Renal vein thrombosis is an acute or chronic occlusion of the venous network of the kidneys. It is manifested by abdominal and lower back pain, macrohematuria, oligoanuria, intoxication syndrome. With a chronic course, it can occur monosymptomically with a persistent increase in blood pressure. It is diagnosed using magnetic resonance, computer, selective renal phlebography, duplex scanning of renal veins. Conservative therapy involves long-term administration of direct and indirect anticoagulants. If there is a threat of thermal insulation, a mesh filter is installed intracavally. According to the indications, regional thrombolysis, percutaneous or open thrombectomy, nephrectomy are performed.
ICD 10
I82.3 Embolism and thrombosis of the renal vein
Meaning
Blockage of the renal veins is traditionally regarded as a casuistically rare pathological condition that usually develops in patients with nephrotic syndrome, less often with other concomitant diseases. According to modern urologists, information about the low (up to 5%) frequency of venous renal thrombosis in nephrological pathology does not correspond to reality.
According to recent studies, chronic occlusion of the renal veins is found in a third of patients suffering from proteinuria for a long time. Thrombosis is more often unilateral, less often affects both renal veins. The urgency of timely diagnosis of the disease is due to its frequent complication of acute or chronic renal failure.
Causes
Venous occlusion of the renal vessels is a polyethological pathology that occurs when the integrity of the vascular endothelium is violated, blood flow is slowed down, and coagulation imbalance. According to the observations of specialists in the field of practical urology, nephrology and angiology, the main causes of thrombotic blockage of one or both renal veins are:
- Hypercoagulation in nephrotic syndrome. The high-risk group includes patients with membranous nephropathy, in whom the risk of venous vessel thrombosis reaches 50%, membranous-proliferative glomerulonephritis, kidney amyloidosis, lipoid nephrosis. Thrombosis can be complicated by diabetic nephropathy, kidney damage in sickle cell anemia, systemic lupus erythematosus.
- Other coagulation disorders. The probability of venous thrombosis of the kidneys increases with congenital deficiency of anticoagulation factors (antithrombin III, proteins S and C), mutations of prothrombin, Leyden factor V. Secondary hypercoagulation with occlusion of the renal veins is possible when taking estrogens, oral contraceptives, gestosis, DIC syndrome, kidney transplantation, dehydration.
- Neoplastic process. Violation of blood flow in the renal vessels with subsequent thrombosis can be observed with the germination of malignant tumors (mainly renal cell carcinoma), external compression of the inferior vena cava and renal veins by enlarged lymph nodes, volumetric neoplasms located in the retroperitoneal space. The aggravating factor in neoplasia is hypercoagulation.
- Vascular pathology. Thrombosis is based on endothelial damage in renal vasculitis, injuries. In some patients, the thrombotic process spreads to the renal vessels from the ovarian, inferior vena cava, occurs when an aortic aneurysm is compressed. Sometimes thrombosis becomes a consequence of migrating thrombophlebitis in myeloma, lymphogranulomatosis, allergies, etc.
Pathogenesis
The starting point of renal vein thrombosis is usually an increase in the activity of coagulating factors in combination with inhibition of coagulation inhibitors and fibrinolytic agents. Increased clotting is promoted by characteristic of nephrotic syndrome hypoalbuminemia (critical level — less than 25-30 g / l), dysproteinemia, increased levels of fibrinogen, prothrombin, platelets. The individual links in the pathogenesis of renal venous thrombosis are the slowing down of renal blood flow during vascular germination by tumors or compression by volumetric neoplasms, damage to the vascular wall due to inflammatory processes, during injuries, operations.
Partial or complete obturation of the vein lumen by a thrombus causes ischemia with reversible or irreversible destruction of the renal parenchyma. With a favorable outcome of phlebothrombosis, fibrinolysis, aseptic autolysis of the clot, the organization of the thrombus with its calcification, petrification is observed. With the slow development of the thrombotic process and the gradual cessation of blood flow, the expansion of compensatory collaterals often occurs.
Symptoms
With simultaneous occlusion of one or two renal veins, a clinical picture of acute kidney injury is revealed, characterized by signs such as sharp pain in the lower back and lateral abdominal regions, the appearance of blood during urination, a decrease in urine volume up to anuria. Due to the accumulation of nitrogen metabolism products in the body, symptoms of intoxication develop — nausea and vomiting, weakness, drowsiness, dizziness. Body temperature may rise.
In the presence of systemic hypercoagulation, manifestations of deep vein thrombosis are observed: pain, swelling and pasty of the lower extremities, visible expansion of venous collaterals. In elderly patients, the disease often proceeds in an erased form, the only symptom is persistent arterial hypertension, resistant to antihypertensive drugs.
Complications
Severe venous stasis as a result of thrombosis can lead to a heart attack and rupture of the kidney. With an increase in the concentration of nitrogenous compounds in the blood due to intoxication damage to the brain, mental disorders occur: alternating periods of excitement and inhibition, disorientation, confusion, delirium, hallucinations. The accumulation of potassium ions in acute renal failure provokes sluggish muscle paresis, bradycardia.
A frequent complication of thrombosis is the suppression of immunity, accompanied by the addition of severe bacterial and viral infections with a tendency to generalization. Retention of urine and electrolytes leads to extracellular hyperhydration, ascites, brain edema. In rare cases, profuse bleeding from the formed ulcers of the gastrointestinal tract is noted. Unstable blood clots can cause pulmonary embolism.
Diagnostics
The diagnosis of renal vein thrombosis is often difficult due to the polymorphism of the clinical picture. It is necessary to suspect venous occlusion in all patients with persistent deterioration of renal function of unexplained etiology, severe nephrotic syndrome. The following studies are the most informative in diagnostic terms:
- Ultrasound. Ultrasound is often used as a starting method for diagnosing the disease, with which it is possible to detect venous thrombosis. With duplex scanning, there is a risk of false positive and false negative results. During ultrasound examination, a change in the contours of the ureters is detected — a characteristic sign that occurs with excessive development of venous collaterals.
- Magnetic resonance phlebography. MRI is a non-invasive, safe diagnostic method that allows obtaining detailed layered images with sufficient magnification to verify the diagnosis. Magnetic resonance imaging is indicated if the glomerular filtration rate is at least 30 ml/min. The advantage of MRI is that it is performed without the introduction of contrast agents into the body.
- CT phlebography. Important advantages of the technique are the speed of implementation, ensuring good detail of anatomical structures, high specificity, sensitivity, and painlessness. The study reveals the exact location of thrombosis well. However, with occlusion of the renal veins, CT phlebography is used with caution due to the nephrotoxicity of radiopaque drugs that are necessary for the study.
- Selective renal phlebography. The method is considered the most informative for confirming thrombosis. The study is carried out by the directional introduction of X-ray contrast through the inferior vena cava, as a result of which the doctor receives sufficient filling of the main trunk and additional branches of the venous vessels of the kidneys. With catheterization of renal veins, there is a risk of thromboembolism.
Additionally, a clinical urine analysis is performed, in which signs of kidney dysfunction are detected — proteinuria, moderate leukocyturia, cylindruria, a decrease in specific gravity, hematuria. In the biochemical analysis of blood, there is an increase in creatinine, urea levels, a decrease in the concentration of potassium and sodium ions, anemia. For a comprehensive assessment of the state of the genitourinary system, intravenous urography and abdominal CT are performed.
Differential diagnosis is performed with renal vein aneurysm, kidney tumor, acute and malignant glomerulonephritis, chronic pyelonephritis, nephropathies in autoimmune diseases, systemic vasculitis, gout, acute tubular, medullary, cortical necrosis, arterial thrombosis, hemolytic-uremic syndrome, hemorrhages in adrenal tissue. In addition to the examination of a nephrologist, the patient is recommended to consult a vascular surgeon, a hematologist, an oncologist, an oncohematologist, an infectious disease specialist.
Treatment
The main medical tasks are the therapy of the underlying disease that caused the formation of a blood clot, the elimination of occlusion, the correction of existing clinical manifestations. Treatment of pathology complicated by thrombosis is carried out according to standard protocols for the corresponding nosological unit. To restore blood flow in the thrombosed renal vein , the following methods are used:
- Anticoagulants. The preferred method of thrombosis therapy is conservative management of the patient with the use of anticoagulant drugs for 6-12 months, and in the presence of hypercoagulation disorders — for life. The most effective are low molecular weight heparins, indirect anticoagulants from the group of semi-synthetic coumarin derivatives. Pharmacotherapy can prevent further thrombosis, recanalize thrombosed venous vessels, and improve the functional abilities of the kidneys.
- Operations on renal vessels and kidneys. In acute bilateral thrombosis of the renal veins, regional thrombolysis may be performed through an angiographic catheter. If anticoagulant therapy is ineffective, the thrombus cannot be dissolved by fibrinolytic agents, there is a threat of thromboembolic complications, suprarenal installation of a cava filter, percutaneous catheter or open thrombectomy is recommended. Massive venous infarction with damage to the entire kidney serves as an indication for nephrectomy.
Since an acute violation of the blood flow in the renal veins is often accompanied by the development of renal insufficiency, taking into account the severity of the patient’s condition, infusion therapy is indicated to correct metabolic disorders, eliminate hemodynamic disorders. With severe acute renal failure, it is possible to prescribe renal replacement therapy (hemodialysis, peritoneal dialysis, hemofiltration, hemodiafiltration). Hypotensive agents are recommended for patients with renal arterial hypertension.
Prognosis and prevention
The probability of full recovery depends on the severity of the underlying pathology that caused the blockage of the renal veins. The prognosis is favorable for young patients who do not have irreversible changes in the kidneys. The long course of the disease in people with intercurrent pathologies leads to a persistent decrease in the glomerular filtration rate.
Specific prevention has not been developed. To prevent venous thrombosis, it is necessary to carry out timely complex therapy of conditions that are naturally complicated by hypercoagulation. In patients with nephrotic syndrome, preventive anticoagulant therapy is prescribed with a decrease in albumin concentration less than 30.0 g / l.