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      Prevalence and outcomes of central venous catheter-related bacteraemia in HIV-infected versus non-HIV-infected patients undergoing haemodialysis treatment for end-stage kidney disease

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          Abstract

          Background

          Central venous catheter (CVC) haemodialysis (HD) to implement renal replacement therapy is the preferred choice in the urgent setting. Unfortunately, CVC placement is associated with multiple complications including nosocomial bloodstream infections. There is a paucity of data on the prevalence and pattern of pathogenic organisms in haemodialysed HIV-infected versus non-HIV-infected patients with end-stage kidney disease.

          Method and results

          We undertook a retrospective study of 228 patients who were dialysed using a CVC at a tertiary referral hospital in KwaZulu-Natal, South Africa. Seventy-eight patients (34.2%) complicated with bacteraemia and sepsis requiring antibiotics. Removal of the catheter was necessary in 58 patients (74.0%). The most common organisms isolated were Staphylococcus aureus (30.8%), Staphylococcus epidermidis (24.4%) and Klebsiella pneumoniae (15.4%). There was no statistically significant difference between HIV-infected and non-infected patients with regards to infection rate, time interval from insertion of CVC to infection and final outcome. However, HIV-infected patients took longer to recover; 54.3% of non-infected patients versus 10.3% HIV-infected patients had their sepsis controlled within one week. Acidosis, hypotension, line malfunction and line discharge were infrequent signs of sepsis. Fever, rigors and raised white cell count occurred in over 80.0% of patients.

          Conclusion

          The infection rate in CVC HD is not more frequent in HIV-infected patients, provided that CD4+ count is ≥ 200 cells/µL and the patient is virologically suppressed. Outcomes following intravenous antibiotic and removal of the CVC are similar in HIV-infected and non-infected patients but response to treatment is slower in HIV-infected patients. A high index of suspicion is needed in detecting CVC-related bacteraemia.

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          Most cited references11

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          Guidelines for the management of chronic kidney disease in HIV-infected patients: recommendations of the HIV Medicine Association of the Infectious Diseases Society of America.

          Lynda Szczech, S. Gupta, A Eustace … (2005)
          Article 0 comments Cited 90 times – based on 0 reviews     Review now
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            HIV-associated renal diseases and highly active antiretroviral therapy-induced nephropathy.

            D. Goebel, R Draenert, M Fischereder … (2006)
            Renal disease is becoming an increasingly prevalent entity in human immunodeficiency virus (HIV)-infected patients; it occurs in a variety of clinical settings and is associated with histopathological changes. HIV-related renal impairment can present as acute or chronic kidney disease; it can be caused directly or indirectly by HIV and/or by drug-related effects that are directly nephrotoxic or lead to changes in renal function by inducing metabolic vaculopathy and renal damage. Acute renal failure is frequently caused by the toxic effects of antiretroviral therapy or nephrotoxic antimicrobial substances used in the treatment of opportunistic infections. Chronic renal disease can be caused by multiple pathophysiological mechanisms, leading to HIV-associated nephropathy, a form of collapsing focal glomerulosclerosis, thrombotic microangiopathy, and various forms of immune complex glomerulonephritis. The increase in life expectancy and alteration of lipid metabolism due to receipt of highly active antiretroviral therapy are expected to result in an increased prevalence of diabetes and hypertension and, thus, to secondary diabetic and hypertensive renal damage. Antiretroviral agents, such as indinavir and tenofovir, have been associated with nephrotoxic drug effects that have been shown to be reversible in most cases. In this article, we review the current knowledge about acute and chronic HIV-associated renal disease, metabolic alterations and related nephropathies, and toxic drug effects of combination antiretroviral pharmacotherapy.
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              HIV-associated nephropathy: pathogenesis.

              P Klotman, Ji C. He, Raj Medapalli (2011)
              HIV-associated nephropathy (HIVAN) is characterized histologically by a collapsing form of focal segmental glomerulosclerosis (FSGS), microcystic tubular dilation, interstitial inflammation and fibrosis. In this review, we provide a summary of the current state of knowledge about the mechanisms involved in the pathogenesis of HIVAN. Two variants in the ApoL1 gene have been identified as the susceptibility alleles that account for a majority of the increased risk of FSGS and nondiabetic end-stage renal disease in blacks. HIVAN1 and HIVAN2 are the other host susceptibility genes that have been identified in animal models for HIVAN. HIV infects renal tubular epithelial cells likely through direct cell-cell transmission. Both in-vivo and in-vitro evidence suggests that Nef and Vpr are the key viral genes mediating HIVAN. Nef induces podocyte dysfunction, whereas Vpr induces renal tubular epithelial cell apoptosis. HIVAN results from direct infection by HIV-1 and expression of viral genes, especially Nef and Vpr, in renal epithelial cells in a genetically susceptible host. The infected renal epithelium acts as a separate viral compartment from the blood and facilitates evolution of strains distant from blood. Dysregulation of several host cellular pathways, including those involved in cell cycle and apoptosis, ultimately results in the unique histopathological syndrome of HIVAN.
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                Author and article information

                Journal
                Journal ID (nlm-ta): South Afr J HIV Med
                Journal ID (iso-abbrev): South Afr J HIV Med
                Journal ID (publisher-id): HIVMED
                Title: Southern African Journal of HIV Medicine
                Publisher: AOSIS
                ISSN (Print): 1608-9693
                ISSN (Electronic): 2078-6751
                Publication date (Electronic): 22 November 2018
                Publication date Collection: 2018
                Volume: 19
                Issue: 1
                Electronic Location Identifier: 859
                Affiliations
                [1 ]Department of Internal Medicine, Grey’s Hospital, University of KwaZulu-Natal, South Africa
                [2 ]Department of Medicine, University of the Free State, South Africa
                [3 ]Department of Family Medicine, Ladysmith Hospital, University of KwaZulu-Natal, South Africa
                Author notes
                Corresponding author: Anand Moodley, moodleyaa@ 123456ufs.ac.za
                Author information
                https://orcid.org/0000-0002-9492-2991
                https://orcid.org/0000-0002-8205-9342
                https://orcid.org/0000-0002-6707-4800
                Article
                Publisher ID: HIVMED-19-859
                DOI: 10.4102/sajhivmed.v19i1.859
                PMC ID: 6295969
                SO-VID: b99c2958-2878-43cd-ae18-261baf5b1758
                Copyright © © 2018. The Authors
                License:

                Licensee: AOSIS. This work is licensed under the Creative Commons Attribution License.

                History
                Date received : 24 April 2018
                Date accepted : 13 September 2018
                Categories
                Subject: Original Research

                Data availability:

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