Changes of coagulation factors IX, VIII, VII, X, and V in nephrotic syndrome

Vaziri, Nosratola D.; Branson, Herman; Ness, Reid M.

doi:10.1097/00000441-198011000-00005

Cited by 53 publications

(25 citation statements)

References 9 publications

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“…[21][22][23] In addition, patients with nephrotic syndrome have decreased antithrombin levels as a result of urinary loss of antithrombin. 24 Increased levels of fibrinogen, 25,26 factor VIII, 27 factor IX, 9 factor XI, 9 and von Willebrand factor 28 have been associated with an increased risk of venous thrombosis in the general population, whereas factor VII was not associated with venous thrombosis in previous studies.…”

Section: Discussionmentioning

confidence: 99%

Role of Hemostatic Factors on the Risk of Venous Thrombosis in People With Impaired Kidney Function

et al. 2014

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Background— Factors explaining the association between impaired kidney function and venous thrombosis have not been identified so far. The aim of our study was to determine whether the association between impaired kidney function and venous thrombosis can be explained by the concurrent presence of genetic or acquired venous thrombosis risk factors. Methods and Results— The glomerular filtration rate was estimated (eGFR) in 2473 venous thrombosis patients and 2936 controls from a population-based case–control study. Kidney function was grouped into 6 categories based on percentiles of the eGFR in the controls (>50th [reference], 10th–50th, 5th–10th, 2.5th–5th, 1st–2.5th, and <1st percentile). Several hemostatic factors showed a procoagulant shift with decreasing kidney function in controls, most notably factor VIII and von Willebrand factor. Compared with eGFR >50th percentile, factor VIII levels (adjusted mean difference, 60 IU/dL for the <1st eGFR percentile category) and von Willebrand factor levels (adjusted mean difference, 60 IU/dL for the <1st eGFR percentile category) increased with each percentile category. The odds ratios for venous thrombosis similarly increased across the categories from 1.1 (95% confidence interval, 0.9–1.3) for the 10th to 50th percentile to 3.7 (95% confidence interval, 2.4–5.7) for the <1st percentile category. Adjustment for factor VIII or von Willebrand factor attenuated these odds ratios, indicating an effect of eGFR on thrombosis through these factors. Adjustments for other risk factors for venous thrombosis did not affect the odds ratios. Conclusion— Impaired kidney function affects venous thrombosis risk via concurrently raised factor VIII and von Willebrand factor levels.

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Section: Discussionmentioning

confidence: 99%

Role of Hemostatic Factors on the Risk of Venous Thrombosis in People With Impaired Kidney Function

et al. 2014

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“…[17][18][19][20]. The most frequent alterations published are: high plasma levels of CFs I [44,45], V [46,47], VII [46], VIII [46], and X [46], low plasma levels of CFs IX [48][49][50], XI [51], and XII [52.531, and decreased levels of ATIII |54| and a 2-APL [44. 55].…”

Section: Intrinsic Pathwaymentioning

confidence: 99%

Abnormalities of Coagulation in Experimental Nephrotic Syndrome

Cruz

Juárez-Nicolás

Tapia

et al. 1994

Nephron

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The human nephrotic syndrome is accompanied by important alterations of the coagulation system related proteins. The purpose of the present study was to examine the activity of coagulation- and fibrinolysis-related proteins in plasma and urine of control and puromycin aminonucleoside injected rats on days 2 (prenephrotic stage) and 10 (nephrotic stage). We measured the prothrombin time (PT), the activated partial thromboplastin time (aPTT), and the activities of (1) the coagulation factors (CFs) I, II, V, and VII-XII; (2) the inhibitor of coagulation antithrombin III (ATIII), and (3) the component of the fibrinolytic system α₂-antiplasmin (α₂-APL). PT and aPTT and the activities of CF, ATIII, and α₂-APL were not measurable in the urine of control and puromycin aminonucleoside injected rats on day 2. On this same day, plasma ATIII and CF VIII decreased. On day 10 (1) PT and aPTT decreased in plasma and were not measurable in urine; (2), plasma CFs I, II, V, VII, VIII, X, and XI increased; (3), plasma ATIII decreased; (4), plasma CFs IX and XII and α₂-APL did not change, and (5) ATIII and CFs II, VII, VIII, IX, X, XI, and XII, but not CFs I and V and α₂-APL, appeared in urine on day 10. ATIII deficiency was secondary probably to the urinary losses; however, the plasma activity of CFs II, VII, VIII, X, and XI increased and that of CFs IX and XII remained unchanged in spite of their urinary losses which suggests that other mechanisms such as deranged catabolism and altered hepatic synthesis may be involved. This model may be useful to study the pathophysiology of the abnormalities of coagulation in humans with nephrotic syndrome.

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“…How ever. factor IX deficiency is not consistent; it could increase [12], Factors II, VII, and X are also increased [13]. Cofactors V and VIII are increased.…”

Section: Discussionmentioning

confidence: 95%