Factor-Ix Deficiency in the Nephrotic Syndrome

Handley, Dean A.; Lawrence, J.R.

doi:10.1016/s0140-6736(67)92651-7

Cited by 40 publications

(9 citation statements)

References 14 publications

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“…2,5,[12][13][14][15] Conversely, increased plasma concentrations of cofactors I, V, and VIII have also been consistently observed in other studies. 16,17 Alterations in other zymogens such as factor X remain controversial, with some investigators reporting an increase and others a decrease or no change in the plasma levels.…”

Section: Zymogens and Co-factorssupporting

confidence: 72%

Blood Coagulation and the Nephrotic Syndrome: Deficiency or Excess?

1990

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Section: Zymogens and Co-factorssupporting

confidence: 72%

Blood Coagulation and the Nephrotic Syndrome: Deficiency or Excess?

1990

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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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“…Acquired factor IX deficiency in NS was first de scribed by Handley and Lawrence [32] who reported 4 such cases in 1967. Corticosteroid administration in these children resulted in improvement of proteinuria, normalization of the thromboplastin generation time (TGT), and factor IX level.…”

Section: Factor IXmentioning

confidence: 99%

Nephrotic Syndrome and Coagulation and Fibrinolytic Abnormalities

Vaziri¹

1983

Am J Nephrol

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Factor-Ix Deficiency in the Nephrotic Syndrome

Cited by 40 publications

References 14 publications

Blood Coagulation and the Nephrotic Syndrome: Deficiency or Excess?

Blood Coagulation and the Nephrotic Syndrome: Deficiency or Excess?

Abnormalities of Coagulation in Experimental Nephrotic Syndrome

Nephrotic Syndrome and Coagulation and Fibrinolytic Abnormalities

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