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Open central and peripheral venous reconstructionComplications and strategies for managing these complications
Published in Sachinder Singh Hans, Mark F. Conrad, Vascular and Endovascular Complications, 2021
Gloria Y. Kim, Dawn M. Coleman, Thomas W. Wakefield
Nutcracker syndrome (NS) describes a phenomenon that occurs when the left renal vein is compressed between the aorta and the superior mesenteric artery (SMA). Posterior nutcracker syndrome is another variant of this condition, which occurs when a retro aortic left renal vein is compressed between the aorta and the vertebral body. The prevalence of nutcracker syndrome is unknown, but is thought to be a rare entity as much of the literature is composed of case reports and small case series.8 This syndrome may present without clinical symptoms and signs, and in these cases, it is considered a normal anatomic variant. If the syndrome is associated with signs and symptoms, most commonly hematuria, it is thought to be secondary to left renal venous congestion. It is hypothesized that the increased intraluminal pressure within the left renal vein contributes to the development of hilar varices around the renal pelvis and ureter, and the rupture of the thin-walled veins within the collecting system lead to both macroscopic and microscopic hematuria.22 The most common symptom associated with this syndrome is flank pain, with other less common signs and symptoms of renal venous hypertension including orthostatic proteinuria, pain of the left flank or the left upper quadrant of the abdomen, left-sided varicocele, and fatigue.9,23
Venous compression syndromes
Published in Ken Myers, Paul Hannah, Marcus Cremonese, Lourens Bester, Phil Bekhor, Attilio Cavezzi, Marianne de Maeseneer, Greg Goodman, David Jenkins, Herman Lee, Adrian Lim, David Mitchell, Nick Morrison, Andrew Nicolaides, Hugo Partsch, Tony Penington, Neil Piller, Stefania Roberts, Greg Seeley, Paul Thibault, Steve Yelland, Manual of Venous and Lymphatic Diseases, 2017
Ken Myers, Paul Hannah, Marcus Cremonese, Lourens Bester, Phil Bekhor, Attilio Cavezzi, Marianne de Maeseneer, Greg Goodman, David Jenkins, Herman Lee, Adrian Lim, David Mitchell, Nick Morrison, Andrew Nicolaides, Hugo Partsch, Tony Penington, Neil Piller, Stefania Roberts, Greg Seeley, Paul Thibault, Steve Yelland
The typical nutcracker syndrome (renal vein entrapment syndrome) results from compression of the left renal vein between the aorta and superior mesenteric artery, sometimes referred to as the anterior nutcracker (Figure 16.2).2 Less frequently, the left renal vein is compressed by the third part of the duodenum. A retro-aortic or circum-aortic renal vein can be compressed between the aorta and vertebral body, referred to as the posterior nutcracker. The left renal vein can be compressed by a pancreatic tumour, retroperitoneal tumour or fibrosis, or para-aortic lymphadenopathy. Predisposing factors may be renal ptosis, abnormal high course of the left renal vein or abnormal origin of the superior mesenteric artery. This causes collateral pathways to open to drain the left kidney with partially obstructed or reversed flow in the left renal vein.
Computed tomography and magnetic resonance imaging in venous disease
Published in Peter Gloviczki, Michael C. Dalsing, Bo Eklöf, Fedor Lurie, Thomas W. Wakefield, Monika L. Gloviczki, Handbook of Venous and Lymphatic Disorders, 2017
Terri J. Vrtiska, James F. Glockner
Nutcracker syndrome describes compression of the left renal vein between the abdominal aorta and superior mesenteric artery, with resultant development of venous varicosities adjacent to the left kidney and ureter and dilatation of the left gonadal vein (Figure 16.36). Demonstration of these findings is most easily accomplished with coronal CE MRA/MRV.
The Vici venous stent for treatment of renal vein entrapment
Published in Baylor University Medical Center Proceedings, 2021
Alex T. Cubberley, Mohanad Hamandi, Courtney Rawitscher, Karim Al-Azizi, Sameh Sayfo, Srinivasa Potluri, Phillip A. Morales, Javier Vasquez, Chadi Dib
The nutcracker syndrome (NCS) is an uncommon vascular anomaly that results from compression of the left renal vein between the superior mesenteric artery and the aorta.1 Patients with NCS usually present with pelvic pain, flank pain, hematuria, gonadal varices, or proteinuria.2,3 Some studies have reported pelvic congestion syndrome and ovarian vein reflux in up to 30% of women who are completely asymptomatic.3 The diagnosis and treatment of NCS is important, as it is associated with an increased risk of chronic kidney disease from long-term left renal vein hypertension, proteinuria, and left renal vein thrombosis.2 Management varies depending on the severity of symptoms, from conservative therapy to endovascular or open surgery.3 We present a 37-year-old woman with severe debilitating left flank and abdominal pain due to NCS. To our knowledge, this is the first reported case of symptomatic left renal vein compression treated with the new Vici stent system.
Surgical aspects of venous pelvic pain treatment
Published in Current Medical Research and Opinion, 2019
S. G. Gavrilov, O. I. Efremova
Aorto-mesenteric compression of the left renal vein (the nutcracker syndrome) is the top second anatomical cause of vein dilation and blood reflux in the left gonadal vein. This syndrome develops when the superior mesenteric artery extends inferiorly at an acute angle with the aorta, causing compression of the left renal vein, which results in the occurrence of left-sided renal phlebohypertension and, eventually, valvular incompetence and dilation of the gonadal and parametrial veins, i.e. PCS development. According to various authors, aorto-mesenteric compression of the left renal vein with pre-stenotic dilation of the vessel by more than 50% was found in 30–40% of studied patients, and the nutcracker syndrome is observed in 15–17% of patients with VPP10. According to White and Holdstock, in some cases duplex ultrasound angioscanning reveals pseudo-nutcracker syndrome caused by a siphon effect of left ovarian vein reflux, rather than true anatomical pathology11. Another syndrome to note is uretero-ovarian conflict, known as right gonadal vein syndrome (RGVS), which occurs due to compression of the right ureter by the dilated unilateral ovarian vein. RGVS was first described by Clark in 1964, who published an analysis of 129 such patients12. He suggested that, during pregnancy, the aberrant right gonadal vein can squeeze the ureter, causing symptoms of ureteral obstruction that persist after delivery. This leads to disruption of the normal passage of urine, the occurrence of signs of urinary infection and the development of chronic pyelonephritis.
Glomerular endothelial expression of type I IFN-stimulated gene, DExD/H-Box helicase 60 via toll-like receptor 3 signaling: possible involvement in the pathogenesis of lupus nephritis
Published in Renal Failure, 2022
Takao Karasawa, Riko Sato, Tadaatsu Imaizumi, Shun Hashimoto, Masashi Fujita, Tomomi Aizawa, Koji Tsugawa, Shogo Kawaguchi, Kazuhiko Seya, Kiminori Terui, Hiroshi Tanaka
Biopsy specimens were obtained during routine diagnostic procedures in clinical practice. In this study, we chose snapped frozen sections, stored in good condition. We performed DDX60 staining for specimens from patients with diffuse proliferative LN [n = 3, Class IV-G (A) in accordance with the International Society of Nephrology/Renal Pathology Society (ISN/RPS) 2003 classification for LN], non-proliferative LN (n = 3, Class II), proteinuric IgA nephropathy (IgAN, n = 3; defined as urinary protein/creatinine ratio greater than 1.0), and nutcracker syndrome (n = 1, as a non-inflammatory control) were stained for DDX60. These biopsy specimens were obtained from the patients before treatment initiation. Because nutcracker syndrome usually presents no inflammation in the kidney, we used this specimen as non-inflammatory control. The OCT-embedded specimens were cut into 5-μm-thick sections using a cryostat, briefly fixed in cold acetone, and air-dried. Sections were transferred to slides, and the slides were washed in phosphate-buffered saline (PBS) (pH 7.4) immediately before the immunohistochemical procedure. Rabbit anti-DDX60 antibody was added at a dilution of 1:1000. After incubation for 60 min at room temperature, the slides were washed in PBS and incubated with fluorescein isothiocyanate (FITC)-conjugated secondary antibody at a dilution of 1:200 for 60 min at room temperature. To examine the localization of the DDX60 expressing cell, we performed a dual-labeling immunofluorescence study with anti-rabbit DDX60 antibody (1:1000) and anti-mouse CD34 antibody (Nichirei Bioscience, Tokyo, Japan, undiluted) as a marker of endothelial cells. The secondary antibodies used for the double-staining study were Alexa fluor 594 conjugated anti-mouse IgG (1:200) and FITC conjugated anti-rabbit IgG (1:200).