Neonatal renal vein thrombosis (RVT) is associated with potentially serious morbidities. Almost 80% of cases
of RVT present within the first postnatal month. The most common risk factors for RVT are birth asphyxia/ in utero fetal
distress, being the infant of a diabetic mother, volume contraction and coagulation abnormalities. Thrombus formation
may be initiated by vascular injury, diminished vascular flow, increased blood viscosity, hyperosmolality or underlying
thrombophilia. The classic triad of RVT includes gross hematuria, flank mass (unilateral or bilateral enlargement of kidneys)
and thrombocytopenia. Laboratory tests may reveal hematuria, proteinuria, polycythemia, hemolytic anemia,
thrombocytopenia and possibly acute kidney injury. The etiology for a hypercoagulable state should be investigated. Renal
ultrasound with Doppler may show increased size of the affected kidney, increased echogenicity and loss of corticomedullary
differentiation. Renal venography remains the gold standard for the diagnosis of RVT. Other causes of renal
enlargement must be considered. Supportive treatment includes correction of fluid and electrolyte disturbances and treatment
of infection and underlying pathophysiologic abnormalities. Use of unfractionated heparin (UFH) or low molecular
weight heparin (LMWH) should be considered if there is evidence of disseminated intravascular coagulation. Conventional
anticoagulants may attenuate hypercoagulability and decrease the risk for thrombus progression and embolism.
Surgery is rarely indicated unless there is bilateral involvement with involvement of the IVC. RVT carries the risk of hypertension
and chronic kidney disease.