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BACKGROUND: Hepatitis viruses have become one of the main infectious problems in patients on maintenance haemodialysis. The aim of this study was to prospectively investigate the incidence of de novo hepatitis C virus (HCV) infection in a haemodialysis unit and to identify factors currently involved in HCV transmission to haemodialysis patients. METHODS: One hundred and fourteen anti-HCV negative and HCV-RNA negative patients who started long-term haemodialysis were followed for a mean period of 36 months (range 18-56). Liver tests and anti-HCV were performed at 6-month intervals. Factors that might be implicated in HCV transmission, such as blood transfusions, sexual habits, surgery and other invasive procedures, were recorded. HCV markers were re-examined in transfused blood and the HCV genotype was investigated in seroconverters to anti-HCV and in patients with previous HCV infection who were treated in the vicinity of those who seroconverted. RESULTS: Eight patients (7%) seroconverted to anti-HCV and seven of them became HCV-RNA positive. HCV markers, including HCV-RNA, were negative in the blood transfused to seroconverters. No differences between seroconverters and non-seroconverters. No differences found in other risk factors not directly related to haemodialysis. The investigation of HCV genotype suggested that HCV transmission was not restricted to patients treated in the vicinity of previously HCV infected patients. Occasional failure to observe strict measures of asepsis was detected in the haemodialysis unit and this was the only factor that might be incriminating. CONCLUSIONS: HCV acquisition in patients on haemodialysis is currently not related to blood transfusion, and nosocomial transmission within the haemodialysis unit seems to be the main mechanism of HCV infection. Extremely careful observation of preventive measures seems essential to eradicate HCV transmission in haemodialysis units. [ABSTRACT FROM PUBLISHER]

Uraemic patients suffer from haemorrhagic disorders and accelerated atherosclerosis. To evaluate the possible role of the vessel wall in these haemostatic alterations associated with uraemia, we investigated the effect of a uraemic milieu on human endothelial cell (EC) cultures and the reactivity of the extracellular matrices (ECM) generated by these cells towards platelets. EC cultures were exposed to a pool of sera (20% in the culture medium) obtained either from uraemic patients or from normal donors, and the following parameters were evaluated: (1) EC viability (trypan blue exclusion test); (2) von Willebrand factor (vWF) levels in supernatants and associated with ECM; (3) the reactivity of EC and EC-derived ECM towards platelets, measured ‘ex vivo’ under flow conditions (5 min, wall shear rate 800 s); and (4) ultrastructure of the ECM. The viability of EC cultured in the presence of uraemic sera was similar to controls. Platelet interaction with ECM generated by EC exposed to uraemic sera was significantly reduced (<0.05). This decrease was mainly related to a reduction in platelet adhesion (9.8 ± 1.9% vs 16.7±1.8% in controls, <0.02). VWF levels in supernatants and associated with ECM were similar to controls. Ultrastructural analysis of the ECM generated by EC exposed to uraemic sera revealed a deficient matrix. An increased removal of EC was observed in experiments in which EC cultured in the presence of uraemic sera were perfused with citrated blood. These results indicate that a uraemic milieu induces quantitative and qualitative changes in the vascular subendothelium, characterized by a less intrincate network of fibrils, as well as a decreased attachment of EC and reduced thrombogenicity to the ECM. These changes may represent another mechanism which contributes to the haemostatic dysfunction observed in uraemic patients. [ABSTRACT FROM PUBLISHER]

To investigate the possible relationships between blood pressure, parathyroid hormone (PTH) and platelet cytosolic Ca concentration ([Ca]) in patients with essential hypertension, we studied 17 patients with this disease aged 48±2 years and 17 normotensive controls aged 44±3 years. Platelet [Ca] was measured by spectrofluorimetry using the dye Fura-2 acetoxymethylester. Patients with essential hypertension displayed lower levels of serum ionized Ca (0.99±0.03 versus 1.1±0.01 mmol/l, <0.05) and higher serum intact PTH levels (37±3 versus 26±2 pg/ml, <0.01) than the normotensive controls. Although serum levels of intact PTH were significantly correlated with mean arterial pressure (MAP) in the combined group of subjects (=0.42, <0.05), there was no correlation when each group was considered separately. Resting platelet [Ca] was also higher in patients than in controls (57±3 versus 48±2nmol/l, <0.005). When platelets were stimulated with thrombin, the increment in [ca] was also greater in patients than in controls in the presence of extracellular Ca (264±24 versus 194±19 nmol/l, <0.05) but not in its absence (123±12 versus 112±10 nmol/l). The thrombin-induced increment in [ca] was correlated with MAP in the hypertensive patients (=0.64, <0.01) and in the combined group of subjects (=0.42, <0.05). There was no relationship between resting or thrombin-induced [Ca] and serum PTH in either group of patients or in the combined group of subjects. Furthermore, preincubation of platelets with PTH had no effect neither on resting platelet [Ca] or on thrombin-induced increments in [ca], both in the presence and in the absence of extracellular Ca in either group of subjects. Therefore, despite platelet [Ca] and serum PTH seem to be related to blood pressure, it appears that PTH does not participate directly in the elevated platelet [Ca] found in patients with essential hypertension. [ABSTRACT FROM PUBLISHER]

Three groups of patients with acute or chronic renal failure (GFR <5 ml/min) and hyperkalaemia (K ≥6 mEq/l), similar in age, serum creatinine and pretreatment K. Group A (=24) received salbutamol 0.5 mg i.v. in 15 min, group B (=10) received glucose 40 g i.v. plus 10 units insulin i.v. in 15 min, and group C (=10) received salbutamol 0.5 mg i.v., glucose 40 g i.v. and insulin 10 units i.v. over a 15-min period. Serum potassium was measured at 30, 60, 180 and 360 min after administration of treatment. All treatments reduced serum potassium, maximal at 30 or 60 min, and ranging from −0.5±0.1 to −1.5±0.2 mEq/l; patients in group C exhibited a significantly greater decrement in serum potassium, when compared to group B at 60 (−1.5±0.2 vs −1±0.1 mEq/l, respectively; <0.01) and 180 min (−1.2±0.2 vs −0.7±0.1 mEq/l, respectively; <0.05). There were no significant differences between groups A and C. Patients from group C had moderate tachycardia and more prolonged hyperglycaemia than those from group B, but all treatments were well tolerated. [ABSTRACT FROM PUBLISHER]