Bacterial infections in hemodialysis patients: Pathogenesis and prevention
2005; Elsevier BV; Volume: 67; Issue: 6 Linguagem: Inglês
10.1111/j.1523-1755.2005.00364.x
ISSN1523-1755
Autores Tópico(s)Infective Endocarditis Diagnosis and Management
ResumoThe Nephrology Forum is funded in part by grants from Amgen, Incorporated; Merck & Co., Incorporated; and Dialysis Clinic, Incorporated. A 62-year-old African American man with end-stage renal disease secondary to hypertension who had been treated with hemodialysis for almost 5 years had multiple vascular access problems. After multiple thrombectomies of right and left arm arterio-venous grafts (AVGs), as well as an episode of life-threatening bleeding from the left arm AVG, he underwent insertion of a LifeSite® catheter in the left internal jugular vein 4 years ago. Four months later, he was hospitalized for an episode of chills and rigors, and was found to have methicillin-resistant Staphylococcus aureus (MRSA) bacteremia, which was treated with intravenous vancomycin and oral rifampin. A trans-esophageal echocardiogram revealed no valvular vegetation. Because he was a nasal carrier of MRSA, he was given a 2-week course of mupirocin ointment to his nares for eradication of MRSA colonization. Extensive discussions ensued with the patient about the future of his vascular access and the likelihood of eradicating the infection with medical therapy alone. Given his history of multiple thrombosed AVGs, and that the implanted catheter might have been his last option for satisfactory dialysis access, the decision was made not to remove the catheter and for him to receive an 8-week course of dual antibiotic therapy. The patient then did well until 13 months later, when erosion of the skin over the arterial port of the LifeSite® catheter required surgical relocation of the port and skin closure. Seventeen months later, he presented with fever and abdominal pain one day following a dialysis session. Blood cultures from a peripheral vein and from the dialysis catheter grew coagulase-negative staphylococcus species. An abdominal CT scan revealed pneumatosis and air tracking in the superior mesenteric and splenic veins consistent with ischemic bowel disease. Broad-spectrum antibiotics were initiated and he was given intravenous fluids prior to undergoing an emergent exploratory surgery. Laparotomy revealed a gangrenous small bowel from the ligament of Treitz to the ileo-cecal valve. Intraoperative Doppler studies revealed no pulse in the arcade of the mesentery of the small intestine. Because of these findings and the overall poor prognosis, no intestinal resection was attempted, and the abdominal surgical wound was closed. As expected, the patient continued to deteriorate clinically and died due to this devastating complication and overwhelming staphylococcal sepsis. No autopsy was performed. Dr. Bertrand L. Jaber (Department of Medicine, Tufts University School of Medicine; and Vice Chairman for Clinical Affairs, Division of Nephrology, Department of Medicine, Caritas St. Elizabeth's Medical Center, Boston, Massachusetts): Bacterial infections represent a common and important health problem for patients with end-stage renal disease (ESRD) who undergo maintenance hemodialysis (HD), and this patient illustrates the challenges inherent to this problem. Considerable gains have been made in deciphering the pathogenesis of bacterial infections in this high-risk population. These gains notwithstanding, the therapeutic goal of preventing bacterial infections in HD patients remains unfulfilled. This Forum reviews the magnitude of the problem in the HD patient population, our progress in understanding the pathogenesis of bacterial infections, the use of novel diagnostic tools, and prospects for preventing such occurrences, while outlining areas of uncertainty. Infection is an important cause of morbidity and mortality among patients with ESRD. According to the United States Renal Data System (USRDS) registry, infection is the second leading cause of death in patients with ESRD (the first is cardiovascular disease), and septicemia accounts for more than 75% of these infectious deaths[1.United States Renal Data System USRDS 2003 Annual Data Report. Bethesda, MD, National Institutes of Health, Diabetes and Digestive and Kidney Diseases, 2003Google Scholar]. Indeed, among ESRD patients undergoing dialysis, the total death rate is 176/1000 patient-years, and septicemia and pulmonary infections combined account for close to 26/1000 patient-years[1.United States Renal Data System USRDS 2003 Annual Data Report. Bethesda, MD, National Institutes of Health, Diabetes and Digestive and Kidney Diseases, 2003Google Scholar]. Annual death rates due to pneumonia and sepsis are markedly higher in dialysis patients compared with the general population; in the 65- to 74-year-old category, the magnitude of difference is on the order of 10- and 100-fold, respectively Figure 1[2.Sarnak M.J. Jaber B.L. Pulmonary infectious mortality among patients with end-stage renal disease.Chest. 2001; 120: 1883-1887Crossref PubMed Scopus (156) Google Scholar],[3.Sarnak M.J. Jaber B.L. Mortality caused by sepsis in patients with end-stage renal disease compared with the general population.Kidney Int. 2000; 58: 1758-1764Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar]. Whereas the presence of diabetes mellitus confers an additional risk for sepsis-related deaths, this comorbid condition appears to exert little influence on pneumonia-related deaths[2.Sarnak M.J. Jaber B.L. Pulmonary infectious mortality among patients with end-stage renal disease.Chest. 2001; 120: 1883-1887Crossref PubMed Scopus (156) Google Scholar],[3.Sarnak M.J. Jaber B.L. Mortality caused by sepsis in patients with end-stage renal disease compared with the general population.Kidney Int. 2000; 58: 1758-1764Abstract Full Text Full Text PDF PubMed Scopus (0) Google Scholar]. Bacterial infections are a major cause of hospitalization. In a recent study on the epidemiology of septicemia in HD patients, hospital admission rates for septicemia during the first year of HD rose by 51% over the 8-year period from 1991 to 1999[4.Foley R.N. Guo H. Snyder J.J. et al.Septicemia in the United States dialysis population, 1991 to 1999.J Am Soc Nephrol. 2004; 15: 1038-1045https://doi.org/10.1097/01.ASN.0000119144.95922.C4Crossref PubMed Scopus (124) Google Scholar]. Hospitalization for septicemia also was associated with an increased risk of myocardial infarction, congestive heart failure, stroke, and peripheral vascular disease at 6 months and 5 years after the original hospitalization[4.Foley R.N. Guo H. Snyder J.J. et al.Septicemia in the United States dialysis population, 1991 to 1999.J Am Soc Nephrol. 2004; 15: 1038-1045https://doi.org/10.1097/01.ASN.0000119144.95922.C4Crossref PubMed Scopus (124) Google Scholar]. These data suggest that septicemia has become more common in dialysis patients in the U.S. and is associated with an increased risk of cardiovascular events and death. Evidence is emerging that HD patients also have a higher incidence of infective endocarditis[5.Cabell C.H. Jollis J.G. Peterson G.E. et al.Changing patient characteristics and the effect on mortality in endocarditis.Arch Intern Med. 2002; 162: 90-94Crossref PubMed Scopus (394) Google Scholar, 6.Abbott K.C. Agodoa L.Y. Hospitalizations for bacterial endocarditis after initiation of chronic dialysis in the United States.Nephron. 2002; 91: 203-209https://doi.org/10.1159/000058393Crossref PubMed Scopus (93) Google Scholar, 7.Hoen B. Infective endocarditis: A frequent disease in dialysis patients.Nephrol Dial Transplant. 2004; 19: 1360-1362https://doi.org/10.1093/ndt/gfh149Crossref PubMed Scopus (32) Google Scholar]. In one study, the proportion of patients with infective endocarditis who were undergoing HD increased from 7% to more than 20% over a 7-year period[5.Cabell C.H. Jollis J.G. Peterson G.E. et al.Changing patient characteristics and the effect on mortality in endocarditis.Arch Intern Med. 2002; 162: 90-94Crossref PubMed Scopus (394) Google Scholar], and this observation was paralleled by a significant increase of Staphylococcus aureus-associated endocarditis from 10% to 68%[5.Cabell C.H. Jollis J.G. Peterson G.E. et al.Changing patient characteristics and the effect on mortality in endocarditis.Arch Intern Med. 2002; 162: 90-94Crossref PubMed Scopus (394) Google Scholar]. In the U.S., the incidence of infective endocarditis in the dialysis population has been estimated at 483 episodes/100,000 patient-years compared with only 7 episodes in the general population[6.Abbott K.C. Agodoa L.Y. Hospitalizations for bacterial endocarditis after initiation of chronic dialysis in the United States.Nephron. 2002; 91: 203-209https://doi.org/10.1159/000058393Crossref PubMed Scopus (93) Google Scholar]. In this study, HD therapy was a strong risk factor for infective endocarditis, which was associated with a 1.5-fold higher risk of death[6.Abbott K.C. Agodoa L.Y. Hospitalizations for bacterial endocarditis after initiation of chronic dialysis in the United States.Nephron. 2002; 91: 203-209https://doi.org/10.1159/000058393Crossref PubMed Scopus (93) Google Scholar]. In a longitudinal cohort study of incident ESRD patients, older age and diabetes were independent risk factors for septicemia in all patients[8.Powe N.R. Jaar B. Furth S.L. Hermann J. Briggs W. Septicemia in dialysis patients: Incidence, risk factors, and prognosis.Kidney Int. 1999; 55: 1081-1090https://doi.org/10.1046/j.1523-1755.1999.0550031081.xAbstract Full Text Full Text PDF PubMed Scopus (352) Google Scholar]. Among HD patients, low serum albumin level, temporary vascular access, and dialyzer reuse also were associated with increased risk[8.Powe N.R. Jaar B. Furth S.L. Hermann J. Briggs W. Septicemia in dialysis patients: Incidence, risk factors, and prognosis.Kidney Int. 1999; 55: 1081-1090https://doi.org/10.1046/j.1523-1755.1999.0550031081.xAbstract Full Text Full Text PDF PubMed Scopus (352) Google Scholar], and septicemia carried a markedly increased risk of death. These data suggest that improving nutrition and avoiding temporary vascular access might decrease the incidence of septicemia, and that dialyzer reuse practices might contribute to this risk. In a recent study reporting on a staged program to stop dialyzer reprocessing, conversion to a single-use dialyzer practice was associated with improved survival[9.Lowrie E.G. Li Z. Ofsthun N. Lazarus J.M. Reprocessing dialysers for multiple uses: recent analysis of death risks for patients.Nephrol Dial Transplant. 2004; 19: 2823-2830https://doi.org/10.1093/ndt/gfh460Crossref PubMed Scopus (30) Google Scholar]. This trend lagged by at least 60 days following abandonment of the dialyzer reuse practice and was ascribed to a cumulative decline in exposure to trace industrial products or repeated inflammatory and infectious insults, which only become clinically manifest over time[9.Lowrie E.G. Li Z. Ofsthun N. Lazarus J.M. Reprocessing dialysers for multiple uses: recent analysis of death risks for patients.Nephrol Dial Transplant. 2004; 19: 2823-2830https://doi.org/10.1093/ndt/gfh460Crossref PubMed Scopus (30) Google Scholar]. In the HEMO study, the incidence of infection-related deaths was not reduced by higher dose of dialysis or by high-flux dialyzers, and most infection-related hospitalizations were not attributed to vascular access[10.Allon M. Depner T.A. Radeva M. et al.Impact of dialysis dose and membrane on infection-related hospitalization and death: Results of the HEMO Study.J Am Soc Nephrol. 2003; 14: 1863-1870https://doi.org/10.1097/01.ASN.0000074237.78764.D1Crossref PubMed Scopus (158) Google Scholar]. However, the frequency of infection-related hospitalizations attributed to vascular access was disproportionately higher among patients with central venous catheters compared with those who had grafts or fistulas[10.Allon M. Depner T.A. Radeva M. et al.Impact of dialysis dose and membrane on infection-related hospitalization and death: Results of the HEMO Study.J Am Soc Nephrol. 2003; 14: 1863-1870https://doi.org/10.1097/01.ASN.0000074237.78764.D1Crossref PubMed Scopus (158) Google Scholar]. In the past two decades, major gains have been realized in our understanding of the pathogenesis of bacterial infections in HD patients. I will emphasize the interaction of three pivotal factors: host immunity, bacterial virulence, and the dialysis procedure per se Figure 2. The following section reviews the various components of this “access of evil,” with special emphasis on the pathogenesis of bacteremia and bacterial pneumonia. Uremia is associated with alterations in primary host defense mechanisms, which increase the risk of bacterial infections. Indeed, neutrophils exhibit impaired chemotaxis, oxidative metabolism, phagocytic activity, degranulation, and intracellular killing, as well as dysregulated programmed cell death or apoptosis[11.Lewis S.L. Van Epps D.E. Neutrophil and monocyte alterations in chronic dialysis patients.Am J Kidney Dis. 1987; 9: 381-395Abstract Full Text PDF PubMed Scopus (82) Google Scholar, 12.Herl W.H. Neutrophil function and infections in uremia.Am J Kidney Dis. 1999; 33: xlv-xlviiiAbstract Full Text Full Text PDF Google Scholar, 13.Cendoroglo M. Jaber B.L. Balakrishnan V.S. et al.Neutrophil apoptosis and dysfunction in uremia.J Am Soc Nephrol. 1999; 10: 93-100https://doi.org/10.1159/000051222Crossref PubMed Scopus (26) Google Scholar, 14.Jaber B.L. Cendoroglo M. Balakrishnan V.S. et al.Kidney Int. 2001; 59: S197-S205Abstract Full Text PDF PubMed Scopus (46) Google Scholar]. A number of factors have been incriminated in neutrophil dysfunction, including malnutrition, trace element deficiencies, iron overload, impaired glucose metabolism, hyperparathyroidism, dialysis per se, and uremic retention solutes[12.Herl W.H. Neutrophil function and infections in uremia.Am J Kidney Dis. 1999; 33: xlv-xlviiiAbstract Full Text Full Text PDF Google Scholar, 15.Vanholder R. Ringoir S. Dhondt A. Hakim R. Phagocytosis in uremic and hemodialysis patients: A prospective and cross sectional study.Kidney Int. 1991; 39: 320-327Abstract Full Text PDF PubMed Scopus (196) Google Scholar, 16.Chervu I. Kiersztejn M. Alexiewicz J. et al.Impaired phagocytosis in chronic renal failure is mediated by secondary hyperparathyroidism.Kidney Int. 1992; 41: 1501-1505Abstract Full Text PDF PubMed Scopus (45) Google Scholar, 17.Patruta S.I. Edlinger R. Sunder-Plassmann G. Herl W.H. Neutrophil impairment associated with iron therapy in hemodialysis patients with functional iron deficiency.J Am Soc Nephrol. 1998; 9: 655-663PubMed Google Scholar, 18.Vanholder R. De Smet R. Glorieux G. et al.Review on uremic toxins: Classification, concentration, and interindividual variability.Kidney Int. 2003; 63: 1934-1943https://doi.org/10.1046/j.1523-1755.2003.00924.xAbstract Full Text Full Text PDF PubMed Scopus (1128) Google Scholar]. Abundant in vitro and clinical studies have linked iron overload to an increased risk of bacterial infections in HD patients[17.Patruta S.I. Edlinger R. Sunder-Plassmann G. Herl W.H. Neutrophil impairment associated with iron therapy in hemodialysis patients with functional iron deficiency.J Am Soc Nephrol. 1998; 9: 655-663PubMed Google Scholar, 19.Weinberg E. Iron and infection.Microbiol Rev. 1978; 42: 45-66Crossref PubMed Google Scholar, 20.Flament J. Goldman M. Waterlot Y. et al.Impairment of phagocyte oxidative metabolism in hemodialyzed patients with iron overload.Clin Nephrol. 1986; 25: 227-230PubMed Google Scholar, 21.Hoen B. Paul-Dauphin A. Hestin D. Kessler M. EPIBACDIAL: A multicenter prospective study of risk factors for bacteremia in chronic hemodialysis patients.J Am Soc Nephrol. 1998; 9: 869-876PubMed Google Scholar], including modest iron storage levels (ferritin level of 100–800 ng/mL and transferrin saturation of 10% to 50%) Figure 3[22.Teehan G. Bahdouch D. Ruthazer R. et al.Iron storage indices: Novel predictors of bacteremia in hemodialysis patients initiating intravenous iron therapy.Clin Infect Dis. 2004; 38: 1090-1094https://doi.org/10.1086/382878Crossref PubMed Scopus (85) Google Scholar],[23.Teehan G. Ruthazer R. Balakrishnan V. et al.Iron storage indices and risk of bacterial infections in hemodialysis patients.Hemodialysis Int. 2004; 8: 226-232https://doi.org/10.1111/j.1492-7535.2004.01100.xCrossref PubMed Scopus (10) Google Scholar]. Iron overload modulates this risk by affecting host defense mechanisms and bacterial virulence. Indeed, iron overload has been associated with reduced phagocytic function and oxidative burst, as well as impaired bacterial killing[17.Patruta S.I. Edlinger R. Sunder-Plassmann G. Herl W.H. Neutrophil impairment associated with iron therapy in hemodialysis patients with functional iron deficiency.J Am Soc Nephrol. 1998; 9: 655-663PubMed Google Scholar, 20.Flament J. Goldman M. Waterlot Y. et al.Impairment of phagocyte oxidative metabolism in hemodialyzed patients with iron overload.Clin Nephrol. 1986; 25: 227-230PubMed Google Scholar, 21.Hoen B. Paul-Dauphin A. Hestin D. Kessler M. EPIBACDIAL: A multicenter prospective study of risk factors for bacteremia in chronic hemodialysis patients.J Am Soc Nephrol. 1998; 9: 869-876PubMed Google Scholar]. Iron dextran, at pharmacologically relevant concentrations, attenuates in vitro the function of polymorphonuclear cells harvested from HD patients with normal iron indices[24.Guo D. Jaber B.L. Perianayagam M. et al.Impact of iron dextran on polymorphonuclear cell function among hemodialysis patients.Clin Nephrol. 2002; 58: 134-142Crossref PubMed Google Scholar]. Also, it is possible that the increased availability of iron can stimulate bacterial growth and increase virulence properties[25.Parkkinen J. von Bonsdorff L. Peltonen S. Catalytically active iron and bacterial growth in serum of haemodialysis patients after i.v. iron administration.Nephrol Dial Transplant. 2000; 15: 1827-1834https://doi.org/10.1093/ndt/15.11.1827Crossref PubMed Scopus (125) Google Scholar]. Consequently, the increased use of parenteral iron might be an important contributory factor to the occurrence of bacterial infections. In recent years, many uremic retention solutes that can adversely affect neutrophil function have been identified, including parathyroid hormone, p-cresol, polyamines, aminoguanidine products, and a series of granulocyte inhibitory proteins, angiogenin and complement factor D[12.Herl W.H. Neutrophil function and infections in uremia.Am J Kidney Dis. 1999; 33: xlv-xlviiiAbstract Full Text Full Text PDF Google Scholar],[18.Vanholder R. De Smet R. Glorieux G. et al.Review on uremic toxins: Classification, concentration, and interindividual variability.Kidney Int. 2003; 63: 1934-1943https://doi.org/10.1046/j.1523-1755.2003.00924.xAbstract Full Text Full Text PDF PubMed Scopus (1128) Google Scholar]. In addition, neutrophil-membrane interactions, mainly with cuprophan membranes, result in transient leukopenia, increased expression of adhesion molecules, degranulation and release of proteolytic enzymes, and release of reactive oxygen species[26.Jaber B.L. Pereira B.J.G. Biocompatibility of hemodialysis membranes.in: Pereira B.J.G. Sayegh M. Blake P. Chronic Kidney Disease, Dialysis and Transplantation: A Companion to Brenner and Rector's The Kidney. 2nd ed. Philadelphia, Elsevier Saunders, 2005: 363-387Crossref Scopus (6) Google Scholar]. These interactions might result in cellular “exhaustion” and decreased responsiveness to subsequent stimuli, such as bacteremia. Other striking abnormalities occur in cell-mediated immunity and primarily involve T-lymphocytes. These include lymphocytopenia, impaired delayed skin reactivity, and decreased in vitro lymphocyte proliferation[26.Jaber B.L. Pereira B.J.G. Biocompatibility of hemodialysis membranes.in: Pereira B.J.G. Sayegh M. Blake P. Chronic Kidney Disease, Dialysis and Transplantation: A Companion to Brenner and Rector's The Kidney. 2nd ed. Philadelphia, Elsevier Saunders, 2005: 363-387Crossref Scopus (6) Google Scholar],[27.Girndt M. Sester U. Sester M. et al.Impaired cellular immune function in patients with end-stage renal failure.Nephrol Dial Transplant. 1999; 14: 2807-2810https://doi.org/10.1093/ndt/14.12.2807Crossref PubMed Scopus (137) Google Scholar]. Alterations in B-lymphocyte function affect humoral immunity and result in decreased immunoglobulin levels and a depressed antibody response to antigens. Dysregulated cytokine synthesis[28.Dinarello C. Cytokines: Agents provocateurs in hemodialysis?.Kidney Int. 1992; 41: 683-694Abstract Full Text PDF PubMed Scopus (157) Google Scholar] and impaired macrophage Fc receptor function[29.Ruiz P. Gomez F. Schreiber A. Impaired function of macrophage Fc gamma receptors in end-stage renal disease.N Engl J Med. 1990; 322: 717-722Crossref PubMed Scopus (141) Google Scholar] further impair immune function in uremic patients. In one study, impaired macrophage Fc receptor function was associated with a higher risk of bacterial infection[29.Ruiz P. Gomez F. Schreiber A. Impaired function of macrophage Fc gamma receptors in end-stage renal disease.N Engl J Med. 1990; 322: 717-722Crossref PubMed Scopus (141) Google Scholar]. Finally, impaired ex vivo cytokine production by mononuclear cells in response to IgG, an Fc-mediated response, was associated with an increased risk of hospitalization for bacterial infections in HD patients[30.Balakrishnan V.S. Schmid C.H. Jaber B.L. et al.Interleukin-1 receptor antagonist synthesis by peripheral blood mononuclear cells: A novel predictor of morbidity among hemodialysis patients.J Am Soc Nephrol. 2000; 11: 2114-2121PubMed Google Scholar]. Additional susceptibility and risk factors that are specific for pulmonary infections in HD patients include obstructive and central sleep apnea, impaired inspiratory muscle strength, uremic pneumonitis/pleuritis, the hyper-hydration syndrome (due to fluid gain during the interdialytic interval), pulmonary metastatic calcification (from an increased calcium × phosphate product), and intradialytic hypoxemia (due to complement activation and transient leukopenia)[2.Sarnak M.J. Jaber B.L. Pulmonary infectious mortality among patients with end-stage renal disease.Chest. 2001; 120: 1883-1887Crossref PubMed Scopus (156) Google Scholar],[31.Gavelli G. Zompatori M. Thoracic complications in uremic patients and in patients undergoing dialytic treatment: State of the art.Eur Radiol. 1997; 7: 708-717Crossref PubMed Scopus (37) Google Scholar]. Bacteria can acquire virulence properties when specific conditions are met. In the normal host, under conditions of low density, bacteria are cleared by primary host-defense mechanisms. However, under conditions of high bacterial density, bacteria can produce extracellular polysaccharides referred to as “quorum sensors”[32.Gray E. Peters G. Verstegen M. Regelmann W. Effect of extracellular slime substance from Staphylococcus epidermidis on the human cellular immune response.Lancet. 1984; 1: 365-367https://doi.org/10.1016/S0140-6736(84)90413-6Abstract PubMed Scopus (205) Google Scholar],[33.Prince A.S. Biofilms, antimicrobial resistance, and airway infection.N Engl J Med. 2002; 347: 1110-1111https://doi.org/10.1056/NEJMcibr021776Crossref PubMed Scopus (151) Google Scholar]. These molecules are secreted by the bacteria and freely diffuse within the bacterial community, where they interact with transcriptional activators such as LasR and RhlR. This interaction increases expression of virulence genes, thereby facilitating bacterial survival by increased production of proteases, superoxide dismutase, and catalase, which enable the organisms to evade neutrophil killing and the bactericidal or bacteriostatic effects of antimicrobial agents. Bacteria also form a matrix of these extracellular polysaccharides, which is called biofilm or “slime.” This slime renders them less susceptible to antimicrobial agents, as the matrix constitutes a barrier between the antimicrobial agent and the bacterial cell wall. In the presence of foreign surfaces such as central venous catheters, biofilm formation is more likely to develop and can potentiate the pathogenicity of the skin bacterial flora (for example, coagulase-negative staphylococci). The adherence properties of bacteria are also important determinants of catheter-related infection[34.Center for Disease Control and Prevention Guidelines for the prevention of intravascular catheter-related infections.MMWR. 2002; 51: 1-29Google Scholar]. For example, S. aureus adheres to host proteins that are commonly present on catheters, such as fibronectin, whereas coagulase-negative staphylococci directly adhere to polymer surfaces. During the normal course of HD, patients are exposed to several infectious risks. Potential sources of infection include the skin (through repeated disruption of the skin barrier and integrity due to the nature of the vascular access type), the dialysis water treatment system, and dialyzer reuse. Central venous catheters used for HD include non-tunneled, tunneled, and totally implantable devices, such as the one described in the case presentation. The risk of bacteremia by device type, site of insertion, and duration of use varies widely. In one study of non-tunneled catheters, the incidence of bacteremia was 5% after three weeks of placement in the internal jugular vein, and 11% after one week in the femoral vein[35.Oliver M.J. Callery S.M. Thorpe K.E. et al.Risk of bacteremia from temporary hemodialysis catheters by site of insertion and duration of use: A prospective study.Kidney Int. 2000; 58: 2543-2545https://doi.org/10.1046/j.1523-1755.2000.00439.xAbstract Full Text Full Text PDF PubMed Scopus (198) Google Scholar]. Four pathogenic pathways have been incriminated in the development of catheter-related bloodstream infections, and include, in order of descending frequency: (1) colonization of the cutaneous catheter tract and tip with skin flora; (2) intraluminal colonization due to contamination of the catheter hub; (3) hematogenous seeding to the catheter from another focus of infection; and (4) very rarely, intraluminal contamination of the catheter with solvent/infusate. In addition to intrinsic bacterial virulence factors, another important determinant of catheter-related infection is the type of the device material[34.Center for Disease Control and Prevention Guidelines for the prevention of intravascular catheter-related infections.MMWR. 2002; 51: 1-29Google Scholar]. For example, catheters made of polyvinyl chloride or polyethylene are less resistant to the adherence of bacteria compared with catheters made of polytetrafluoroethylene (PTFE), silicone elastomer, or polyurethane[36.Ashkenazi S. Weiss E. Drucker M. Bacterial adherence to intravenous catheters and needles and its influence by cannula type and bacterial surface hydrophobicity.J Lab Clin Med. 1986; 107: 136-140PubMed Google Scholar]. Finally, surface irregularities and thrombogenicity of the catheter material are also likely to influence microbial adherence and therefore increase the risk of catheter colonization and catheter-related infection. Bacteremia also can result from contamination of dialysis fluids or equipment, inadequate dialyzer reprocessing procedures, or inadequate treatment of municipal water for use in dialysis[37.Jaber B.L. Pereira B.J.G. Dialysis reactions.Semin Dial. 1997; 10: 158-165Crossref Scopus (18) Google Scholar],[38.Tokars J. Alter M. Arduino M. Favero M. Nosocomial infections in hemodialysis units: Strategies for control.in: Pereira B. Sayegh M. Blake P. Chronic Kidney Disease, Dialysis and Transplantation: A Companion to Brenner and Rector's The Kidney. 2nd ed. Philadelphia, Elsevier Saunders, 2005: 429-450Crossref Scopus (4) Google Scholar]. Contaminated medication vials also are a potential source of bacteremia[39.Grohskopf L.A. Roth V.R. Feikin D.R. et al.Serratia liquefaciens bloodstream infections from contamination of epoetin alfa at a hemodialysis center.N Engl J Med. 2001; 344: 1491-1497https://doi.org/10.1056/NEJM200105173442001Crossref PubMed Scopus (110) Google Scholar]. The confirmation of peripheral bacteremia is paramount in the diagnosis of catheter-related infections. Unfortunately, for practical purposes often only one set of blood cultures is collected from the catheter lumen itself. Although blood culture testing is relatively inexpensive and easy to process, 24 to 48 hours often elapse before a preliminary report is provided to the clinician. In addition, if a catheter removed on suspicion of causing infection proves not to be infected, the patient is exposed unnecessarily to the risks associated with reinsertion. Consequently, rapid diagnostic approaches that help confirm a suspected catheter-related infection in HD patients and that implement the proper use of antibiotics are needed. Several novel but rather cumbersome diagnostic approaches include the use of an endoluminal brush, catheter hub culture, and electron microscopy[40.Dobbins B.M. Kite P. Wilcox M.H. Diagnosis of central venous catheter related sepsis—A critical look inside.J Clin Pathol. 1999; 52: 165-172Crossref PubMed Scopus (39) Google Scholar],[41.Dobbins B.M. Kite P. Endoluminal brushing in catheter–related sepsis: A “sweeping” statement.Nutrition. 1999; 15: 66-67https://doi.org/10.1016/S0899-9007(98)00115-4Abstract Full Text PDF PubMed Scopus (6) Google Scholar]. One rapid diagnostic technique, however, merits discussion. The acridine-orange leukocyte cytospin test (AOLC) is rapid (30 min), inexpensive, and requires only 100 µL of catheter blood and the use of ultraviolet microscopy[42.Tighe M.J. Kite P. Thomas D. et al.Rapid diagnosis of catheter-related sepsis using the acridine orange leukocyte cytospin test and an endoluminal brush.JPEN. 1996; 20: 215-218Crossref PubMed Scopus (35) Google Scholar]. In a study of diagnostic approaches of catheter-related bloodstream infections in adult surgical patients, the AOLC provided a diagnostic sensitivity and
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