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Renal Disease; Fluid and Electrolyte Disorders
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
The most common cause of renal vein thrombosis is the nephrotic syndrome, which predisposes to venous thrombosis, but renal vein thrombosis can arise from other risk factors for venous thromboembolism.
Urinary system
Published in A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha, Clark’s Procedures in Diagnostic Imaging: A System-Based Approach, 2020
A Stewart Whitley, Jan Dodgeon, Angela Meadows, Jane Cullingworth, Ken Holmes, Marcus Jackson, Graham Hoadley, Randeep Kumar Kulshrestha
MRI is also the gold standard for assessing renal vein thrombosis along with renal venography and CT. MRI can be used in the assessment of suspected renal cell carcinoma, where CT and ultrasound are non-diagnostic or where radiographic contrast is contraindicated.
Acquired Bleeding Disorders Associated with Disease and Medications
Published in Harold R. Schumacher, William A. Rock, Sanford A. Stass, Handbook of Hematologic Pathology, 2019
William A. Rock, Sue D. Walker
b. Nephrotic Syndrome. In nephrotic syndrome the renal tubules cease to function, resulting in the urinary loss of AT-III, F IX, factor XII, and prekallikrein (64). Patients present with thrombosis but rarely with bleeding. Renal vein thrombosis, lower-extremity deep vein thrombosis, pulmonary embolus, stroke, and acute myocardial infarction do occur, but the exact mechanism has not been well defined. Treatment with anticoagulants may be required and may result in a risk for bleeding.
Comparison of the prophylactic antithrombotic effect of indobufen and warfarin in patients with nephrotic syndrome: a randomized controlled trial
Published in Renal Failure, 2023
Xin-Yi Gao, Yue-Ming Liu, Dan-Na Zheng, Yi-Wen Li, Hua Li, Xiao-Ling Xiong, Hong-Yu Chen, Hua Wang, Xiao-Yong Yu, Kai Qu, Juan Jin, Bo Lin, Qiang He
The primary outcomes were the incidence rates of thrombosis and bleeding. Thromboembolic events were confirmed by ultrasound (for deep vein thrombosis), renal magnetic resonance venography (for renal vein thrombosis), or computed tomography pulmonary ventilation-perfusion scan (for pulmonary embolism). Major bleeding referred to any of the following: fatal bleeding, two symptomatic bleeding events at a critical site, bleeding causing the Hb level to drop by ≥ 20 g/L (1.24 mmol/L), or bleeding requiring the transfusion of two or more units of whole blood or red blood cells [15]. Minor bleeding events were defined as bleeding not meeting the criteria for major bleeding but associated with medical intervention; contact with a physician; interruption of the study drug; or discomfort/impairment in performing daily activities, including gastrointestinal bleeding, nasal bleeding, subcutaneous hemorrhage, fundus bleeding, and non-glomerular origin hematuria. The secondary outcome was coagulation function (APTT, PT, TT, and D-dimer). In group C, INR values were also collected. The incidences of AEs and SAEs were recorded from the initial treatment until the final follow-up visit. AEs were summarized using the MedDRA system organ class and the preferred term. An independent data monitoring committee reviewed the cumulative safety data.
The forgotten urinalysis: an integral part of unmasking thrombophilia
Published in Journal of Community Hospital Internal Medicine Perspectives, 2019
Marvi Qureshi, Fortune Alabi, Francis Christian, Claudia Romero
In general, thromboses of abdominal veins that are outside the iliac-caval axis are not common, but when such thromboses do occur they are clinically relevant [16]. Renal vein thrombosis has been shown to have numerous etiologies, but one of the most common causes has been shown to be nephrotic syndrome [1]. Renal vein thrombosis has been shown in many accounts to have an association with membranous glomerulopathy mainly, but less frequently in other forms of glomerulopathy such as membranoproliferative [8]. Thromboembolic consequences are more likely when the underlying nephrotic syndrome is taking place due to membranous nephropathy. The exact pathogenic mechanism of this association is not known, but it has been well established that the hypercoagulable state produced by nephrotic syndrome further increases the risk of renal vein thrombosis [8]. Specific reasons as to why the renal vein is more susceptible to thrombosis is unclear [1]. In fact, though the thromboembolic consequences of nephrotic syndrome can involve both the venous and arterial sides of the systemic circulation, it is has been found that arterial thrombosis is a less common occurrence than venous thrombosis, but the exact reasoning behind this as well is unknown [4].
Budd Chiari syndrome associated with AL amyloidosis: a coagulation paradox
Published in Amyloid, 2018
Guilherme Grossi Lopes Cançado, Luciana Costa Faria, Fernanda Maria Farage Osório, Paula Vieira Teixeira Vidigal, Cláudia Alves Couto, Teresa Cristina de Abreu Ferrari
To our knowledge this is the first case of AL amyloidosis complicated with BCS. Increased bleeding is a recognized complication of amyloidosis, which is frequently associated with amyloid infiltration of blood vessels, reduced activity of factor X, impaired synthesis of clotting factors due to amyloid liver involvement, and enhanced fibrinolytic activity [3]. On the other hand, plasma cell dyscrasias can also present with thrombotic rather than haemorrhagic manifestations, or even both in the same patient. Impairment of the thrombin-antithrombin pathway, in association with the low antithrombin biological activity, was recognized as a possible pathogenic player in the paradox of coagulation observed in amyloidoisis patients [3]. In our case, the patient presented both haemorrhagic and thrombotic tendencies. Paliard et al. [4] described a similar case BCS in a patient with secondary hepatic and intestinal amyloidosis presenting with thrombosis of inferior vena cava. Tsuji et al. [5] also observed the BCS in a woman with multiple myeloma. The thrombotic tendency in amyloidosis was suggested by Srkalovic et al., who showed an increased incidence of venous thromboembolism (11% at 10 years review) in these patients as compared to the general population [6]. The loss of haemostatic proteins due to nephrotic syndrome certainly contributed to the imbalance between clotting factors and inhibitors observed in our patient. It is well known that the incidence of both venous and arterial thrombosis are much higher in patients with nephrotic syndrome compared with estimates in general population, particularly deep vein and renal vein thrombosis [7]. The involvement of several factors has been reported, such as the alteration of coagulation factors, increased fibrinogen concentration, defects in the fibrinolytic system, platelet dysfunction, increased blood viscosity and co-administration of diuretics and steroids [7]. On the other hand, acquired factor X deficiency has been described as the most common coagulation factor deficiency in patients with AL amyloidosis complicating with unexpected bleeding [8].