Evaluating Proteinuria and Nephrotic Syndrome in Patients With Venous Thromboembolism

Htike, Naing; Superdock, Keith; Teehan, Geoffrey; Thiruveedi, Sampath; Surkis, William

doi:10.1097/maj.0b013e318223b95c

Cited by 7 publications

(8 citation statements)

References 14 publications

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“…The results suggest that KC cells introduce mucinous substances, such as CA125 and CEA, into the bloodstream to induce a hypercoagulable state, which in turn leads to embolic stroke. In addition, previous studies have shown that many types of chronic kidney disease are associated with increased proteinuria and venous thromboembolism [24,25]. Severe proteinuria was not only found to be an independent risk factor for stroke, but was also an independent predictive factor for a poor prognosis of stroke [26–28].…”

Section: Discussionmentioning

confidence: 99%

Potential Pathogenesis and Biomarkers of Kidney Cancer-Related Stroke

et al. 2017

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BackgroundStroke risk and stroke recurrence are increased in cancer patients, but the pathogenesis and biomarkers of kidney cancer-related stroke (KCS) are generally unclear. The aim of the present research was to investigate the pathogenesis and plasma biomarkers of kidney cancer-related stroke.Material/MethodsA retrospective review was conducted on acute stroke patients with kidney cancer (KC) who were admitted to the hospital between January 2006 and December 2015. A total of 106 patients with KCS (active KC patients with acute stroke but without conventional vascular risks) were identified. In addition, 106 age- and sex-matched patients with KC alone were recruited.ResultsKCS patients had higher plasma D-dimer, cancer antigen (CA) 125, and CEA levels and greater proteinuria levels than did KC patients. Multiple logistic regression analysis showed that the risk of stroke in patients with KC increased independently by 0.8% (odds ratio [OR] 1.008; 95% confidence interval [CI] 1.002, 1.013; p=0.004) with a 1 ng/mL increase in D-dimer levels, by 1.2% (OR 1.012; 95% CI 1.007, 1.018; p=0.000) with a 1 U/mL increase in CA125, by 2.5% (OR 1.025; 95% CI 1.012, 1.038; p=0.000) with a 1 U/mL increase in CEA by 1.4% (OR 1.014; 95% CI 1.005, 1.024; p=0.004) with a 1 mg increase in urine protein in 24 hours.ConclusionsElevated plasma D-dimer, CA125 and CEA levels, and increased urine protein levels might lead to hypercoagulability and then KCS; however, they may also be biomarkers of KCS.

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Section: Discussionmentioning

confidence: 99%

Potential Pathogenesis and Biomarkers of Kidney Cancer-Related Stroke

et al. 2017

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“…This may be partly explained by a reduction of thrombotic risk in patients who enter remission - 72% of our cohort achieved at least transient remission. Thirty-three percent of those who had VTE experienced it as part of their NS presentation highlighting the importance of checking for NS in patients who present with VTE [13]. …”

Section: Discussionmentioning

confidence: 99%

Venous Thromboembolism in Primary Nephrotic Syndrome - Is the Risk High Enough to Justify Prophylactic Anticoagulation?

Rankin

McQuarrie²,

Fox³

et al. 2016

Nephron

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Background: The reported incidence of venous thromboembolism (VTE) in patients with nephrotic syndrome (NS) varies widely, as does the approach to prophylactic anticoagulation. We aimed to assess the incidence of VTE in patients with primary NS in order to inform a sample size calculation to determine if a future clinical trial will ever be feasible. Methods: All adults undergoing native renal biopsy for NS between 2008 and 2013 yielding a diagnosis of primary glomerulonephritis were identified. Baseline serum albumin, urine protein:creatinine ratio, estimated glomerular filtration rate, date of biopsy and histological diagnosis were recorded. Episodes of objectively verified VTE were identified using the electronic patient record. Sample size calculations were performed based on 2 independent samples with a dichotomous outcome and to achieve a power of 80% and p < 0.05. Results: Two hundred six patients were included of which 60% were male and mean age at biopsy was 55 years (SD 19). Median follow-up was 2.9 years (interquartile range (IQR) 1.6-4.7). Fourteen (6.8%) patients suffered VTE. Median time to diagnosis of VTE from renal biopsy was 36 days (IQR -22 to 178), with 6 VTEs occurring prior to biopsy and 1 during remission. In a total of 270 patient years of NS, there were 7 VTE that could potentially have been avoided if anticoagulation was given for the duration of NS, that is, 2.6% risk per year of NS; this risk was highest for patients with minimal change nephropathy at 13.3% per year of NS, compared to 0.65% per year of NS for those with idiopathic membranous nephropathy. Assuming a 75% reduction in the incidence of VTE with prophylactic anticoagulation, 972 participants would be required for a future clinical trial to have 80% power. Conclusions: Patients with primary NS are at an increased risk of VTE. The timing of VTE means that only half of episodes would be targeted by prophylactic anticoagulation. Given the low frequency of events, a well-powered clinical trial would be challenging to achieve.

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“…In both pediatric and adult studies, worsening proteinuria is directly correlated with increasing VTE probability [9, 40]. In fact, even sub-nephrotic proteinuria has been identified as a prothrombotic risk marker [41–43]. Hypoalbuminemia, which is closely correlated to proteinuria severity, has been identified as an additional significant VTE risk marker in some adult studies [44, 45], but not in all [40], and was reported not to be a significant marker in a recent large pediatric cohort [9].…”

Section: Risk Stratification and Diagnostic Approachmentioning

confidence: 99%

Venous thromboembolism in pediatric nephrotic syndrome

2013

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Childhood nephrotic syndrome (NS) is one of the most common pediatric kidney diseases, with an incidence of 2-7 per 100,000. Venous thromboembolism (VTE) is associated with significant morbidity and mortality, and occurs in ∼3 % of children with NS, though incidence approaches 25 % in high-risk groups. VTE etiology is multifactorial, with disease-associated coagulopathy thought to be a significant contributor. Other risks include age, disease severity, and treatment-related hazards, such as the presence of central venous catheters. Non-pharmacologic preventive measures such as ambulation and compression stockings are recommended for patients with identified VTE risks. Central venous catheters should be avoided whenever possible. Symptoms of VTE include venous catheter dysfunction, unilateral extremity symptoms, respiratory compromise, flank pain, and gross hematuria. When VTE is suspected, confirmatory imaging studies should be obtained, followed by appropriate laboratory evaluation and treatment. Therapeutic goals include limiting thrombus growth, extension, and embolization by early institution of anticoagulant therapy. Anticoagulation is recommended for a minimum of 3 months, but should be continued until NS remission is achieved. Further studies are necessary to identify VTE-risk biomarkers and optimal therapeutic regimens. Observational cohort studies are needed to identify VTE-risk groups who may benefit from thromboprophylaxis and to define disease-specific treatment algorithms.

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Evaluating Proteinuria and Nephrotic Syndrome in Patients With Venous Thromboembolism

Cited by 7 publications

References 14 publications

Potential Pathogenesis and Biomarkers of Kidney Cancer-Related Stroke

Potential Pathogenesis and Biomarkers of Kidney Cancer-Related Stroke

Venous Thromboembolism in Primary Nephrotic Syndrome - Is the Risk High Enough to Justify Prophylactic Anticoagulation?

Venous thromboembolism in pediatric nephrotic syndrome

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