The mechanism for producing hematuria is thought to be due to increased left renal vein pressure, resulting in small venous ruptures into the collecting system or between dilated venous sinuses and adjacent renal calyces.
Other etiologic hypotheses of nutcracker syndrome include posterior renal ptosis with resultant stretching of the left renal vein over the aorta, and abnormal branching of the superior mesenteric artery from the aorta.
Although it can be invasive and uncomfortable for the patient, renal venography combined with measurement of the pressure gradient between the left renal vein and the IVC is the gold standard for demonstrating renal vein hypertension.
Doppler ultrasound measurements of the anterior-posterior (A-P) diameter and peak velocities of the left renal vein may be helpful in diagnosing nutcracker syndrome.
CT and CT angiography are other noninvasive modalities that can demonstrate compression of the left renal vein in the aortomesenteric angle and collateral veins.
A confounding factor is that distended left renal vein can be a normal variant without collateral veins and with normal pressure gradient.
Conservative management with routine urinalysis is proposed for mild hematuria, since the development of collateral veins may resolve the hypertension in the left renal vein and alleviate symptoms.