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ANATOMICAL CONFIGURATION AND PATHOPHYSIOLOGY
LRV entrapment divided into 2 types: anterior and posterior. Anterior NCS is the compression of a normally situated LRV by the abdominal aorta and the superior mesenteric artery (Figure 1). Posterior NCS is rare. It is presented with retroaortic LRV compressed usually between abdominal aorta and vertebral column. Other uncommon causes such as pancreatic neoplasm, paraaortic lymphadenopathy, retroperitoneal tumor, abdominal aortic aneurysm, overarching testicular artery, LRV duplication, and ectopic ventral right renal artery and strangulating fibrolymphatic tissue may play a role on the etiology of posterior NCS. Left renal ptosis, lordosis and decreased retroperitoneal and mesenteric fat tissue may cause to NCS[1-3].
Right-sided NCS is a more rare condition. Pregnancy is defining as a factor contributing to right-sided NCS by compression of large veins[1]. Left-sided IVC, hemiazygos continuation and persistent left superior vena cava combination is another rare cause of right NCS[4].
All of the anatomic mechanisms involved in renal vein compression are resulting with outflow obstruction leads to LRV hypertension with a measurable renocaval pressure gradient. The normal pressure gradient between the distal renal vein and IVC is < 1 mmHg. A renocaval pullback pressure gradient of ≥ 2 mmHg is highly suggestive of a nutcracker phenomenon[5]. LRV hypertension is the underlying mechanism which may result in formation of varices and collaterals. Venous sinuses in the neighboring of renal calyces were taken in form by these varices and collaterals. Hematuria and proteinuria are the results of these venous sinuses[6].
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