Sunday, May 21, 2017

Renal vein thrombosis

Clotting in the renal vein results in renal congestion, engorgement and, possibly, infarction. Renal vein thrombosis may affect both kidneys and may occur in an acute or a chronic form.
Chronic thrombosis usually impairs renal function, causing nephrotic syndrome. Abrupt onset of thrombosis that causes extensive damage may precipitate rapidly fatal renal infarction.
If thrombosis affects both kidneys, the prognosis is poor. However, less-severe thrombosis that affects only one kidney or gradual progression that allows development of collateral circulation may preserve partial renal function.

Renal vein thrombosis results from trauma to the abdomen or back, stricture (scar formation), or a tumor that obstructs the renal vein (usually hypernephroma).
Other causes include thrombophlebitis of the inferior vena cava (may result from abdominal trauma) or blood vessels of the legs, heart failure, and periarteritis. In infants, renal vein thrombosis usually follows diarrhea that causes severe dehydration.
Chronic renal vein thrombosis is a common complication of other glomerulopathic diseases, such as amyloidosis, systemic lupus erythematosus, diabetic nephropathy, and membranoproliferative glomerulonephritis.

Signs and symptoms
Signs and symptoms of renal vein thrombosis vary with the speed of onset.

Rapid onset of venous obstruction produces severe lumbar pain and tenderness in the epigastric region and the costovertebral angle. Other characteristic features include fever, leukocytosis, pallor, hematuria, proteinuria, peripheral edema and, when the obstruction is bilateral, oliguria and other uremic signs. The kidneys enlarge and become easily palpable. Hypertension is unusual but may develop.
Gradual onset causes symptoms of nephrotic syndrome. Peripheral edema is possible, but pain is generally absent. Other signs include proteinuria, hypoalbuminemia, and hyperlipemia.

  • Abdominal X-ray, computed tomography scan, magnetic resonance imaging, or ultrasonography shows occlusion of the renal vein.
  • Excretory urography provides reliable diagnostic evidence. With acute renal vein thrombosis, the kidneys appear enlarged and excretory function diminishes. The contrast medium seems to “smudge” necrotic renal tissue. With chronic thrombosis, ureteral indentations resulting from collateral venous channels may be present.
  • Renal arteriography and a kidney biopsy may confirm the diagnosis.
  • Urinalysis reveals gross or microscopic hematuria, proteinuria (more than 2 g/day in chronic disease), casts, and oliguria.
  • Blood studies show leukocytosis, hypoalbuminemia, and hyperlipidemia.
  • Venography confirms thrombosis.
Anticoagulant therapy may be given to prevent formation of new clots. Conservative treatment may also be ordered; the patient may be placed on bed rest or limited activity for a brief period, allowing the thrombosis to resolve over time.
Surgery must be performed within 24 hours of thrombosis, but even then it has only limited success because thrombi often extend into the small veins. Extensive intrarenal bleeding may necessitate nephrectomy.
In patients who are nephritic, reduction in proteinuria is essential; the current standard is angiotensin-converting enzyme inhibition. Patients who survive abrupt thrombosis with extensive renal damage develop nephrotic syndrome and require treatment of renal failure, such as dialysis and possible transplantation. Some infants with renal vein thrombosis recover completely after heparin therapy or surgery; others suffer irreversible kidney damage.

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