A pathogenetic role for fibrin deposition and platelet activation in the kidney is thought to play a role in the pathogenesis of acute renal failure (ARF). Thus, some fibrinolytic parameters and platelet function have been studied in 17 patients with ARF and compared to healthy volunteers and subjects with chronic renal failure (CRF). Since serotonin may participate in pathological processes resulting from platelet/vessel wall interactions, its level in the whole blood and plasma was also assayed. In ARF and CRF platelet aggregatory responses in both whole blood and in platelet rich plasma upon stimulation with various agonists (collagen, arachidonic acid, ADP, ristocetin) were lower than those obtained in healthy volunteers. Increased levels of lipoprotein (a), von Willebrand factor (VWF) and fibronectin were found in ARF relative to controls. Protein C activity was significantly lower in patients with ARF. Euglobulin clot lysis time was prolonged in ARF and CRF, reflecting a decreased overall fibrinolytic activity. Activity of tissue plasminogen activator (tPA) inhibitor (PAI) and PAI:Ag were higher in ARF, whereas tPA:Ag, urokinase, tPA/PAI complexes, thrombin-antithrombin complexes (TAT), plasmin-antiplasmin (PAP) complexes, fibrinogen, and F-1+2 did not differ between ARF and controls. In CRF elevated levels of TAT, PAP, fibrinogen and prothrombin fragments F-1+2 were found, whereas concentration of fibronectin was lowered when compared to controls. In both groups of renal failure patients increased levels of fibrin monomers and d-dimer were found relative to healthy volunteers. Whole blood serotonin was significantly lower, whereas plasma serotonin was significantly higher in patients with ARF and CRF relative to controls. Serotonin uptake and its release from platelets were markedly diminished in patients with ARF and CRF. Chronic renal failure exhibit a slightly different pattern of coagulopathies that acute renal failure. Acute renal failure (ARF) is a potentially reversible yet life-threatening condition, resulting from different etiological factors acting through complex, still unclear pathophysiological mechanisms but consistently leading to renal vasoconstriction and ischemia (1). Most factors that affect vascular tone come from the endothelium. Its damage leads also to local blood platelets aggregation and release of TxA(2) and serotonin which amplify vasoconstriction (1). There is an evidence that glomeruli can release a number of factors like PAF and procoagulant tissue factor that can activate intracapillary coagulation and alter renal hemodynamics (2). Although glomeruli posses activators of fibrinolysis such as tissue plasminogen activator-tPA and urokinase -uPA which provide some protective fibrinolysis, an exaggerrated or unbalanced activation of prothrombotic factors may trigger local coagulation and microvascular occlusion (2). Thus, a pathogenetic role for fibrin deposition in the kidneys, thought to play a role in the pathogenesis since the earliest description of ARF, is amplified today. On the other hand, chronic renal failure exhibit a slightly different pattern of coagulopathies that acute renal failure (1,3). Moreover, the precise relationship of uremic retention products to platelet dysfunction, abnormal plasma vWF, inhibitors of blood coagulation and fibrinolysis and their effects on the properties of the vessel wall, is not well defined. Disturbances in serotonin metabolism were also reported in uremic patients (4). Taking all these data into consideration and the fact that a few data is available, we performed the comprehensive study on platelet function, hemostasis and peripheral serotonergic system in patients with acute renal failure in comparison to subjects with chronic renal failure and healthy volunteers.
