Fourteen cases of malposition of a permanent central vein catheter for hemodialysis or poor blood flow associated with thrombosed central veins but correct catheter positioning, in 13 patients suffering from end stage renal disease, presented from September 1991 to December 2003 among 385 permanent central vein catheters for hemodialysis (3.6%). There were 8 episodes of catheter tip malplacement in the azygos vein (1 case), hemiazygos vein (1), left internal thoracic (mammalian) vein (1), contralateral innominate vein (5) and 6 cases with correct anatomical catheter tip placement but with blood inflow from the catheter through the collateral vein system because of thrombosis of a major vein trunk (hemiazygos vein system (2), azygos vein (2), ascending lumbar veins (1), or portal vein system (1)). The malposition was diagnosed using roentgenography, with or without contrast, and computer tomography. In 3 cases the catheter was removed, in 5 cases the position was corrected. In the remaining 6 cases its function was maintained using anticoagulation or/and thrombolytic therapy. In conclusion, the placement of a permanent central vein catheter for hemodialysis must be followed by simple or contrast medium x-ray evaluation of its correct position or function. The malposition must be corrected whereas in the case where there is no alternative solution the function of the catheter may be maintained in the incorrect position using a combination of anticoagulation or/and thrombolytic therapy.
Replacement therapy may contribute to the quantitative alterations of immune subsets found in HD and CAPD patients compared to normal subjects. We speculate that these changes account, at least in part, for the immune dysregulation observed in patients with chronic renal failure. Analysis of lymphocyte subsets will help the research and the evaluation of the possible causes of immunodeficiency in uremic patients undergoing replacement therapy and will probably contribute to more efficient and preventive strategies.
Hepatitis C virus (HCV) infection is frequent in patients with end-stage renal disease treated by chronic dialysis, with a prevalence varying from 10-65% according to the geographical data. The prevalence is significantly associated with the duration of dialysis and the number of transfused blood products [1,2] and has dramatically declined with efficient blood screening. [3] We studied patients with acute HCV infection in a dialysis unit. The diagnosis was based on both anti-HCV detection and HCV-RNA detection. Other virological tools including HCV genotype determination was also used to tailor treatment to the individual patient and determine its efficacy for a one-year follow-up period. Seventeen patients (7 male and 10 female, mean age: 63.7 ± 11.6 SD) with acute hepatitis C were enrolled to our study. All of them were followed up for a period of one year after the diagnosis was established. Phylogenetic analysis distinguished two separate HCV subtypes 1b, which were both responsible for this acute infection (see Figure 1). These types did not differ in their behavior on the clinical situation of our patients, as confirmed by the fact that in both groups of patients, there was only one patient who presented with acute illness. Six patients of our study group, three months after the acute infection, received pegylated interferon (Peg-IFNa2a) 135 μg for a six-month period. Four of them responded very well to therapy and at the first determination HCV RNA was below the cutoff point. One of our patients with very high HCV levels (HCV RNA > 50,000,000 IU/ mL), despite receiving the same therapy, did not respond well and developed cirrhosis. In conclusion, it is clear from our experience that better information is needed about the current incidence, prevalence, and risk factors for HCV infection in dialysis patients. Algorithms for the diagnosis and management of hepatitis C should be developed by academic societies. Routine screening for hepatitis C also would allow for better definition of the natural history of hepatitis C in patients with end stage renal disease.
The combination of elevated IL-6 and CRP levels was associated with an altered nutritional status. The concomitant elevations in PCT, CRP, and IL-6 could be more sensitive in the evaluation of inflammation.
Replacement therapy may contribute to the quantitative alterations of immune subsets found in HD and CAPD patients compared to normal subjects. We speculate that these changes account, at least in part, for the immune dysregulation observed in patients with chronic renal failure. Analysis of lymphocyte subsets will help the research and the evaluation of the possible causes of immunodeficiency in uremic patients undergoing replacement therapy and will probably contribute to more efficient and preventive strategies.
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