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Intradialytic hypotension (IDH) is a still-frequent and poorly-understood complication of haemodialysis. Haemofiltration has recently been shown to reduce the phenomenon of IDH. HFR-Aequilibrium adds to traditional HFR and is, in practice, a variant comprising endogenous re-infusion of haemodiafiltration with dialysate sodium concentration and ultrafiltration rate profiles elaborated by the 'Profiler' plasma sodium biofeedback system, and measurement of plasma sodium via the on-line Natrium sodium sensor.

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One hundred sixty-five patients with cirrhosis diagnosed by needle liver biopsy were followed for 2 years to evaluate the relation between clotting factors and survival. Patients with spontaneous bacterial peritonitis, hepatic carcinoma, and cholestatic liver diseases were excluded. Patients were classified as A (n = 34), B (n = 75), or C (n = 56) according to Child-Pugh criteria. During the follow-up 45 patients died of liver failure or gastrointestinal hemorrhage. Nonsurvivor patients had significantly higher values of bilirubin and D-dimer, a marker of fibrinolysis in vivo, lower values of albumin, prothrombin activity, fibrinogen, prekallikrein, factor VII, and a more prolonged activated partial thromboplastin time than survivors. All these variables and Child-Pugh classification were significantly associated with survival in a univariate analysis. Multivariate analysis (Cox's model) showed that only prekallikrein and factor VII were independently predictors of survival. Ninety-three percent of patients with prekallikrein values < 32% died within 32 months of follow-up, whereas factor VII < 34% identified 93% of patients who died within 10 months of follow-up. This study suggests that factor VII is an early predictor of survival and may be a useful test to better identify cirrhotic patients who should be candidates for liver transplantation.

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Patients with cirrhosis suffer from a complex haemostatic disturbance, due to abnormalities in clotting and fibrinolytic system activation and in primary haemostasis. The latter is indicated by a prolongation of bleeding time, which is a reliable indicator of platelet function in vivo. To further assess the relationship between bleeding time, degree of liver failure and clotting abnormalities in patients with cirrhosis, bleeding time was investigated in a prospective study of 70 consecutive patients with cirrhosis diagnosed by liver-needle biopsy, of whom 19 belonged to Child-Pugh class A, 29 to B and 22 to C. Among patients with cirrhosis, 40% had an abnormal bleeding time (> 10 min), and 42% had a platelet count < 100,000/microliters. Patients with severe liver failure (class C) had a lower platelet count and a more prolonged bleeding time than patients in classes A and B. Bleeding time was significantly inversely correlated to platelet count, fibrinogen, prothrombin activity and packed cell volume, and directly correlated to serum bilirubin and D-dimer. However, in class C patients, only a significant inverse correlation between bleeding time and fibrinogen was observed. These findings indicate that in cirrhosis worsening of platelet function is closely related to the degree of liver failure. The inverse correlation between bleeding time and fibrinogen indicates that a low value of this clotting parameter may account in part for platelet dysfunction.

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Effects of subcutaneous calcium-heparin and vitamin K administration were studied in 30 cirrhotic patients showing low values of prothrombin time, antithrombin III, fibrinogen, platelet count, plasminogen, alpha 2-antiplasmin, raised levels of fibrin(ogen) degradation products and prolonged activated partial thromboplastin time. A group of 10 patients was first treated with K vitamin for 15 d; after vitamin K therapy interruption, a treatment with 5000 IU (8000 IU in 1 patient) every 12 h of subcutaneous calcium-heparin was started. In another group of 20 patients a treatment with 5000 IU (8000 IU in 2 patients) every 12 h of subcutaneous calcium-heparin was started immediately. The heparin administration in both groups had been performed for at least 2 weeks. No significant changes of blood coagulation picture were observed after vitamin K administration, while calcium-heparin treatment showed an increase in prothrombin time, fibrinogen, platelet count, plasminogen, alpha 2-antiplasmin, a decrease in fibrin(ogen) degradation products and a shortened activated partial thromboplastin time. There was no significant change in antithrombin III values.

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Eighteen diabetic patients with abnormal platelet function were treated for 1 month with gliclazide (80 to 160 mg/day). Platelet aggregation, circulating beta-thromboglobulin levels and platelet malondialdehyde concentrations were significantly reduced after 30 (but not 15) days of treatment. Although fasting and post-prandial glycaemia significantly improved in these patients, similar changes in platelet function were noted in 5 other patients in whom glycaemia did not change. Gliclazide therapy, therefore, brought about an improvement in platelet function and a reduction activation in the thromboxane metabolic pathway, possibly by a direct on the platelets.

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