Renal venous hypertension

Renal venous hypertension - increased pressure in the renal vein system.

[1], [2], [3], [4], [5], [6]

Causes of the renal venous hypertension

The frequency of renal venous hypertension is associated with vascular renal anomalies and other pathological conditions that lead to obstruction of venous outflow from the kidney.

The most common cause of renal venous hypertension is aortomethovenous "tweezers." Of purely venous vascular anomalies, renal venous hypertension is most often caused by ring-shaped left renal vein (17% of cases), retroaortic left renal vein (3%). Extremely rare causes - the congenital absence of the ordering department of the renal vein and its congenital stenosis. Renal venous hypertension leads to stagnant processes in the kidney, proteinuria, micro- or macrohematuria occur. About renal venous hypertension is also evidenced by varicocele. Sometimes, against the background of stagnant processes in the kidney, there is an increase in the formation of renin and arterial hypertension of a nephrogenic nature occurs.

[7], [8], [9], [10], [11]

Pathogenesis

Based on the results of renal phlebotometric and phlebographic studies performed in patients with arterial normotension and hypertension of renal and non-renal genesis, the following concept of mechanisms of renal venous hypertension has been put forward.

Renal venous hemodynamics is determined by arterial inflow to the kidney and the state of venous outflow in the direction from the kidney to the heart. Disturbance of outflow in the renal vein as a result of narrowing of the lumen of the venous trunk or its branch leads to stagnant renal vena hypertension. This is the mechanism of increasing venous pressure in the kidney during nephroptosis, thrombosis of the renal vein, compression of its abnormal arterial trunks, scar tissue,

Any obstruction of a dynamic or organic nature that violates the outflow in the inferior vena cava above the confluence of the renal veins (heart failure, compression of the inferior vena cava with fibrous lobes, membranous or scar occlusion of the inferior vena cava at the level of the liver or diaphragm, thrombosis of the inferior vena cava, etc.). . Leads to hypertension in the inferior vena cava system and can cause venous congestion in both kidneys. This form of renal hypertension is entirely determined by the conditions of venous outflow from the kidney.

A completely different mechanism for increasing venous pressure in the kidney is characteristic of systemic arterial hypertension. It is based on anatomical and functional features of the vascular bed of the kidney. High pressure in the renal artery with systemic arterial hypertension, increased tone of the sympatoadrenal system, causing vasoconstriction in the cortical layer, an increase in the medullary renal blood flow, the multifaceted arteriovenous shunting that provides the venous network with a large mass of blood in conditions of increased arterial delivery, are the main elements of the pathogenesis of increased venous pressure in both kidneys of patients with non-hypertensive arterial hypertension, as well as in contralateral intact kidney in b with nephrogenic arterial hypertension. With the discharge of a part of the kidney blood by short-circuiting in the arched veins or switching to a non-circular circulation path, much less resistance to blood flow is created than when circulating through the glomerular vasculature. For the kidney, it is a compensatory-adaptive mechanism that ensures the protection of the glomeruli from the destructive pressure of the arterial blood.

Some role in increasing venous pressure in the kidneys is played by general venous hypertension in patients with systemic arterial hypertension, for example, nephrogenic.

As research has shown, the venous pressure in the kidneys in patients with arterial hypertension depends on the level of systemic arterial pressure at the time of renal phlebotonometry. In the transient stage of arterial hypertension, intermittent renal venous hypertension corresponds to fluctuations in arterial pressure. This form of renal venous hypertension is secondary to systemic arterial hypertension. This compensatory-adaptive response of the vascular bed of the kidney to the arterial perfusion of the organ under increased pressure. This type of hypertension is referred to as "secondary renal venous hypertension of systemic arterial genesis."

If the venous pressure in the kidney increases with systemic arterial hypertension under the influence of the mechanisms of physiological shunting of the renal blood flow, then with congenital or acquired arteriovenous fistulas that cause the restructuring of the vascular architectonics of the kidney, the pressure in the renal venous bed increases due to shunting the blood flow through pathological arteriovenous messages. Blood from the arterial bed is discharged into the venous under an unusual pressure for veins. Develops the so-called fistulous renal venous hypertension - secondary renal venous hypertension of the local arterial genesis.

The pathological process in the kidney leads to complex changes in intraorganic hemodynamics, which causes combined disturbances of renal venous circulation. There are mixed forms of renal venous hypertension, in the mechanism of which both local factors and general factors that exist before the disease or have arisen in connection with it take part.

[12], [13]

Symptoms of the renal venous hypertension

Symptoms of renal venous hypertension depend on conditions arising from this urological disease.

When varicocele patients complain about the presence of volumetric education, swelling of the half of the scrotum, corresponding to the side of the lesion. Complaints are possible about drawing pains. Often the only complaint is infertility. In women with varicose veins of the ovary, menstrual irregularities are possible.

Hematuria with renal venous hypertension is of varying intensity and character. Often observed painless hematuria, which occurs without provocation (especially in the presence of arteriovenous fistula) or with physical exertion. Intensive hematuria may be accompanied by the formation of blood clots of worm-like form. Deviations of clots can provoke classical renal colic.

With acute thrombosis of the renal vein, pain occurs in the projection of the affected kidney, hematuria.

When collecting an anamnesis, you should pay attention to several situations in which it is possible to suspect with a high degree of renal venous hypertension.

A typical situation is when a small proteinuria of 600-800 mg / l (usually no more than 1 g / day) is detected in an apparently healthy, sportive adolescent with varicocele during clinical examination or at an outpatient examination before routine surgical treatment. Such a patient, despite the complete absence of characteristic clinical manifestations, is usually diagnosed with "nephritis?" And offers in-patient examination. In a hospital, proteinuria is significantly less or nonexistent, which forces one to reject the diagnosis. This condition can easily be explained by the fact that proteinuria with uncomplicated renal venous hypertension is tightly connected with physical activity, which strengthens the renal lymphatic flow and causes an increase in pressure in the renal vein system, as a result of which proteinuria and sometimes hematuria are observed. In a hospital, usually a mobile teenager is forced to lie more than to move. Varicocele in such patients exists since childhood and very slowly progresses.

Varicocele, which arose in adulthood, especially on the right, and rapidly progressing, is very suspicious of renal venous hypertension due to compression of the renal vein by a tumor of the kidney or retroperitoneal space.

Recurrent haematuria, often for no apparent reason, in a child of preschool age or in anyone who has recently undergone a severe trauma to the lumbar region, suggests an arteriovenous fistula of the kidney.

The appearance of pain in the projection of the kidney and hematuria in a patient with severe nephrotic syndrome, erythremia or decompensated circulatory insufficiency, except for the most common cause - renal colic, - requires the exclusion and thrombosis of the renal veins. The probability of thrombosis of the renal veins increases against the background of already developed thrombosis of veins of another localization. It is worth paying attention to proteinuria: a significant proteinuria is not characteristic of renal colic, but it is natural for thrombosis of the renal vein.

Palpatory it is easy to establish the presence and severity of varicocele.

Visually assess the severity of hematuria, the presence and shape of blood clots in the urine.

Forms

Renal venous hypertension is divided into four groups according to the features of pathogenesis.

• Congestive renal venous hypertension associated with impaired blood flow to the renal vein due to a decrease in its lumen under the following conditions:
  • vascular anomalies - aortomethasenteral "tweezers" (the most frequent abnormality), annular left renal vein, retroaortal left renal vein, congenital absence of the renal vein ordering department, congenital stenosis of the renal vein, etc .;
  • compression of the renal vein by a tumor, scars, organized by a hematoma;
  • nephroptosis;
  • thrombosis of the renal vein.
• Fistulous renal venous hypertension resulting from the formation of arteriovenous fistulas with the following conditions:
• vascular anomalies (the most common cause);
• kidney tumors;
• kidney trauma.
• with non-invasive arterial hypertension (bilateral);
• with renal arterial hypertension due to unilateral damage to the contralateral kidney.
• Secondary renal venous hypertension of systemic arterial genesis:
• Mixed form of renal venous hypertension.

[14], [15], [16], [17], [18]

Diagnostics of the renal venous hypertension

Laboratory diagnostics of renal venous hypertension

[19], [20], [21], [22], [23]

General urine analysis

Characteristic proteinuria from 300 to 600 mg / l, it is possible the appearance of a small number of cylinders. Hematuria can be any degree of severity - from a slight erythrocyturia to profuse bleeding.

Erythrocytes do not pass the glomerular filter, so they are described as unchanged. With renal venous hypertension, reabsorption suffers little.

Determination of daily proteinuria

More informative for assessing protein excretion than a general urine test. Characteristic proteinuria, not exceeding 1000 mg / day, increasing with intense physical exertion. With thrombosis of the renal veins, proteinuria can be of any severity, including nephrotic level.

[24], [25], [26], [27], [28], [29], [30], [31], [32], [33]

Provocative tests

For the diagnosis of renal venous hypertension, the definition of proteinuria is a more sensitive diagnostic method than the definition of erythrocyturia. This is due to the fact that one of the main mechanisms of proteinuria in renal venous hypertension is an increase in intra-cerebral pressure, while a vascular defect is needed to form a pronounced hematuria. Obviously, there will not be proteinuria if renal venous hypertension is fully compensated at the time of the analysis, for example by discharging blood into the testicle vein. This dictates the need for provocative samples that create conditions

To decompensate the renal circulation.

• Marching test. Conduct a general urine analysis before and after exercise. The appearance or strengthening of proteinuria or hematuria is evidence in favor of renal venous hypertension. The sample is simple in execution, but its results are difficult to interpret, since physical activity in most cases is dosed formally or not at all, and its tolerability depends heavily on the body's fitness.
• A sample with dopamine is performed in controversial cases. The drug is administered as a constant infusion at a rate of 1.5 μg / (kghmin) for 2 hours. Such a small dose of dopamine does not alter systemic hemodynamics, but increases renal blood flow and increases GFR by 10-15% (normal). If there is a violation of the outflow of blood through the renal vein, the increase in renal blood flow can lead to the appearance or strengthening of proteinuria or even hematuria. A coagulogram is needed as soon as possible to assess the coagulation system of the blood. Without a coagulogram, the appointment of anticoagulants or hemostatic drugs is highly undesirable.

Instrumental diagnosis of renal venous hypertension

Cystoscopy

Hematuria of unclear etiology is an indication for cystoscopy. Isolation of blood-colored urine along one of the ureters allows one to determine the side of the lesion, and also unambiguously exclude glomerulonephritis.

[34]

Ultrasonography of kidneys with dopplerography

Allows you to assess the condition of the kidneys and trunk renal vessels. The study is especially indicated for suspected thrombosis of the kidney vessels. Sometimes with the help of dopplerography it is possible to identify arteriovenous fistula.

Radioisotope renography and dynamic nephroscintigraphy

These studies are performed to assess the symmetry of nephropathy. For renal venous hypertension, asymmetric lesion is characteristic, whereas in immune nephropathies it is always symmetrical.

Selective renal venography

The main method of diagnosis, which allows to reliably determine the nature and extent of renal veins.

Phlebonometry

The research is performed in the process of angiography. The method allows to estimate the hemodynamic significance of the revealed changes.

Indications for consultation by other specialists

All persons with suspected renal venous hypertension are advised by a urologist (if absent - a vascular surgeon) and a roentgenologist, an angiography specialist. If the patient has proteinuria and, if necessary, to exclude glomerulonephritis, the consultation of the nephrologist is indicated.

Differential diagnosis

Renal venous hypertension must be differentiated with all diseases that regularly occur with painless hematuria, but without gross intoxication.

Chronic glomerulonephritis (especially mesangioproliferative) can occur with isolated painless hematuria. The principal difference between all immune nephropathies is the symmetry of kidney damage. Sometimes there is a clear association of relapses of jade with acute respiratory viral infection, angina and other similar acute diseases. However, neither hematuria nor proteinuria are ever provoked by physical exertion. Very high proteinuria leading to nephrotic syndrome can become a predisposing factor in the development of renal vein thrombosis.

Tumors of the kidney and urinary tract. Tumors of the kidney are often observed in the elderly or, conversely, in early childhood. Characterized by the presence of palpable formation in the projection of the kidney, the increase of hematuria with effleurage on the lumbar region from the side of the lesion, symptoms of cancer intoxication are possible - weakness, weight loss, reduction or perversion of appetite. Anemia due to intoxication hypoplastic (hyporegenerative), while classical posthemorrhagic anemia proceeds with high reticulocytosis, that is, it is hyperregenerative. In most cases, a kidney tumor can be ruled out with ultrasound. With tumors of the urinary tract, it is more difficult to have a complete X-ray examination, CT, sometimes a urethrocystoscope and ureteropyeloscopy with a biopsy of suspicious areas.

Benign family hematuria is a rare benign non-progressive hereditary lesion of the kidney that does not lend itself to specific treatment. The basis of pathology - congenital thinning of the basal glomeruli membranes. Often such patients, after numerous examinations, carry out angiography that does not reveal any changes in the vascular bed of the kidney, or a kidney biopsy, in which no jade-like changes are detected. To confirm the diagnosis, an electron microscopy is necessary to measure the thickness of the basal membrane of the glomerulus. This study is performed only in the largest nephrological clinics.

[35], [36], [37], [38], [39], [40], [41], [42], [43]

Treatment of the renal venous hypertension

The goals of treatment of renal venous hypertension

The goal of treatment of renal venous hypertension depends on the manifestation of the disease - from the prevention of infertility in varicocele to saving the life of the patient with profuse fornic hemorrhage.

Indications for hospitalization

If there is a suspicion of renal venous hypertension, the initial stage of the examination is quite possible in an outpatient setting. Hospitalization of the patient is necessary to perform angiographic examination and subsequent surgical treatment.

Emergency hospitalization is necessary for all patients with foremic bleeding and hematuria of unclear etiology.

Non-pharmacological treatment of renal venous hypertension

Restriction of physical activity is necessary in the event that it provokes hematuria. In the case of severe hematuria, a strict bed rest is indicated.

Drug treatment of renal venous hypertension

The role of drug treatment of renal venous hypertension is low. Fornatural bleeding shows the appointment of hemostatic therapy. Usually, treatment starts with intramuscular or intravenous administration of etamzilate at a dose of 250 mg 3-4 times a day. "Whether bleeding is not stopped, perhaps the appointment of drugs with the expression of antifibrinolytic activity - aprotinin (countercracker, gordoks), aminomethylbenzoic acid (ambene), etc. The use of antifibrinolytic drugs is risky, especially with intensive hematuria, because if with their help the bleeding is quickly stopped it will not be possible, the drug along with the blood will pass through the defect of the vessel - the patient will develop a tamponade of the renal pelvis, obstruction of the ureter with blood clots, and sometimes even a tamponade of the bladder.

With confirmed renal vein thrombosis, the appointment of direct anticoagulants - heparin or low-molecular heparins, for example sodium enoxaparin (kleksan) at a daily dose of 1-1.5 mg / kg, is quite logical.

It is important to properly manage the patient after reconstructive surgery on the veins for renal venous hypertension. In order to prevent thrombosis of the anastomosis from the moment of performing the operation to discharge from the hospital, the patient is prescribed direct anticoagulants daily in preventive doses (for example, sodium enoxaparin in the vine 20 mg / day intradermally). After discharge for 1 month or more antiplatelet agents are used - acetylsalicylic acid in a dose of 50-100 mg / day after meals.

[44], [45], [46], [47], [48]

Operative treatment of renal venous hypertension

The main method of treating renal venous hypertension is surgical intervention.

The purpose of surgical treatment of renal venous hypertension

Depending on the specific situation, different goals may be set - normalization of renal hemodynamics and prevention of progression of nephrosclerosis on the side of defeat, prevention and treatment of infertility, stopping bleeding.

Types of surgical treatment of renal venous hypertension

• Reconstructive surgery aimed at the formation of bypass renocaval anastomosis testikuloiikalny, testukulosaphenic or testikuloepigastral anastomosis.
• Resection of the kidney with a single arteriovenous fistula.
• Nephrectomy with multiple arteriovenous fistulas and forecal hemorrhage, resistant to all other types of treatment.
• Thrombectomy with renal vein thrombosis and unsuccessful conservative therapy.

Varicocele is a sign of an anomaly or a disease of the inferior vena cava or one of the renal veins, so operations that do not ensure the discharge of venous blood from the kidney are pathogenetically unfounded. They contribute to the onset of hypertension and can provoke the emergence of fornatural bleeding, impairment of kidney function, etc. That is why, in the presence of a confirmed renal venous hypertension and varicocele, the Ivanissevich surgery and X-ray endovascular occlusion of the testicular vein are contraindicated, as this destroys the natural bypass Renocaval anastomosis. Due to these interventions, renal hemodynamics is sharply decompensated. Complications are possible. At best, a recurrence of varicocele develops; in the worst case, long-term venous hypertension may lead to progressive nephrosclerosis or recurrent fornic hematuria.

The most physiological surgical interventions for varicocele are the operations aimed at creating vascular anastomoses (proximal testicular and testiculosafenic anastomoses), preservation of venous renocaval anastomosis in renal hypertension. Various variants of vascular anastomoses between the distal end of the testicular vein and the proximal part of the deep vein that surrounds the iliac bone (proximal testicular-epigastric anastomosis) are suggested.

To improve the results of vascular surgery suggest using a microsurgical method. Through the skin incision parallel to the inguinal ligament, having retreated from it 1.5-2 cm upwards, the spermatic cord is excreted. Further, the proximal part of the deep vein, surrounding the iliac, and the lower epigastric vein are identified for 2-3 cm. The location and usefulness of the valves in the mouths of the veins are determined, and the vessels are crossed 10-12 cm distal to the location of the valves. The vein of the testicle is crossed and anastomoses are placed between its distal portion and the proximal portion of the deep vein of the ileal envelope, as well as between the proximal areas of the testicular vein and the lower epigastric vein. The vein should be of adequate diameter and contain high-grade valves. Carry out a thorough revision and dressing of additional veins, which can be the cause of varicocele. Microsurgical correction of blood outflow with varicocele allows to disentangle collateral venous outflow from the testicle and reduce the influence of retrograde blood flow along the main trunk of the testicular vein.

Further management

The patient who underwent reconstructive surgical treatment on veins, with the aim of preventing anastomosis thrombosis, received antiplatelet agents for at least 1 month after discharge from hospital (acetylsalicylic acid in a dose of 50-100 mg / day).

Prevention

Screening is not carried out, since cheap and non-invasive diagnostic methods that allow us to conclude with any reasonable certainty about the presence or absence of renal venous hypertension are lacking.

Renal venous hypertension is prevented by the prevention of renal vein thrombosis. It is concluded in the adequate treatment of diseases that are naturally complicated by thrombosis (nephrotic syndrome, antiphospholipid syndrome, decompensation of circulatory insufficiency, erythremia, etc.).

[49], [50], [51], [52], [53], [54], [55]

Forecast

With adequate treatment of renal venous hypertension, the prognosis is favorable. The disease has no tendency to relapse. The continued existence of non-severe renal vascular hypertension without treatment leads to a slow but steady progression of nephrosclerosis on the affected side. With adequate surgical treatment of arteriovenous fistulas, the prognosis is favorable. With the technical impossibility of surgical treatment (for example, in the case of multiple fistulas), the prognosis is significantly worse. It is determined by the frequency and severity of episodes of hematuria. With thrombosis of renal veins, the prognosis is usually determined by the underlying disease that led to such a complication. It is worth noting that the thrombosis of the renal veins develops only with a severe, extremely unfavorable course of the underlying disease.

[56], [57], [58], [59], [60]