after the crisis. Exacerbations of chronic nephritis occur with more or less long periods of proteinuria and microhematuria.

It is necessary to remember one more feature of the urinary syndrome in chronic glomerulonephritis. Proteinuria is considered a characteristic sign of this disease, but in 15-20% of cases of hypertensive form of chronic glomerulonephritis, urine tests periodically turn out to be normal. As already indicated, chronic pyelonephritis can also occur with sterile urine and without changes in its sediment. In many cases, their differentiation can be achieved by determining the number of leukocytes and erythrocytes in the urine. Chronic glomerulonephritis, which occurs with minor urinary syndrome, is still characterized by a higher excretion of red blood cells in the urine than in a healthy person. The number of erythrocytes in the urine of a patient with chronic glomerulonephritis prevails over the number of leukocytes. In the daily urine of a patient with chronic pyelonephritis, the number of erythrocytes is less than the number of leukocytes.

Kidney biopsy in such diagnostically difficult cases is a method that is more reliable than others in distinguishing chronic glomerulonephritis from pyelonephritis and from hypertension. In the kidneys with hypertension, changes in the walls of small arteries and arterioles are detected. Kidney changes in chronic glomerulonephritis are very diverse. Morphological signs of nephritis are found in the glomeruli, tubules, vessels and connective tissue. Immunomorphological studies of renal biopsy can detect the deposition of immunoglobulins in the mesangium and in the walls of the glomerular capillaries in chronic glomerulonephritis.

The results of a puncture biopsy are of extremely great diagnostic value. Unfortunately, this method cannot be used in every diagnostically unclear case of arterial hypertension, both due to the difficulties in obtaining renal tissue and due to possible complications.

A diagnostic conclusion can be made only from a biopsy sample that contains at least 5-6 renal glomeruli. The percutaneous biopsy method makes it possible to obtain a biopsy sample of the specified volume in approximately 80% of cases (Baykova D. A. 1969). The more pronounced the sclerotic changes in the organ, the less often it is possible to obtain renal tissue through biopsy.

Each case of renal biopsy is accompanied by microhematuria, which lasts for several days. Gross hematuria is much less common. The most serious complication is retroperitoneal hematoma, the growth of which in two cases known to us required surgical intervention. The use of needle biopsy of the kidneys is associated with some degree of risk. This method is used only in cases where it is impossible to determine the diagnosis using other methods.

Hypertension, chronic glomerulonephritis and pyelonephritis are the most common causes of arterial hypertension, occurring without changes in urine or in combination with moderate urinary syndrome. The methods described above for separate assessment of the functional state of the right and left kidneys in most cases make it possible to identify objective differential diagnostic criteria between pyelonephritis and chronic glomerulonephritis. Taking into account the peculiarities of the course of both diseases can provide some assistance in this regard. Signs of nephrotic syndrome, even if they are mildly expressed, should always be assessed as a strong argument in favor of chronic glomerulonephritis. Indications of short-term edema in the past have the same differential diagnostic value as edema during examination of the patient. The protein content in urine with pyelonephritis rarely exceeds 1-2 g/l. More intense proteinuria, other things being equal, should be assessed as evidence in favor of chronic glomerulonephritis. Malignant hypertension differs from chronic glomerulonephritis and pyelonephritis in the course of chronic renal failure developing in terminal stages these diseases.

Symptoms of kidney pressure and methods of its treatment

Kidney pressure tends to appear after a person is diagnosed with symptoms of ordinary hypertension. The main characteristic of this disease is persistent high pressure. Damage to the kidney tissue usually leads to such a development of events. In addition, the reason may lie in the narrowing of the renal artery. If this disease is not treated, it has a tendency to develop further.

Signs of kidney pressure

How the disease develops

Due to the appearance of symptoms of this disease in a person, the kidneys begin to perform their functions in an incorrect rhythm, which leads to an increase in the volume of blood circulating in this organ. At the same time, the patient’s body begins to retain water. As a result, renal pressure changes from low or normal to high, and the normal process of sodium excretion is disrupted.

A blood test taken from the patient at this moment will certainly show an increased content of this element in the body. The next predicted symptom will be the sensitivity of the walls of blood vessels to the effects of hormonal substances, which will certainly lead to an increase in their tone.

The main role in the development of the disease is played by receptors located in the kidneys. These “sensors” performing their functions are characterized by a sensitive reaction to every change in hemodynamics. Disruption of the blood circulation process leads to irritation of the receptors, which provokes the release of renin. This hormone has the property of activating blood substances responsible for increasing peripheral vascular resistance, which leads to their hardening. The result of this is renewed irritation of the kidney receptors, which turns this process into a vicious circle.

High blood pressure in older people

Renal hypertension develops and tends to continue also because kidney tissue begins to die, which leads to low levels of substances in the blood that reduce vascular tone. This disease Elderly people are most often affected.

However, its symptoms can also occur in fairly young representatives who, as a result of the examination, were found to have high blood pressure. The high-risk group is also supplemented by the male part of the population, which by nature has a greater body weight and, as a consequence, a large volume of the vascular bed.

The danger of the disease and how to recognize it

It is difficult to envy a person who is familiar firsthand with the phrase “high blood pressure and kidneys.” Kidney pressure tends to lead to the following complications:

• disturbances in the blood circulation of the brain;
• leading to changes in the properties of blood, which can become more viscous;
• renal or heart failure;
• lipid metabolism disorders;
• corrosion of blood vessels, gradually losing elasticity and putting more and more strain on the heart.

Main signs of the disease

High blood pressure

Besides being so bright pronounced symptom, like high blood pressure, the body of a renal hypertensive person can give other signals. One patient may have several of the following symptoms, and some of them appear only in certain cases. Symptoms of a disease occurring in a person who consults a doctor include:

• the presence of systolic or diastolic murmurs present in the area of ​​the renal arteries;
• manifestation of blood pressure asymmetry in the arms;
• dysfunction of nitrogen excretion (this sign is characteristic of the late stage of the disease);
• slight presence of proteinuria and hyposthenuria;
• constant pain in the head area, relieved only with the help of potent tablets;
• complaints of increased heart rate;
• the appearance of so-called goosebumps before the eyes.

Renal hypertension is accompanied by the same symptoms as essential hypertension. Therefore, to make a more clear diagnosis, the patient must be referred for laboratory and instrumental treatment.

Diagnosis and treatment

Among the examination methods that make it possible to accurately diagnose and subsequently treat this disease, they usually resort to checking the morning urine test, collected after carefully carried out hygiene procedures; ultrasound examination of the kidneys; excretory urography; renography and angiography.

Diagnosis of the disease

Only the totality of the indicators obtained as a result of a complete examination will help in making an appropriate diagnosis and, accordingly, choosing the most optimal algorithm for selecting tablets and other treatment agents.

How to treat renal hypertension

First of all, renal hypertension categorically does not accept self-medication and advice from people who have no knowledge of medicine on the choice of treatment methods and magically helping pills. This can lead to a further significant deterioration in health and distort the overall picture of the disease when diagnosing it.

Treatment of renal pressure should only be carried out under the close supervision of a qualified specialist. After the diagnostic procedures, the doctor will prescribe medications, taking into account the sensitivity of the microflora, and treat the patient in strict accordance with his individual characteristics.

As a rule, doctors try to treat renal hypertension using two basic principles: possible treatment diseases and therapy designed to lower blood pressure.

In addition to pills designed to alleviate the patient’s condition, the doctor may recommend the use of traditional methods of treatment. If, when monitoring the course of the disease, a negative trend is detected that has arisen as a result of changes in the structure and functioning of the renal arteries, then surgical treatment may be indicated for the patient.

If, during the next examination, the patient has a narrowing of the renal artery, he is prescribed a referral for a procedure called balloon angioplasty, which consists of inserting a special catheter into the patient’s artery, the design of which involves the presence of a small balloon at its end.

Having reached the designated problem area, the balloon begins to slowly inflate inside the artery, thereby expanding it. After this, the catheter is removed. The stent left after this manipulation can have a beneficial effect on blood flow, which will reduce blood pressure and subsequently give up some pills.

Preventive procedures

After the body’s condition has been restored, it is necessary to adhere to some rules that will prevent a return to the previous diagnosis. To prevent further development hypertension, just follow a few tips.

is a complex and insidious disease that is diagnosed in every fifth patient with a complaint of high blood pressure. This disease is growing younger faster than classic hypertension - in most cases it affects people under 40 years of age, develops rapidly and requires immediate and long-term therapy. What is hypertension in kidney disease, how does it manifest itself and how to treat it?

Renal hypertension device

The disease develops with any impairment of kidney function. The main role of the urinary organs in the body is filtration. arterial blood, timely withdrawal excess liquid, sodium, protein breakdown products and harmful substances, accidentally entered our blood.

If the kidneys suddenly stop working fully, blood flow to them decreases, water and sodium begin to linger inside, causing edema. Accumulating in the blood, sodium ions provoke swelling vascular walls, sharpening their sensitivity. Damaged kidney receptors actively secrete a special enzyme “renin”, which is converted into “angiotensin”, then into “aldosterone”. These substances increase the tone of blood vessels and reduce the gaps in them, which inevitably leads to an increase in pressure. At the same time, the production of substances that reduce arterial tone is sharply reduced, and the kidney receptors are irritated even more.

This creates a vicious circle that feeds on itself and causes a constant increase in blood pressure.

Causes

The reasons why patients experience high renal pressure depend on the type of disease. There are two types:

• renovascular hypertension;
• hypertension associated with diffuse kidney damage.

First type. Vasorenal (renovascular) hypertension- These are disturbances in the functioning of the arteries of the kidneys.

This problem is caused by renal vascular pathologies, congenital or acquired.

Congenital causes:

• hyperplasia (proliferation) of the walls of the renal artery;
• coarctation (narrowing of the isthmus) of the aorta;
• artery aneurysm.

Acquired reasons:

• atherosclerosis of kidney vessels;
• embolism (blockage) of the renal artery;
• sclerosing paranephritis,
• external compression of the renal arteries.

Renovascular hypertension is the most common type high blood pressure for kidney pathologies: in children it is diagnosed in 90% of all cases, in adults – in 50-60%.

Second type. Hypertension in diffuse kidney damage is caused by damage to the organ tissue itself. Factors that cause pressure surges in this disease can also be divided into 2 groups.

Developmental anomalies:

• congenital reduction in kidney size (hypoplasia);
• organ duplication, complete or incomplete;
• cyst.

Tissue inflammation:

• pyelonephritis;
• glomerulonephritis.

Note! In rare cases, experts also note a mixed form of the disease, when pathological changes in the kidney tissue are combined with the destruction of the arteries.

Symptoms

Renal hypertension in its manifestation is quite similar to traditional cardiac hypertension, but may include typical signs of kidney disease. Doctors indicate 2 scenarios for its development, the symptoms of which differ significantly.

Symptoms of a benign course

In this form, the disease develops rather slowly, without obvious deterioration. The pressure is steadily increased, does not decrease, but does not make sharp jumps upward. Patients feel dull headache, weakness, dizziness and shortness of breath, a feeling of causeless anxiety. I suffer from discomfort and pain in the area of ​​the heart, and rapid heartbeat.

Symptoms of malignancy

The disease begins quickly. The “lower” (diastolic) pressure increases to 120 mmHg. Art., the boundary between the upper and lower readings of the tonometer becomes minimal. The optic nerve is affected, leading to irreversible visual impairment. Patients suffer from severe headaches in the back of the head, nausea, vomiting, and dizziness.

General symptoms

In addition to the specific ones, there are also general signs of increased renal pressure for both cases, which make it possible to exclude cardiac hypertension and begin appropriate treatment:

• blood pressure can jump suddenly, without obvious stress or physical overload;
• problems can begin at a young age, up to 30 years;
• there are no chronic hypertensive patients or heart disease sufferers in the family;
• in parallel with the main symptoms, characteristic lower back pain occurs;
• suffer from severe swelling of the extremities.

Complications

If a patient develops renal hypertension, the so-called target organs are primarily affected - the organs that are most susceptible to morphological and functional changes due to high blood pressure. These are the heart, kidneys and brain.

Complications of high blood pressure caused by kidney damage are:

• renal and heart failure;
• disruption of proper cerebral circulation;
• hemorrhages in the retina of the eye;
• severe damage to arterial vessels;
• lipid metabolism disorders.

Operational disruptions internal organs with such hypertension entail severe and incurable diseases. If the disease is not treated promptly, high blood pressure can cause partial or even complete loss of vision, atherosclerosis, stroke and heart attack, as well as impaired kidney function, including kidney failure.

Diagnostics

Only an experienced therapist can determine renal hypertension in a patient - in order to give an accurate diagnosis and prescribe treatment, it is necessary to exclude an impressive number of reasons that can provoke surges in blood pressure.

The first thing that is necessary to establish the disease is continuous monitoring of blood pressure over a sufficiently long period. So, if within a month a person’s readings are recorded above 140/90 mm Hg. Art., then the diagnosis is obvious - “hypertension”. If there are also any disturbances in the functioning of the kidneys, then the disease is defined as secondary hypertension in renal diseases, and comprehensive treatment must be started immediately.

To identify renal pathologies, a number of studies are needed:

• Analysis of urine;
• Ultrasound of the kidneys;
• urography;
• dynamic scintigraphy;
• renal angiography;
• MRI and computed tomography;
• biopsy.

Treatment

Increased renal pressure requires the participation of two specialists, a urologist and a therapist, in the treatment. The entire complex of rehabilitation measures can be combined into 2 large groups - normalization of kidney function and lowering blood pressure.

Kidney treatment comes in two forms: surgery and medications.

Procedures/operations

At congenital defects(organ duplication, cyst, etc.) surgery is necessary; if there is blockage or stenosis of the renal arteries, surgical intervention is also necessary.

In the latter case (with arterial stenosis), doctors usually use balloon angioplasty - widening and strengthening the walls of blood vessels using a stent that is inserted inside. But surgery is possible only if the kidney has at least partially retained its function - in the most severe cases, removal is inevitable.

Experts often suggest treating renal hypertension in such a way as phonation - this is a method of non-surgical impact on organs using vibroacoustic waves. Vibration helps cleanse the blood, break up plaques that have formed in the vessels, reduce the risk of subsequent blockage of the arteries and reduce blood pressure.

Drug therapy

This type involves receiving special drugs to treat the underlying disease (usually prescribed for kidney inflammation) and reduce the production of the enzyme renin.

It is possible to reduce blood pressure in renal pathologies with the help of ACE inhibitors (captopril, fozzinopril, enalapril, etc.), which are prescribed only by the attending physician. In agreement with the therapist, treatment is sometimes also used traditional methods– herbal preparations, decoctions and freshly squeezed juices.

If you have been diagnosed with renal hypertension, treating the problem within hospital walls and using gentle folk methods is not enough - you need to change your lifestyle and diet. If you have high blood pressure, you will have to stop junk food– sour, peppery and fried, exclude strong black coffee and alcohol. In some cases, a special salt-free diet is necessary, which is usually prepared by the attending physician. In addition, hypertension requires avoidance of elevated physical activity– about special courses therapeutic therapy You can also ask your doctor.

Kidneys are an element of an integral system of the body. They are directly related to circulatory system, the health of blood vessels and the heart and themselves have a direct impact on them. This determines the relationship between kidney function and blood pressure. Changes in their work, provoked by any factors, can cause an increase in pressure, which negatively affects not only the cardiovascular system, but also the kidneys themselves, resulting in renal hypertension.

Causes of the disease

Nephrogenic hypertension (or renal) is a disease that causes pathological change blood pressure with simultaneous disruption of the blood supply to organs. The kidneys act as a filter, removing waste products from the body with urine.

Any disturbances in the functioning of these organs lead to changes in their blood supply - fluid retention occurs and the walls of blood vessels become enlarged due to the lack of natural blood circulation. The increased blood pressure (hypertension) that occurs in this case may be accompanied by other symptoms characterizing hypertension.

The kidneys also produce enzymes (renin) and hormones (angiotensin, aldosterone), which affect the lumens of blood vessels, either reducing or expanding them, and also regulate the water-salt balance of the entire body.

This work makes them a direct participant in hypertensive processes - salts (sodium) cause swelling and narrowing of the walls of blood vessels, provoke their tone, leading to an increase in blood pressure. This condition is accompanied by edema, and the kidneys become even more irritated, their work is disrupted.

The reasons why nephrogenic hypertension develops are very diverse:

The relationship between age and nephrogenic hypertension has not been proven. Thus, congenital vascular anomalies can lead to this disease in childhood.

The risk of developing renal hypertension before the age of 40 is quite high in the absence of a healthy approach to nutrition and an active lifestyle. After 50 years, renal-type hypertension is on a par with arterial hypertension in terms of detection frequency.

Symptoms and diagnosis

The difficulty of diagnosing renal hypertension lies in the invisibility of symptoms, which can be confused with many other diseases. The leading symptom that determines the development of hypertension (upper pressure can reach 140 mm Hg and higher, and lower pressure can reach 90 and higher).

In the renal form of hypertension, symptoms such as:

• confusion of consciousness;
• pain in the back of the head;
• prostration;
• dyspnea;
• periodic discomfort in the heart area.

The above symptoms can be a sign of many diseases, among them there are no specific ones that are characteristic only of nephrogenic hypertension. If they have a history of urological diseases or the patient complains of pain in the lumbar region, it is worth examining more closely in order to exclude damage to the organ due to hypertension and prevent the consequences of the disease in a timely manner.

Renal hypertension has two forms:

To combat kidney pathology, it is necessary to consult a doctor in time for an accurate diagnosis of the disease. Diagnosis is carried out comprehensively, taking into account constant monitoring of the patient.

Diagnosis requires daily monitoring of blood pressure for one to two months. If kidney pathologies are detected with constantly elevated blood pressure, arterial hypertension is diagnosed as nephrogenic. Basic diagnostic measures:

These diagnostic measures are prescribed after collecting anamnesis and examination by a doctor. These methods assume:

• assessment of the condition and presence of edema;
• attention to pain in the lumbar region;
• finding out the reasons for the increase in blood pressure (presence or absence of psycho-emotional stress, heavy physical labor, etc.);
• attention to age - high blood pressure in patients under 35 years of age is often caused by nephrological reasons;
• collection of data on the presence of renal failure and arterial hypertension in relatives.

Prevention and treatment

Damage to the kidneys due to hypertension leads to their dysfunction up to complete failure. Renal hypertension in these cases has an extremely unfavorable prognosis, and treatment turns out to be quite difficult, because it is necessary not only to stabilize blood pressure, but also to do everything possible to restore kidney function and improve its tissue. Self-medication is unacceptable. Treatment of renal hypertension should be prescribed only by specialists - a therapist and a nephrologist and includes a set of drugs aimed at:

All medications taken under the supervision of a physician. The course of treatment is long and, as a rule, lasts for years. For anatomical abnormalities or a malignant course of the disease, surgery in combination with drug treatment can be used. If there is blockage or severe reduction in the lumen in the renal arteries, balloon angioplasty is prescribed, aimed at dilating blood vessels and normalizing blood circulation.

As the most in a safe way impact on renal hypertension, it is proposed to use phonation, which, thanks to sound vibrations can reduce blood pressure and improve kidney health.

Given the complexity of treating renal hypertension, special attention should be paid to prevention. The severe consequences of kidney failure, which may be caused by blood pressure, are easier to eliminate in time.

Renal hypertension involves the following basic preventive measures:

The above preventive measures should become part of the lifestyle of the patient with diagnosed nephrogenic hypertension.

Treatment of renal hypertension is quite complex, lengthy and not always successful. This disease cannot be ignored, since disturbances in the functioning of the kidneys lead to the development of heart diseases and cerebrovascular accidents.

All body systems are interconnected and experience severe stress during renal failure.

Preventive measures can reduce the risk of developing the disease, including preventing the development of inflammatory kidney diseases that affect hypertension. It is necessary to treat and observe a nephrologist if arterial hypertension is accompanied by any renal disorders - this will eliminate the risks of developing a malignant form of the disease and maximally prolong the patient’s life.

The high frequency of kidney changes in hypertension, especially in its late stages, makes clear the attention paid to the renal factor in hypertension.

It is natural to first of all find out whether (and if so, how often) in hypertension there is an obstruction to the flow of blood into the kidneys through their arteries. We may be talking about a narrowing of these arteries due to atherosclerosis or, as well as their thrombosis. Similar changes could be clinical analogue stenosis of the renal arteries, which in the experiment leads to the development of arterial hypertension.

Atherosclerosis undoubtedly often affects the main renal arteries. Atherosclerotic changes usually found in the area of ​​the mouths of the main renal arteries, i.e., at their origin from the aorta. Atherosclerotic plaques at the mouths of the main renal arteries can, of course, narrow their lumen. In addition, atherosclerotic changes occur at the site of division of the main renal artery into first-order branches entering the kidneys; they can also, of course, narrow the vascular lumen and lead to a decrease in blood supply to the kidney tissue. Atherosclerotic changes in the renal arteries can be bilateral or unilateral. Do atherosclerotic narrowings of the renal arteries occur in hypertension? Undoubtedly, they meet. But in order to recognize them as the cause of hypertension in appropriate cases, it is necessary to establish the presence or absence of arteriolosclerosis in the kidneys. As G. F. Lang correctly pointed out, only in those cases in which atherosclerotic narrowing of the renal arteries is not accompanied by the development of arteriolosclerosis in the corresponding (ischemic) kidney can it be considered that this narrowing was the cause of hypertension. It is known that in experimental hypertension caused by narrowing of the arteries of the kidneys during hypertension, arteriolosclerotic changes in the kidneys are not observed, whereas they are usually found in other organs; because, due to the narrowing of the renal arteries, the arterioles of the kidneys are not exposed to increased pressure; thus, one of the essential factors contributing to arteriolosclerosis is missing.

If in hypertension there is atherosclerosis of the main renal arteries, then only in isolated cases there are no signs of renal arteriolosclerosis; in most cases, atherosclerosis of the main renal arteries is combined with severe arteriolosclerosis (hyalinosis, arteriolonecrosis) of the renal arteries. In such cases, obviously, we must assume that atherosclerotic narrowing of the renal arteries has already developed during hypertension, which managed to cause renal arteriolosclerosis even before the narrowing of the large renal arteries.

As with the coronary and cerebral arteries, there is good reason to believe that hypertension promotes faster and intensive development atherosclerosis of the main renal arteries.

Attention was also paid to individual findings in hypertensive conditions of aneurysms of the main renal arteries or aneurysms of the abdominal aorta near the point where the renal arteries originate from it, followed by their stenosis or compression.

The detection of thrombosis and embolism in the main renal arteries in hypertension is very demonstrative. B

The presented data are of interest from the point of view of the pathogenesis of renal hypertension. They demonstrate the important role of renal ischemia in the development of high blood pressure. But they do not directly relate to the question of the origin of hypertension. In the vast majority of cases with hypertension, autopsy does not reveal narrowing of the lumen of the large renal arteries.

Both thrombosis and various other forms of narrowing of the large renal arteries are more common in malignant or rapidly progressing hypertension at a young age. Therefore, when figuring out possible reasons, contributing to rapidly progressing hypertension in young people, these changes that disrupt the blood supply to the kidneys must be taken into account.

Attention was also paid to the features of the large arteries of the kidneys in hypertension; to their greater than normal length, to their departure from the aorta at a more acute angle, to sharper bends of the arteries, especially in the area of ​​their penetration into the kidney tissue, to congenital narrowing of their lumen (small caliber), to congenital atresia of one of them .

All these findings were collected with great diligence by American authors who sought to support Goldblatt’s theory.

There is a very extensive series of reports on various kinds of changes in the kidneys, renal arteries, pelvis, and also the urinary tract, some congenital, some acquired, which are sometimes found in patients who during their lifetime suffered from hypertension, diagnosed as hypertension.

The most common changes in the kidneys in hypertension are changes in the renal arterioles. They occur in the form of either arteriolohyalinosis or arteriolonecrosis. Hyalinosis of the renal arteries in hypertension occurs so regularly at autopsy that it has long been considered as a cause of hypertension. It was believed that only in rare cases of severe hypertension are arteriolosclerotic changes in the kidneys absent in hypertension.

Studied initial stages development of renal arteriolohyalinosis, and it was found that hyaline deposition is preceded by hyperplastic changes in the walls of arterioles. This first stage of changes in the arterioles should be considered functional, depending on fluctuations in blood pressure and vascular tone, and only after it does the process of infiltration of the vascular walls with protein masses occur.

Arteriolohyalinosis of the kidneys in hypertension is found along the small arteries of the kidneys, starting from distal section interlobular arteries, including vasa afferentia, and extends to the capillaries of the glomeruli. As hypertension progresses, hyalinosis of renal arterioles becomes more common, although it undoubtedly develops slowly.

Another type of arteriolar damage - renal arteriolonecrosis in hypertension - is characteristic of a more rapidly progressing (“malignant”) form of hypertension. It is localized in the same places as hyalinosis, but affects the glomeruli more often. “Fibrinoid necrosis” of the walls of arterioles leads to reactive changes in the surrounding tissue, in the vessel wall, similar to those characteristic of inflammation. Therefore, they talk about arteritis (endarteritis, periarteritis). Suggestions have been repeatedly made about the infectious-toxic or allergic nature of arteriolonecrosis. Later, in the etiology and pathogenesis of arteriolonecrosis, as well as glomerulonephritis, they began to attach great importance factor, since elements of similarity, and sometimes close relationships, were found between glomerulonephritis, periarteritis nodosa of the renal vessels and renal arteriolonecrosis.

As mentioned above, the cause of arteriolonecrosis is plasmorrhagia, the saturation of the walls of arterioles with blood protein. It is difficult to judge to what extent this protein, infiltrating the vessel walls, acts as an allergen, sensitizing and causing a hyperergic reaction. In any case, it is unlikely that any exogenous factors should be invoked to explain arteriolenecrosis. toxic substances. It is more correct to think that plasma impregnation and subsequent arteriolononecrosis are the result of a malnutrition of the vascular walls arising from vasospasm or narrowing of the vascular bed.

Both with hyalinosis of arterioles and with arteriolonecrosis, changes in the glomeruli are observed. Of particular importance in the development of changes is the narrowing of the lumen of the afferent arteries. Thickening of the walls of the capillaries of the glomerulus occurs, and then its blockage: the glomeruli undergo hyalinosis, necrosis, and cicatricial wrinkling. With arteriolohyalinosis, only a small number of glomeruli are usually affected, while with arteriolonecrosis, a much larger number is affected. The glomeruli are often affected by thrombosis of the afferent arterioles; in this case, hemorrhages are observed in the Shumlyansky-Bowman capsule. The remaining unaffected glomeruli are often hypertrophied.

From damage to the glomeruli, the corresponding tubules can successively undergo atrophy. If the changes depend on insufficient blood supply (since blood enters the tubules through vessels extending from the glomeruli), part of the tubules adjacent to normal glomeruli hypertrophies. Changes in the glomeruli and tubules in hypertensive nephrosclerosis occur late and only in a minority of cases.

Extremely important for understanding the nature of the relationship between kidney changes and hypertension is the discovery of a special cellular system in the kidneys that produces renin: this is the perinephric cellular apparatus, first described by Goormaghtigh. Renin is found in the kidneys in these periglomerular cells. The number of these cells in some forms of hypertension is increased and the content of renin in them is increased. This is also observed with more severe forms hypertension.

Nephrosclerosis as an outcome of arteriolonecrosis and arteriolohyalinosis is also called primary wrinkled kidney. “Primary” is a term, of course, that is absolutely inconsistent with the modern understanding of the nature of this process (in the sense of the relationship of renal changes to hypertension itself).

As for the appearance and size of arteriolosclerotic kidneys in hypertension, they are different in different cases. Sometimes, upon autopsy, the kidneys turn out to be not only not reduced, but rather even enlarged, with a smooth surface. This is observed either in the very initial forms of renal changes, or in a rapidly progressing disease, when cicatricial changes have not yet had time to develop. Typically, the kidneys in hypertension are reduced in size, with a granular and sometimes lumpy surface as a result of scarring.

The article was prepared and edited by: surgeon