++
Diseases of the renal veins, as with other diseases of the venous system, tend to be forgotten in the study of both renal disease and peripheral vascular disease. The full functional impact of renal venous disease remains to be established; however, adequate experience with anatomic derangements in the renal venous system has led to some appreciation of the importance of the "passive" side of renal circulation. As a part of the deep venous system, the renal veins may suffer from thrombosis in a similar fashion as other manifestations of venothromboembolic disease. Renal venous thrombosis, however, is the predominant primary disease of the renal veins. The other syndromes—renal venous tumors, renal vein entrapment, and renal arteriovenous malformations (AVMs)—result more from the anatomic environment the renal veins are surrounded by (i.e., in these disease processes, the renal veins tend to be injured as bystanders in local pathology). Finally, increasing interest is developing on functional disease of the renal venous system, primarily in the form of renal venous congestion.
+++
RENAL VEIN THROMBOSIS
++
As with all deep veins, the renal venous system is at risk for the formation of luminal thrombus, the syndrome known as renal vein thrombosis (RVT) (Table 25-1). Although similar to deep venous thrombosis (DVT) in other circulatory beds with regard to risk factors, pathophysiology, diagnosis, and, even treatment, unique aspects of RVT are present. The renal vein's intrinsic connection to a vital organ subject to specific injuries related to hemodynamic, immunologic, and physiologic derangements, makes RVT is distinct from other DVTs in certain aspects. Specifically, RVT carries a higher risk in selected patient populations with underlying disease states, requires a higher index of suspicion given the absence of physical examination clues to its presence, and requires specific treatment at underlying risk factors for its development to not only preserve vital organ function but also to prevent extension of existing thrombosis and recurrence of thrombotic events.
++
++
The development of RVT requires the pathologic environment shared by all sites of DVT; one or more elements of Virchow's triad—low blood flow (stasis), hypercoagulable state and/or vascular injury. Although occasionally only a single ...