Renal venous hypertension

Renal venous hypertension is an increase in pressure in the renal vein system.

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Causes renal venous hypertension

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

The most common cause of renal venous hypertension is aortomesenteric "tweezers". Of purely venous vascular anomalies, renal venous hypertension is most often caused by the annular left renal vein (17% of cases), retroaortic left renal vein (3%). Extremely rare causes are congenital absence of the pericaval part of the renal vein and its congenital stenosis. Renal venous hypertension leads to congestion in the kidney, proteinuria, micro- or macrohematuria occur. Varicocele also indicates renal venous hypertension. Sometimes, against the background of congestion in the kidney, there is an increase in the formation of renin and arterial hypertension of a nephrogenic nature occurs.

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Pathogenesis

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

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

Any obstruction of a dynamic or organic nature that disrupts the outflow through the inferior vena cava above the confluence of the renal veins (heart failure, compression of the inferior vena cava by fibrotic lobes of the liver, membranous or cicatricial 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 of increasing venous pressure in the kidney is characteristic of systemic arterial hypertension. It is based on the anatomical and functional features of the renal vascular bed. High pressure in the renal artery in systemic arterial hypertension, increased tone of the sympathoadrenal system causing vasoconstriction in the cortex, increased medullary renal blood flow, the versatility of arteriovenous shunting ensuring the acceptance of a large mass of blood by the venous network under conditions of its increased arterial delivery are the main elements of the pathogenesis of increased venous pressure in both kidneys of patients with nonrenal arterial hypertension, as well as in the contralateral intact kidney in patients with nephrogenic arterial hypertension. When part of the renal blood is discharged by short-circuiting into the arcuate veins or switching to the non-glomerular circulation pathway, much less resistance to blood flow is created than when circulating through the glomerular vascular network. For the kidney, this is a compensatory-adaptive mechanism that ensures protection of the glomeruli from the destructive pressure of arterial blood.

General venous hypertension in patients with systemic arterial hypertension, such as nephrogenic hypertension, also plays a certain role in increasing venous pressure in the kidneys.

As studies have shown, the venous pressure in the kidneys of 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, fluctuations in arterial pressure correspond to intermittent renal venous hypertension. This form of renal venous hypertension is secondary to systemic arterial hypertension. This is a compensatory-adaptive response of the renal vascular bed to arterial perfusion of the organ under increased pressure. This type of hypertension is designated by the term "secondary renal venous hypertension of systemic arterial genesis".

If in systemic arterial hypertension the venous pressure in the kidney increases under the action of physiological shunting mechanisms of renal blood flow, then in congenital or acquired arteriovenous fistulas, causing restructuring of the vascular architecture of the kidney, the pressure in the renal venous bed increases due to shunting of blood flow along pathological arteriovenous communications. Blood from the arterial bed is discharged into the venous bed under pressure unusual for veins. The so-called fistula renal venous hypertension develops - secondary renal venous hypertension of local arterial genesis.

The pathological process in the kidney leads to complex changes in intraorgan hemodynamics, generating combined disorders of renal venous circulation. Mixed forms of renal venous hypertension arise, in the mechanism of which both local factors and general ones, existing before the disease or arising in connection with it, participate.

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Symptoms renal venous hypertension

Symptoms of renal venous hypertension depend on the conditions that arise as a result of this urological disease.

With varicocele, patients complain of a voluminous formation, swelling of half of the scrotum corresponding to the affected side. Complaints of nagging pain are possible. Often the only complaint is infertility. In women with varicose veins of the ovary, menstrual irregularities are possible.

Hematuria in renal venous hypertension can be of varying intensity and nature. Most often, painless hematuria is observed, occurring without provocation (especially in the presence of an arteriovenous fistula) or during physical exertion. Intense hematuria can be accompanied by the formation of worm-shaped blood clots. The passage of clots can provoke classic renal colic.

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

When collecting anamnesis, attention should be paid to several situations in which renal venous hypertension can be suspected with a high degree of probability.

A typical situation is when a seemingly healthy, athletic teenager with varicocele is found to have slight proteinuria of 600-800 mg/l (usually no more than 1 g/day) during a medical examination or outpatient examination before planned surgical treatment. Such a patient, despite the complete absence of characteristic clinical manifestations, is usually diagnosed with "nephritis?" and offered inpatient examination. Inpatient proteinuria turns out to be significantly less or absent altogether, which forces the diagnosis to be rejected. The described condition is easily explained by the fact that proteinuria in mild renal venous hypertension is strictly related to physical activity, which increases renal lymph flow and causes an increase in pressure in the renal vein system, as a result of which proteinuria and sometimes hematuria are observed. Inpatient treatment usually forces an active teenager to lie down more than move. Varicocele in such patients exists since childhood and progresses very slowly.

Varicocele that occurs in adulthood, especially on the right, and progresses rapidly, is highly suspicious for renal venous hypertension due to compression of the renal vein by a renal or retroperitoneal tumor.

Recurrent hematuria, often without apparent cause, in a preschool-aged child or in any person who has recently suffered severe lumbar trauma suggests a renal arteriovenous fistula.

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

The presence and severity of varicocele can be easily determined by palpation.

The severity of hematuria and the presence and shape of blood clots in the urine are visually assessed.

Forms

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

• Congestive renal venous hypertension associated with impaired blood outflow through the renal vein due to a decrease in its lumen in the following conditions:
  • anomalies in the development of blood vessels - aortomesenteric "tweezers" (the most common anomaly), annular left renal vein, retroaortic left renal vein, congenital absence of the pericaval part of the renal vein, congenital stenosis of the renal vein, etc.;
  • compression of the renal vein by a tumor, scars, or organized hematoma;
  • nephroptosis;
  • renal vein thrombosis.
• Fistular renal venous hypertension resulting from the formation of arteriovenous fistulas in the following conditions:
• vascular developmental anomalies (the most common cause);
• kidney tumors;
• kidney injuries.
• in non-renal arterial hypertension (bilateral);
• in renal arterial hypertension caused by unilateral damage to the contralateral kidney.
• Secondary renal venous hypertension of systemic arterial genesis:
• Mixed form of renal venous hypertension.

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Diagnostics renal venous hypertension

Laboratory diagnostics of renal venous hypertension

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General urine analysis

Proteinuria from 300 to 600 mg/l is typical, a small number of cylinders may appear. Hematuria can be of any degree of severity - from minor erythrocyturia to profuse bleeding.

The erythrocytes do not pass through the glomerular filter, so they are described as unchanged. In renal venous hypertension, reabsorption suffers little.

Determination of daily proteinuria

More informative for assessing protein excretion than general urine analysis. Typical proteinuria is not exceeding 1000 mg/day, increasing with intense physical activity. In renal vein thrombosis, proteinuria can be of any severity, including nephrotic levels.

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Provocative tests

For the diagnosis of renal venous hypertension, proteinuria determination is a more sensitive diagnostic method than erythrocyturia determination. This is due to the fact that one of the main mechanisms of proteinuria in renal venous hypertension is an increase in intraglomerular pressure, while a vascular defect is needed to form pronounced hematuria. Obviously, there will be no proteinuria if renal venous hypertension is completely compensated at the time of analysis, for example, by blood discharge into the testicular vein. This dictates the need for provocative tests that create conditions

For decompensation of renal circulation.

• Marching test. A general urine analysis is performed before and after physical activity. The appearance or increase of proteinuria or hematuria indicates renal venous hypertension. The test is easy to perform, but its results are quite difficult to interpret, since physical activity is in most cases dosed formally or not dosed at all, and its tolerance strongly depends on the body's fitness.
• A dopamine test is performed in controversial cases. The drug is administered as a constant infusion at a rate of 1.5 mcg/(kg x min) for 2 hours. Such a small dose of dopamine does not change systemic hemodynamics, but increases renal blood flow and increases the SCF by 10-15% (normally). If the blood outflow through the renal vein is impaired, increased renal blood flow can lead to the appearance or increase of proteinuria or even hematuria. A coagulogram is necessary as soon as possible to assess the blood coagulation system. Without a coagulogram, the administration of anticoagulants or hemostatic drugs is highly undesirable.

Instrumental diagnostics of renal venous hypertension

Cystoscopy

Hematuria of unclear etiology is an indication for cystoscopy. The release of blood-stained urine through one of the ureters allows one to determine the side of the lesion, as well as to clearly exclude glomerulonephritis.

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Ultrasound examination of the kidneys with Dopplerography

Allows to assess the condition of the kidneys and main renal vessels. The study is especially indicated if thrombosis of the renal vessels is suspected. Sometimes, Dopplerography can detect an arteriovenous fistula.

Radioisotope renography and dynamic nephroscintigraphy

These studies are performed to assess the symmetry of nephropathy. Renal venous hypertension is characterized by asymmetrical damage, while in immune nephropathies it is always symmetrical.

Selective renal venography

The main diagnostic method that allows one to reliably determine the nature and extent of damage to the renal veins.

Phlebotonometry

The study is performed during angiography. The method allows assessing the hemodynamic significance of the detected changes.

Indications for consultation with other specialists

All persons with suspected renal venous hypertension are advised to consult a urologist (if unavailable, a vascular surgeon) and a radiologist - an angiography specialist. If the patient has proteinuria and if it is necessary to exclude glomerulonephritis, a nephrologist is advised.

Differential diagnosis

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

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

Tumors of the kidney and urinary tract. Tumors of the kidney are more often observed in the elderly or, conversely, in early childhood. Characteristic is the presence of a palpable formation in the projection of the kidney, increased hematuria when tapping on the lumbar region on the side of the lesion, symptoms of cancer intoxication are possible - weakness, weight loss, decreased or perverted appetite. Anemia due to intoxication is hypoplastic (hyporegenerative), while classic posthemorrhagic anemia occurs with high reticulocytosis, that is, it is hyperregenerative. In most cases, a kidney tumor can be excluded by ultrasound. With tumors of the urinary tract, it is more difficult - a complete X-ray examination, CT, sometimes a urethrocystoscope and ureteropyeloscopy with a biopsy of suspicious areas are necessary.

Benign familial hematuria is a rare benign non-progressive hereditary kidney disorder that does not respond to specific treatment. The basis of the pathology is congenital thinning of the glomerular basement membranes. Often, after numerous examinations, such patients undergo angiography, which does not reveal any changes in the renal vascular bed, or a kidney biopsy, which does not reveal changes similar to nephritis. To confirm the diagnosis, electron microscopy with measurement of the thickness of the glomerular basement membrane is necessary. This study is performed only in the largest nephrology clinics.

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Treatment renal venous hypertension

Treatment goals for renal venous hypertension

The goal of treatment of renal venous hypertension depends on the manifestation of the disease - from preventing infertility in varicocele to saving the life of a patient with profuse fornical bleeding.

Indications for hospitalization

If renal venous hypertension is suspected, the initial stage of examination can be carried out on an outpatient basis. The patient must be hospitalized to perform an angiographic examination and subsequent surgical treatment.

Emergency hospitalization is necessary for all patients with fornicational bleeding and hematuria of unknown etiology.

Non-drug treatment of renal venous hypertension

Limiting physical activity is necessary if it provokes hematuria. In case of severe hematuria, strict bed rest is indicated.

Drug treatment of renal venous hypertension

The role of drug treatment of renal venous hypertension is small. In case of fornical bleeding, hemostatic therapy is indicated. Usually, treatment begins with intramuscular or intravenous administration of etamzilat at a dose of 250 mg 3-4 times a day. If the bleeding is not stopped, it is possible to prescribe drugs with antifibrinolytic activity - aprotinin (contrycal, gordox), aminomethylbenzoic acid (amben), etc. The use of antifibrinolytics is risky, especially with intense hematuria, due to the fact that if they fail to quickly stop the bleeding, the drug will pass through the vessel defect together with the blood - the patient will develop tamponade of the renal pelvis, obstruction of the ureter with blood clots, sometimes even tamponade of the bladder.

In case of confirmed renal vein thrombosis, it is quite logical to prescribe direct anticoagulants - heparin or low molecular weight heparins, for example, enoxaparin sodium (Clexane) in a daily dose of 1-1.5 mg/kg.

Proper management of the patient after reconstructive surgery on veins for renal venous hypertension is important. In order to prevent anastomotic thrombosis, direct anticoagulants are prescribed daily in prophylactic doses (e.g., sodium enoxaparin in a vein 20 mg/day intradermally) from the time of surgery until discharge from the hospital. After discharge, antiplatelet agents are used for 1 month or more - acetylsalicylic acid in a dose of 50-100 mg/day after meals.

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Surgical treatment of renal venous hypertension

The main method of treating renal venous hypertension is surgery.

The goal 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 affected side, prevention and treatment of infertility, stopping bleeding.

Types of surgical treatment for renal venous hypertension

• Reconstructive surgeries aimed at forming a bypass renocaval anastomosis: testiculoiliac, testiculosaphne or testiculoepigastric anastomosis.
• Kidney resection for a single arteriovenous fistula.
• Nephrectomy for multiple arteriovenous fistulas and fornicational bleeding resistant to all other treatments.
• Thrombectomy for renal vein thrombosis and failure of conservative therapy.

Varicocele is a sign of anomaly or disease of the inferior vena cava or one of the renal veins, therefore operations that do not ensure the discharge of venous blood from the kidney are not pathogenetically justified. They contribute to venous hypertension and can provoke the occurrence of fornical bleeding, deterioration of kidney function, etc. That is why, if the patient has confirmed renal venous hypertension and varicocele, the Ivanissevich operation and X-ray endovascular occlusion of the testicular vein are contraindicated, since this destroys the natural bypass renocaval anastomosis. As a result of the listed interventions, renal hemodynamics is sharply decompensated. Complications are possible. In the best case, a relapse of varicocele develops, in the worst case, long-term venous hypertension can lead to progressive nephrosclerosis or recurrent fornical hematuria.

The most physiological surgical interventions for varicocele are those aimed at creating vascular anastomoses (proximal testicular-iliac and testicular-saphenous anastomoses), preserving venous renocaval anastomosis in venous renal hypertension. Various variants of vascular anastomoses between the distal end of the testicular vein and the proximal part of the deep vein encircling the iliac bone (proximal testicular-epigastric anastomosis) have been proposed.

To improve the results of vascular surgeries, it is suggested to use a microsurgical method. Through a skin incision parallel to the inguinal ligament, stepping back from it 1.5-2 cm upward, the spermatic cord is isolated. Then the proximal section of the deep vein encircling the ilium and the inferior epigastric vein are isolated for 2-3 cm. The location and adequacy of the valves in the vein mouths are determined, the vessels are crossed 10-12 cm distal to the location of the valves. The testicular vein is crossed and anastomoses are applied between its distal section and the proximal section of the deep vein encircling the ilium, as well as between the proximal sections of the testicular vein and the inferior epigastric vein. The vein should be of adequate diameter and contain adequacy of the valves. A thorough revision and ligation of additional veins that may be the cause of varicocele is performed. Microsurgical correction of blood outflow in varicocele allows to separate collateral venous outflow from the testicle and reduce the influence of retrograde blood flow along the main trunk of the testicular vein.

Further management

A patient who has undergone reconstructive surgery on veins is recommended to take antiplatelet agents for at least 1 month after discharge from the hospital (acetylsalicylic acid at a dose of 50-100 mg/day) in order to prevent anastomotic thrombosis.

Prevention

Screening is not performed because there are no inexpensive and non-invasive diagnostic methods that would allow one to draw a conclusion about the presence or absence of renal venous hypertension with acceptable reliability.

Renal venous hypertension is prevented by prophylaxis of renal vein thrombosis. It consists of adequate treatment of diseases that are naturally complicated by thrombosis (nephrotic syndrome, antiphospholipid syndrome, decompensation of circulatory failure, erythremia, etc.).

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Forecast

With adequate treatment of renal venous hypertension, the prognosis is favorable. The disease does not tend to relapse. Long-term existence of mild renal venous hypertension without treatment leads to slow but steady progression of nephrosclerosis on the affected side. With adequate surgical treatment of arteriovenous fistulas, the prognosis is favorable. If surgical treatment is technically impossible (for example, in the case of multiple fistulas), the prognosis is significantly worse. It is determined by the frequency and severity of hematuria episodes. In renal vein thrombosis, the prognosis is usually determined by the underlying disease that led to such a complication. It is worth noting that renal vein thrombosis develops only with a severe, extremely unfavorable course of the underlying disease.

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