Comprehensive Study of Haemostasis in Nephrotic Syndrome

Abstract

A comprehensive study of haemostasis has been performed in a homogeneous group of 20 patients with nephrotic syndrome without renal failure. We have found unchanged number of platelets and a significant increase of platelet adhesiveness and aggregation; increased levels of activity and related antigen of fibrinogen, of factor VIII, of activity of factors II, VII and X and of antigens of factors XIII. Antithrombin III was unchanged in plasma and was detected in the urine. Euglobulin lysis times were decreased, and levels of plasminogen and its activators were increased after a venous occlusion test. At the same time urokinase inhibitors and antiplasmins were increased not only after, but also before a venous occlusion test. Fibrinogen degradation products have been found in the urine of all our patients but not in their sera.

Blood Coagulation and the Nephrotic Syndrome: Deficiency or Excess?

“…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.…”

“…19,[33][34][35] It appears that, except for one report, the most consistent pattern has been decreased fibrinolytic activity. 5,17,34,35 The mechanism, or mechanisms, leading to decreased fibrinolysis remain uncertain. Defective formation or release of plasminogen activator, or an increase in antiplasmin activity, or both mechanisms, have been suggested.…”

“…38 Findings suggesting an increased rather than decreased fibrinolytic activator release have also been reported. 5 These conflicting reports may reflect variations in the degree of in vivo depletion of endothelial stores of the activator by an ongoing activation of coagulation factors or platelets. In this regard, the increased platelet aggregability along with the activation of coagulation factors described in nephrotic patients could promote a relative depletion of activators from endothelial cells, 39 thereby explaining such a variability.…”

“…[1][2][3] Although the association between nephrotic syndrome and thromboembolic complications has been recognized for more than a century, the precise causal relationship is not entirely understood. [4][5][6] Moreover, the association between the increased bleeding tendency and nephrotic syndrome is also somewhat unclear. [2][3][4][5][6][7] In this review, we present a current synopsis on the subject and discuss some of the controversial aspects that have emerged during the past decade.…”

“…[4][5][6] Moreover, the association between the increased bleeding tendency and nephrotic syndrome is also somewhat unclear. [2][3][4][5][6][7] In this review, we present a current synopsis on the subject and discuss some of the controversial aspects that have emerged during the past decade. 8,9 An in-depth understanding of the underlying pathogenesis should pave the way to better clinical methods for preventing these grave complications.…”