Renal vein thrombosis (RVT) is the formation of a clot in the vein that drains blood from the kidneys, ultimately leading to a reduction in the drainage of one or both kidneys and the possible migration of the clot to other parts of the bodyfirst described by German pathologist Friedrich Daniel von Recklinghausen in 1861, RVT most commonly affects two subpopulations: newly born infants with blood clotting abnormalities or dehydration and adults with nephrotic syndrome

Nephrotic syndrome, a kidney disorder, causes excessive loss of protein in the urine, low levels of albumin in the blood, a high level of cholesterol in the blood and swelling, triggering a hypercoagulable state and increasing chances of clot formation. Other less common causes include hypercoagulable state, cancer, kidney transplantation, Behcet syndrome, antiphospholipid antibody syndrome or blunt trauma to the back or abdomen

Treatment of RVT mainly focuses on preventing further blood clots in the kidneys and maintaining stable kidney function. The use of anticoagulants has become the standard treatment in treating this abnormality.Membranous glomerulonephritis, the most common cause for nephrotic syndrome in adults, peaks in people ages 40–60 years old and it is twice as likely to occur in men than in women. Since nephrotic syndrome is the most common cause of RVT, people over 40 years old and men are most at risk to develop a renal vein thrombosis

Signs and symptoms[edit]

Aside from the occasional flank or lower back pain caused by a sudden clot in the major veins to the kidneys, RVT produces few symptoms. Some patients may not display any symptoms while other patients may experience bloody urine, decrease in urine output, edema and worsening proteinuria. Usually the diagnoses of RVT is first made when a nephrotic syndrome patient experiences a pulmonary embolism or a sudden decrease in kidney function or kidney failure. These symptoms may vary in duration since a blood clot can resolve itself, but precautions should be taken to prevent the migration of the clot to other parts of the body. The most severe complication of RVT is a pulmonary embolism, caused by a clot, also called a thrombus, that originates from the renal vein or any other vein in the body and migrates to the pulmonary artery. A pulmonary embolism is a serious condition because; it can damage the lungs due to pulmonary hypertension and cause low blood oxygen, damaging other organs in the body. This condition can cause death if left untreated; about 30% percent of patients who have a pulmonary embolism will die, usually within one hour.

Infants and young children experiencing dehydration induced RVT, may experience dehydration symptoms (dry mouth, low urine output, loss of skin turgidity) as while as vomiting, nausea and fever, and the usual RVT symptoms like flank pain, blood in the urine, anaemia, edema, enlarged kidneys and kidney failure.

Mechanism[edit]

The mechanism behind RVT is no different from other types of blood clots in other parts of the body. Rudolf Virchow, was the first to describe the physiological mechanism behind venous thrombosis (blood clots) using three related factors, known as Virchow's Triad; damage to the blood vessel (endothelial damage), decrease in blood flow (stasis) and increased coagulability of the blood (thrombophilia or hypercoagulability). it is possible for one of these factors alone to cause a blood clot, but in most cases, a combination or all of these factors induce the formation of a blood clot. Decreased urine output or kidney function may be the only observable symptoms caused by a blood clot renal vein. Other less common causes include hypercoagulable state, invasion by renal cell carcinoma, kidney transplantation, Behcet syndrome, antiphospholipid antibody syndrome or blunt trauma to the back or abdomen

Vein tissue damage[edit]

Damage to the endothelial tissue of the vein can be caused by blunt damage, trauma during venography, a renal transplant, tumors, acute rejection, vasculitis or spontaneous micro-trauma to the endothelium due to homocystinuria.[6] Cystathionine beta synthase deficiency, also known as homocystinuria, is an autosomal recessive inherited disorder in which the body is not able to process certain building blocks of proteins correctly due to a mutation to the CBS gene. This mutation causes the amino acid homocystine not to be used properly thus high levels build up in the blood, damaging the endothelial tissue and increasing the likelihood of RVT

The most common cause of RVT in infants is dehydration. Dehydration may be caused by reduction in both volume and circulatory blood volume due to water depleting abnormalities like diarrhea or vomiting. The decrease in blood volume due to dehydration will cause blood flow to be diverted away from the kidneys to other organs, resulting in slower blood flow to the kidneys, increasing chances of a blood clot occurrence. "RVT is known to occur in the absence of clinically obvious shock e.g. following neonatal distress and placement of central venous catheters." RVT can also be induced by post transplant distortion or physical distortion or compression of the renal vein, which depending on the shape distortion can affect the rate of flow through the vein.

Best regards,
John Mathews
Editorial Assistant
Journal of Phlebology and Lymphology