Mesoaortic compression of the left renal vein (nutcracker syndrome): case reports and review of the literature.

Compression of the left renal vein between the aorta and the superior mesenteric artery has been termed the nutcracker syndrome. Obstruction of left renal vein outflow results in venous hypertension with the formation of intra- and extrarenal collaterals and/or the development of gonadal vein reflux. To date, a variety of clinical symptoms due to mesoaortic compression of the left renal vein (nutcracker syndrome) have been described. It is not known what pathophysiological variables play a role in the different clinical manifestations of nutcracker syndrome. We report two patients representing the two different forms of the condition. In the first, hematuria and left flank pain resolved in a young man after successful renocaval reimplantation. In the second, symptoms of pelvic congestion due to pelvic varices improved in a middle-aged woman after successful embolization of the gonadal vein and pelvic collaterals. This report reviews the pathophysiology, presentation, diagnosis including radiographic findings, management options, as well as the current literature on nutcracker syndrome.

Reduced protease inhibitory capacity in patients with abdominal aortic aneurysms is reversed with surgical repair.

BACKGROUND: Abdominal aortic aneurysm (AAA) disease is a complex degenerative process that is associated with elevated proteolytic activity. This increased proteolytic activity may be linked to an imbalance in the protease regulatory mechanisms. We hypothesize that reduced AAA plasma inhibitory capacity is related to increased elastolytic activity observed in patients with AAA, which promotes matrix degradation in the aortic wall and AAA expansion. METHODS: Preoperative plasma from patients with AAA (n = 86; mean age, 75 +/- 8 years) and healthy controls (n = 30; mean age, 72 +/- 10 years) was assayed for inhibitory capacity. Postoperative plasma inhibitory capacity was evaluated with comparison of the activity of porcine pancreatic elastase on succinylated elastin substrate, in the presence and absence of AAA and control plasma. RESULTS: AAA plasma showed a significantly reduced capacity to inhibit porcine pancreatic elastase (71.31% +/- 1.47%) compared with control plasma (85.52% +/- 1.70%; P <.001). Within the AAA group, the inhibitory capacity increased with AAA diameter (P <.05). In addition, surgical repair of AAA resulted in a significant increase in plasma inhibitory capacity (79.83% +/- 1.86%) as compared with preoperative levels (63.98% +/- 2.69%; P <.001). Of note, the postoperative plasma inhibitory capacity is not significantly different than that of control. CONCLUSION: AAA plasma has a significantly reduced inhibitory capacity, which varies with aortic diameter and returns to control levels after surgical repair of the AAA. This suggests that protease regulation is a dynamic balance that changes with AAA progression and may play an important role in AAA progression.