Hypercoagulability, Intraglomerular Coagulation, and Thromboembolism in Nephrotic Syndrome

Sagripanti, A; Barsotti, Giovanni

doi:10.1159/000188604

Cited by 52 publications

(41 citation statements)

References 68 publications

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“…1 These conditions result, most probably, from the conjunction of hypoalbuminemia and hyperlipemia with several changes in blood coagulation, fibrinolysis, and platelet functions. 5,51 Marked lipid abnormalities, such as elevation of lipoproteins containing apo B, ie, VLDL, LDL, and Lp(a), have been previously reported 52 and were confirmed by results of the present studies. Nephrotic children have significantly higher plasma concentrations of Lp(a) than do healthy children 14,15,[53][54][55][56] ; these high levels of Lp(a) are an abnormality currently considered to be an independent risk factor for the development of cardiovascular disease in the general population.…”

Section: Discussionsupporting

confidence: 91%

Effect of Individual Plasma Lipoprotein(a) Variations In Vivo on Its Competition With Plasminogen for Fibrin and Cell Binding

Soulat

Loyau

Baudouin

et al. 2000

ATVB

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Abstract-Simultaneous natural changes in lipoprotein(a) [Lp(a)] and plasminogen occur in the nephrotic syndrome and offer a unique opportunity to investigate their effects on plasminogen activation under conditions fashioned in vivo. Plasminogen, Lp(a), and apolipoprotein(a) in plasma were characterized, and their competitive binding to carboxyterminal lysine residues of fibrin and cell membrane proteins was determined in nephrotic children during a flare-up of the disease (61 cases) and after 6 weeks (33 cases) and 6 months (42 cases) of remission. Low plasminogen concentrations (median 1.34 mol/L, range 0.39 to 1.96 mol/L) and high Lp(a) levels (median 0.27 g/L, range 0.07 to 2.57 g/L) were detected at flare-up. These changes were associated with an increased Lp(a) binding ratio onto fibrin (3.13Ϯ0.48) and cells (1.53Ϯ0.24) compared with binding ratios of control children (1.31Ϯ0.19 and 1.05Ϯ0.07, respectively) with normal plasminogen and low Lp(a) (median 0.071 g/L). After 6 weeks and 6 months of remission, the values for net decrease in Lp(a) binding to fibrin were 1.7Ϯ0.22 (after 6 weeks) and 1.88Ϯ0.38 (after 6 months) and were correlated with low Lp(a) concentrations (median 0.2 g/L, range 0.07 to 0.8 g/L; and median 0.12 g/L, range 0.07 to 1.34 g/L) and inversely associated with increased plasminogen levels (median 1.82 mol/L, range 1.4 to 2.1 mol/L; and median 1.58 mol/L, range 1.1 to 2.1 mol/L). These studies provide the first quantitative evidence that binding of Lp(a) to lysine residues of fibrin and cell surfaces is directly related to circulating levels of both plasminogen and Lp(a) and that these glycoproteins may interact as competitive ligands for these biological surfaces in vivo. This mechanism may be of relevance to the atherothrombotic role of Lp(a), particularly in nephrotic patients.

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Section: Discussionsupporting

confidence: 91%

Effect of Individual Plasma Lipoprotein(a) Variations In Vivo on Its Competition With Plasminogen for Fibrin and Cell Binding

Soulat

Loyau

Baudouin

et al. 2000

ATVB

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“…SVT has been associated with left-sided PH in non-cirrhotic subjects [24] . Therefore, acenocumarol may have exerted an additive portal hypotensive effect in our patient by restoring SVT, possibly related to PTHR A20210 mutation [25] or NS per se [26] . Renal vein thrombosis [26] or spontaneous splenorenal shunt [27] , which might have been involved in the development and progress of IgAN in our patient, were not confirmed by computed tomography and venography.…”

Section: Discussionmentioning

confidence: 99%

Association of liver cirrhosis related IgA nephropathy with portal hypertension

Kalambokis

Christou²,

Stefanou³

et al. 2007

WJG

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A high incidence of IgA nephropathy has been reported in patients with liver cirrhosis, though, clinically evident nephrotic syndrome is very uncommon. Impaired hepatic clearance of circulating IgA immune complexes and subsequent deposition in renal glomeruli has been considered principally in the pathogenesis of liver cirrhosis associated IgA nephropathy. Here we report on a patient with cryptogenic liver cirrhosis and splenic vein thrombosis, who presented with nephrotic syndrome. Renal biopsy showed findings consistent with IgA nephropathy. Lower endoscopy showed features of portal hypertensive colopathy. Following initiation of propranolol and anticoagulant treatment to reduce portal pressure, a gradual decrease of proteinuria and hematuria to normal range was noted. The potential p a t h o g e n e t i c ro l e o f p o r t a l hy p e r t e n s i o n i n t h e development of IgA nephropathy in cirrhotic patients is discussed.

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“…1,2 In the ensuing half-century, VTE rates ranging from 2% in children to as high as 42% in adults [3][4][5][6] and a relative risk of ATE ranging from 1 to 5.5 have been reported in these patients. 7,8 Whereas NS resulting from membranous glomerulopathy has been correlated with an exceptionally high risk of VTE, especially renal vein thrombosis, 9,10 likewise correlations have not been described for ATE.…”

mentioning

confidence: 99%

High Absolute Risks and Predictors of Venous and Arterial Thromboembolic Events in Patients With Nephrotic Syndrome

et al. 2008

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Background-No data are available on the absolute risk of either venous thromboembolism (VTE) or arterial thromboembolism (ATE) in patients with nephrotic syndrome. Reported risks are based on multiple case reports and small studies with mostly short-term follow-up. We assessed the absolute risk of VTE and ATE in a large, single-center, retrospective cohort study and attempted to identify predictive factors in these patients. Methods and Results-A total of 298 consecutive patients with nephrotic syndrome (59% men; mean age, 42Ϯ18 years)were enrolled. Mean follow-up was 10Ϯ9 years. Nephrotic syndrome was defined by proteinuria Ն3.5 g/d, and patients were classified according to underlying histological lesions accounting for nephrotic syndrome. Objectively verified symptomatic thromboembolic events were the primary study outcome. Annual incidences of VTE and ATE were 1.02% (95% confidence interval, 0.68 to 1.46) and 1.48% (95% confidence interval, 1.07 to 1.99), respectively. Over the first 6 months of follow-up, these rates were 9.85% and 5.52%, respectively. Proteinuria and serum albumin levels tended to be related to VTE; however, only the predictive value of the ratio of proteinuria to serum albumin was significant (hazard ratio, 5.6; 95% confidence interval, 1.2 to 26.2; Pϭ0.03). In contrast, neither the degree of proteinuria nor serum albumin levels were related to ATE. Sex, age, hypertension, diabetes, smoking, prior ATE, and estimated glomerular filtration rate predicted ATE (PՅ0.02). Conclusions-This study verifies high absolute risks of symptomatic VTE and ATE that were remarkably elevated within the first 6 months. Whereas the ratio of proteinuria to serum albumin predicted VTE, estimated glomerular filtration rate and multiple classic risk factors for atherosclerosis were predictors of ATE. (Circulation. 2008;117: 224-230.)

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Hypercoagulability, Intraglomerular Coagulation, and Thromboembolism in Nephrotic Syndrome

Cited by 52 publications

References 68 publications

Effect of Individual Plasma Lipoprotein(a) Variations In Vivo on Its Competition With Plasminogen for Fibrin and Cell Binding

Effect of Individual Plasma Lipoprotein(a) Variations In Vivo on Its Competition With Plasminogen for Fibrin and Cell Binding

Association of liver cirrhosis related IgA nephropathy with portal hypertension

High Absolute Risks and Predictors of Venous and Arterial Thromboembolic Events in Patients With Nephrotic Syndrome

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