FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2065835830> ?p ?o ?g. }

• W2065835830 endingPage "678" @default.
• W2065835830 startingPage "668" @default.
• W2065835830 abstract "Human immunodeficiency virus (HIV) infection started in Africa circa 1930. South Africa has the highest prevalence rate in the world. Although reports of HIV-associated nephropathy (HIVAN) appeared in the early 1980s, the earliest report from sub-Saharan Africa (SSA) came in 1994. Geographical, socioeconomic, political, and ethical factors have worked in concert to shape the character of HIV disease as it is seen in SSA. Political leaders within SSA have, through their actions, significantly contributed to the incidence of HIV infection. Black females, who often face cultural suppression and disadvantage, have a higher prevalence of HIV than males. Too few studies and outcomes data have bedeviled the statistics in SSA in relation to HIVAN prevalence and its management. Much of what is written is approximation and anecdotal. The largest reliable biopsy series comes from the University of Cape Town, where a workable classification of HIVAN has been developed to enable standardization of terminology. Histologic and clinical prognostic indicators with outcomes have been evaluated using this classification. Patients with HIV who present with acute kidney injury appear to have mainly acute tubular necrosis due to sepsis, dehydration, and nephrotoxic drugs. Since the rollout of combination antiretroviral therapy, the extent of HIV infection and kidney disease continues to be modified and possibly retarded. Human immunodeficiency virus (HIV) infection started in Africa circa 1930. South Africa has the highest prevalence rate in the world. Although reports of HIV-associated nephropathy (HIVAN) appeared in the early 1980s, the earliest report from sub-Saharan Africa (SSA) came in 1994. Geographical, socioeconomic, political, and ethical factors have worked in concert to shape the character of HIV disease as it is seen in SSA. Political leaders within SSA have, through their actions, significantly contributed to the incidence of HIV infection. Black females, who often face cultural suppression and disadvantage, have a higher prevalence of HIV than males. Too few studies and outcomes data have bedeviled the statistics in SSA in relation to HIVAN prevalence and its management. Much of what is written is approximation and anecdotal. The largest reliable biopsy series comes from the University of Cape Town, where a workable classification of HIVAN has been developed to enable standardization of terminology. Histologic and clinical prognostic indicators with outcomes have been evaluated using this classification. Patients with HIV who present with acute kidney injury appear to have mainly acute tubular necrosis due to sepsis, dehydration, and nephrotoxic drugs. Since the rollout of combination antiretroviral therapy, the extent of HIV infection and kidney disease continues to be modified and possibly retarded. The world is a dangerous place; not because of people who are evil, but because of the people who don't do anything about it.Albert Einstein1Fitzhenry R.I. The Harper Book of Quotations. 3rd ed. Quill, New York, NY1993: 356Google Scholar In 1984, Pardo et al2Pardo V. Aldana M. Colton R.M. et al.Glomerular lesions in the acquired immunodeficiency syndrome.Ann Intern Med. 1984; 101: 429-434Crossref PubMed Scopus (247) Google Scholar described what is now widely known as the “collapsing glomerulopathy” of human immunodeficiency virus (HIV)-associated nephropathy (HIVAN). This initial description has been substantiated by the works of Rao et al3Rao T.K. Filippone E.J. Nicastri A.D. et al.Associated focal and segmental glomerulosclerosis in the acquired immunodeficiency syndrome.N Engl J Med. 1984; 310: 669-673Crossref PubMed Scopus (495) Google Scholar and D'Agati et al.4D'Agati V. Suh J.I. Carbone L. Appel G. Pathology of HIV-associated nephropathy: a detailed morphologic and comparative study.Kidney Int. 1989; 35: 1358-1370Crossref PubMed Scopus (339) Google Scholar HIVAN, with a predilection for black Africans, is now known to consist of a constellation of findings involving glomerular, interstitial, and tubular changes. Genetic factors appear to involve the apolipoprotein L1 (APOL1) gene,5Tzur S. Rosset S. Shemer R. et al.Missense mutations in the APOL1 gene are highly associated with end stage kidney disease risk previously attributed to the MYH9 gene.Hum Genet. 2010; 128: 345-350Crossref PubMed Scopus (443) Google Scholar which is in strong linkage disequilibrium with nonmuscle myosin heavy chain 9 (MYH9).6Kopp J.B. Smith M.W. Nelson G.W. et al.MYH9 is a major-effect risk gene for focal segmental glomerulosclerosis.Nat Genet. 2008; 40: 1175-1184Crossref PubMed Scopus (579) Google Scholar The role of these genes in sub-Saharan Africa (SSA) has yet to be determined. The interference of HIV-1 viral proteins with the fully differentiated podocyte causes it to proliferate. There also appears to be disruption of contact between the glomerular basement membrane and the podocyte, allowing the podocyte to “fall off” into Bowman space, with loss of glomerular integrity and ultimately collapse of the glomerulus. This gives rise to the well described collapsing focal segmental glomerulosclerosis (FSGS) seen in HIVAN. Renal epithelial cell infection by HIV-1 was demonstrated in 2000.7Bruggeman L.A. Ross M.D. Tanji N. et al.Renal epithelium is a previously unrecognized site of HIV-1 infection.J Am Soc Nephrol. 2000; 11: 2079-2087PubMed Google Scholar However, renal epithelial cells lack CCR5 and CXCR4 receptors, the mechanism by which the virus classically enters to infect T cells, macrophages, and dendritic cells. Evidence suggests that T cells have virologic synapses that allow transfer of the virus from T cells to epithelial cells.8Chen P. Chen B.K. Mosoian A. et al.Virological synapses allow HIV-1 uptake and gene expression in renal tubular epithelial cells.J Am Soc Nephrol. 2011; 22: 496-507Crossref PubMed Scopus (53) Google Scholar Thus, a significant complication of HIV infection is kidney disease. Because up to 30% of HIV-positive patients may have abnormal kidney function, HIV-associated kidney disease has emerged as a relatively common cause of end-stage renal disease and death.9Gupta S.K. Mamlin B.W. Johnson C.S. et al.Prevalence of proteinuria and the development of chronic kidney disease in HIV-infected patients.Clin Nephrol. 2004; 61: 1-6Crossref PubMed Scopus (99) Google Scholar, 10Szczech L.A. Hoover D.R. Feldman J.G. et al.Association between renal disease and outcomes among HIV-infected women receiving or not receiving antiretroviral therapy.Clin Infect Dis. 2004; 39: 1199-1206Crossref PubMed Scopus (156) Google Scholar In Africa, the first report of a biopsy-proven case of HIVAN, featuring a collapsing focal segmental glomerulopathy with tubular microcysts, was published in the South African Medical Journal in 1994.11Bates W.D. Muller N. van de Wal B.W. Jacobs J.C. HIV-associated nephropathy—an initial presentation in an HIV-positive patient.S Afr Med J. 1994; 84: 223-224PubMed Google Scholar By that time, the epidemic of HIV in Africa had commenced many years before. In the ensuing years, there have been very few studies from Africa addressing HIVAN and other HIV-related kidney diseases, and most of what we know today about HIVAN comes from non-African countries. HIV-1 is the dominant type of HIV found in SSA. Its viral ancestor appears to have been a simian immunodeficiency virus found in several chimpanzee colonies in Cameroon, Western Africa.12Keele B.F. Van Heuverswyn F. Li Y. et al.Chimpanzee reservoirs of pandemic and nonpandemic HIV-1.Science. 2006; 313: 523-526Crossref PubMed Scopus (620) Google Scholar The first transfer of simian immunodeficiency virus to humans is believed to have occurred around 1930.13Korber B. Muldoon M. Theiler J. et al.Timing the ancestor of the HIV-1 pandemic strains.Science. 2000; 288: 1789-1796Crossref PubMed Scopus (719) Google Scholar It is likely that HIV-2 originated in the 1940s after transfer from monkeys in Guinea-Bissau (Fig 1).14Lemey P. Pybus O.G. Wang B. Saksena N.K. Salemi M. Vandamme A.M. Tracing the origin and history of the HIV-2 epidemic.Proc Natl Acad Sci U S A. 2003; 100: 6588-6592Crossref PubMed Scopus (265) Google Scholar, 15AVERTHistory of HIV and AIDS in Africa.www.avert.org/history-aids-africa.htmGoogle Scholar The prevalence of this HIV type remains low in SSA. By the 1970s, the Congolese capital of Kinshasa was experiencing the first epidemic of HIV-1. It is thought that the virus was carried to the Congo by an infected individual from Cameroon and the virus entered an urban sexual network. The epidemic spread from west to east, and by the 1980s, the Ugandan population in particular had a high level of infection. At this time, physicians were aware of acquired immunodeficiency syndrome (AIDS) in the United States; however, the connection was not yet made with the epidemic occurring in Africa. Interactions of itinerant groups, such as truck drivers and soldiers, with sex workers hastened the spread along transport and trade routes. As the decade progressed, the epidemic moved south and SSA became the epicenter of the HIV epidemic by the early 1990s. SSA now accounts for more than two-thirds of all people living with HIV and was the site of almost three-quarters of the AIDS-associated deaths that occurred in 2008.16UNAIDSAnnual report 2009.http://www.unaids.org/en/media/unaids/contentassets/dataimport/pub/report/2010/2009_annual_report_en.pdfGoogle Scholar In 2009, an estimated 1.8 million people in SSA became infected with HIV, and the overall population of those living with HIV in this region reached 22.5 million. The country with the largest number of people living with HIV (5.6 million) is South Africa. Blacks are affected more commonly than any other race group. In almost all SSA countries, most of those living with HIV are women, particularly girls and young women aged 15-24 years. In South Africa, there is an ∼21% prevalence in women aged 20-24 years versus ∼7% in men of the same age group.17UNAIDSGlobal report facts sheet sub-Saharan Africa 2010.http://www.unaids.org/documents/20101123_FS_SSA_em_en.pdfGoogle Scholar There has been an absence of surveillance, documentation, and confirmation of renal histologic types in HIV-positive patients in SSA. In addition, little is known about the prevalence and effects of treatment on outcome, and most areas of Africa lack access to analysis by biopsy. The prevalence of HIVAN in the United States has been calculated to be 3.5%-12%18Ross M.J. Klotman P.E. Recent progress in HIV-associated nephropathy.J Am Soc Nephrol. 2002; 13: 2997-3004Crossref PubMed Scopus (121) Google Scholar; its prevalence in SSA has been reported as 6%-45%.19Fabian J. Naiker S. HIV and kidney disease in sub-Saharan Africa.Nat Rev Nephrol. 2009; 5: 591-598Crossref PubMed Scopus (66) Google Scholar However, these prevalence rates have been derived mostly from studies making assumptions of HIVAN without actual histologic confirmation of the disease. Studies from South Africa have tended to more accurately report the prevalence of kidney disease in HIV-positive patients using histologic data.20Han T.M. Naicker S. Ramdial P.K. Assounga A.G. A cross-sectional study of HIV-seropositive patients with varying degrees of proteinuria in South Africa.Kidney Int. 2006; 69: 2243-2250Crossref PubMed Scopus (161) Google Scholar, 21Gerntholtz T.E. Goetsch S.J. Katz I. HIV-related nephropathy: a South African perspective.Kidney Int. 2006; 69: 1885-1891Crossref PubMed Scopus (127) Google Scholar, 22Okpechi I.G. Rayner B.L. Swanepoel C.R. Nephrotic syndrome in adult black South Africans: HIV-associated nephropathy as the main culprit.J Natl Med Assoc. 2010; 102: 1193-1197PubMed Scopus (10) Google Scholar, 23Arendse C.G. Wearne N. Okpechi I.G. Swanepoel C.R. The acute, the chronic and the news of HIV-related renal disease in Africa.Kidney Int. 2010; 78: 239-245Crossref PubMed Scopus (19) Google Scholar, 24Arendse C. Okpechi I. Swanepoel C. Acute dialysis in HIV-positive patients in Cape Town, South Africa.Nephrology. 2011; 16: 39-44Crossref PubMed Scopus (14) Google Scholar Data from our center in Cape Town has shown that the diagnosis of HIVAN was made in 25% of all renal biopsies performed in 2009.25Okpechi I. Swanepoel C. Duffield M. et al.Patterns of renal disease in Cape Town South Africa: a 10-year review of a single-centre renal biopsy database.Nephrol Dial Transplant. 2011; 26: 1853-1861Crossref PubMed Scopus (72) Google Scholar In the past in South Africa, a deliberate decision was made not to perform biopsy on patients with kidney disease in HIV-positive patients. This decision was made due to the poor prognosis of HIVAN without the availability of combination antiretroviral therapy (cART). Since the arrival of cART, this attitude has changed. The largest reliable kidney biopsy series in HIV-positive patients has recently been published by us.26Wearne N, Swanepoel CR, Boulle A, et al. The spectrum of renal histologies seen in HIV with outcomes, prognostic indicators and clinical correlations [published online ahead of print February 7, 2012]. Nephrol Dial Transplant. doi:10.1093/ndt/gfr702.Google Scholar We describe the spectrum of renal pathology seen in 192 biopsies from HIV-positive patients. The patients were predominantly black Africans and there were no whites in the study. We viewed HIVAN as a disease not only of the glomerulus, but accepted that, in addition, HIVAN encompassed interstitial and tubular changes. However, glomerular changes predominated in HIVAN. Collapsing FSGS was found to be the most common variant of HIVAN, and pseudocrescents also featured in this series (Fig 2). There were other histologic subtypes, including the perihilar variant of FSGS. In the case of any variant of FSGS, additional histologic features needed to be present (these included parietal or podocyte hypertrophy or hyperplasia, microcysts, and plasma cell interstitial infiltrate) to be able to attribute the pathology to HIV infection. We described a new variant of FSGS we termed the “fetal” variant,26Wearne N, Swanepoel CR, Boulle A, et al. The spectrum of renal histologies seen in HIV with outcomes, prognostic indicators and clinical correlations [published online ahead of print February 7, 2012]. Nephrol Dial Transplant. doi:10.1093/ndt/gfr702.Google Scholar which resembles the histologic conformation of a fetal glomerulus (Fig 3). The interstitial component of HIVAN has a characteristic lymphocytic infiltrate that is composed predominantly of plasma cells. The diagnostic clincher for HIV involvement in the interstitium is the presence of microcysts (Fig 4).Figure 3The glomerulus shows global collapse and prominence of the epithelial cells. This resembles the histologic configuration of a fetal glomerulus (hematoxylin and eosin stain; original magnification, ×400).View Large Image Figure ViewerDownload Hi-res image Download (PPT)Figure 4Typical microcysts. Massively distended tubules with atrophied and flattened epithelial cells. They contain acellular eosinophilic material (hematoxylin and eosin stain; original magnification, ×400).View Large Image Figure ViewerDownload Hi-res image Download (PPT) Immune complex glomerulonephritis may be seen in conjunction with HIVAN. The most common pattern is mesangiocapillary glomerulonephritis. A second variant is characterized by large subepithelial deposits surrounded by basement membrane extensions.21Gerntholtz T.E. Goetsch S.J. Katz I. HIV-related nephropathy: a South African perspective.Kidney Int. 2006; 69: 1885-1891Crossref PubMed Scopus (127) Google Scholar, 23Arendse C.G. Wearne N. Okpechi I.G. Swanepoel C.R. The acute, the chronic and the news of HIV-related renal disease in Africa.Kidney Int. 2010; 78: 239-245Crossref PubMed Scopus (19) Google Scholar This lesion can be seen on hematoxylin and eosin–stained sections (Fig 5). These deposits may represent either a form of postinfectious glomerulonephritis or a variant of membranous glomerulopathy. Immune complex glomerulonephritis seen without features of HIVAN also appears in this series.26Wearne N, Swanepoel CR, Boulle A, et al. The spectrum of renal histologies seen in HIV with outcomes, prognostic indicators and clinical correlations [published online ahead of print February 7, 2012]. Nephrol Dial Transplant. doi:10.1093/ndt/gfr702.Google Scholar The most common coincidental immune complex glomerulonephritis was membranous glomerulonephritis (Box 1).Box 1The UCT Classification of HIVANGlomerulus •Glomerular variants of HIVAN ◊FSGS collapsing variant◊FSGS noncollapsing variant with additional features◊Global sclerosis with epithelial cell involvement: “fetal” variant•Additional features to glomerular variants of HIVAN ◊Parietal and or visceral epithelial cell hypertrophy and hyperplasia◊Presence of pseudocrescentsInterstitium •Fibrosis•Lymphocytic infiltrate•Plasma cells within the lymphocytic infiltrate•Diffuse inflammatory lymphocytic syndromeTubules •Presence of microcysts•Epithelial cell hyperplasia and hypertrophyHIV + ICGN •With additional features of HIVAN (as described) ◊Mesangiocapillary glomerulonephritis◊Ball in cup: very large subepithelial immune deposits◊Any other type of glomerulonephritis•Without additional features of HIVAN (immune complex disease alone)Others •Diseases unrelated to HIV, eg, granulomas, acute tubular necrosis, drug reactions, lymphomaAbbreviations: FSGS, focal segmental glomerulosclerosis; HIVAN, human immunodeficiency virus–associated nephropathy; ICGN, immune complex glomerulonephritis; UCT, University of Cape Town. Glomerulus •Glomerular variants of HIVAN ◊FSGS collapsing variant◊FSGS noncollapsing variant with additional features◊Global sclerosis with epithelial cell involvement: “fetal” variant•Additional features to glomerular variants of HIVAN ◊Parietal and or visceral epithelial cell hypertrophy and hyperplasia◊Presence of pseudocrescents Interstitium •Fibrosis•Lymphocytic infiltrate•Plasma cells within the lymphocytic infiltrate•Diffuse inflammatory lymphocytic syndrome Tubules •Presence of microcysts•Epithelial cell hyperplasia and hypertrophy HIV + ICGN •With additional features of HIVAN (as described) ◊Mesangiocapillary glomerulonephritis◊Ball in cup: very large subepithelial immune deposits◊Any other type of glomerulonephritis•Without additional features of HIVAN (immune complex disease alone) Others •Diseases unrelated to HIV, eg, granulomas, acute tubular necrosis, drug reactions, lymphoma Abbreviations: FSGS, focal segmental glomerulosclerosis; HIVAN, human immunodeficiency virus–associated nephropathy; ICGN, immune complex glomerulonephritis; UCT, University of Cape Town. Data from Groote Schuur Hospital, Cape Town, South Africa, showed 50% mortality at 4.47 months for patients with HIVAN not receiving cART.26Wearne N, Swanepoel CR, Boulle A, et al. The spectrum of renal histologies seen in HIV with outcomes, prognostic indicators and clinical correlations [published online ahead of print February 7, 2012]. Nephrol Dial Transplant. doi:10.1093/ndt/gfr702.Google Scholar The outcome for all forms of the disease was improved greatly with the initiation of cART (Fig 6). Although HIVAN and the components thereof have come to represent the common manifestations of kidney disease in HIV, the occurrence of acute kidney injury (such as acute tubular necrosis) is common in HIV-positive patients. Studies have reported the incidence of acute kidney injury to be as high as ∼59% for all HIV-infected patients presenting with decreased kidney function.24Arendse C. Okpechi I. Swanepoel C. Acute dialysis in HIV-positive patients in Cape Town, South Africa.Nephrology. 2011; 16: 39-44Crossref PubMed Scopus (14) Google Scholar, 27Williams D.I. Williams D.J. Williams I.G. Unwin R.J. Griffiths M.H. Miller R.F. Presentation, pathology, and outcome of HIV associated renal disease in a specialist centre for HIV/AIDS.Sex Transm Inf. 1998; 74: 179-184Crossref PubMed Scopus (60) Google Scholar The cause of acute tubular necrosis in such instances has been shown to vary, but often is attributed to sepsis, malaria, diarrheal illnesses, rhabdomyolysis, or nephrotoxins (aminoglycosides, co-trimoxazole, antituberculosis drugs, and tenofovir; Box 2).Box 2Causes of Kidney Failure in HIV-Positive Patients in Cape Town Acute •Sepsis•Rhabdomyolysis•Drug toxicity ◊Rifampicin◊Co-trimoxazole◊Aminoglycosides•GN•Pyelonephritis•Renal tuberculosisAcute-on-chronic •HIVAN (± immune complex disease) with ◊ATN◊Nephrotoxic drug◊Granulomatous disease◊Malignant hypertension◊LymphomaChronic •HIVAN•HIVAN + other GN ◊Membranous GN◊Mesangiocapillary GN◊IgA nephropathy◊Mesangioproliferative GN•Idiopathic FSGS•Hypertensive nephrosclerosis•Diabetic nephropathyAbbreviations: ATN, acute tubular necrosis; FSGS, focal segmental glomerulosclerosis; GN, glomerulonephritis; HIVAN, human immunodeficiency virus–associated nephropathy; IgA, immunoglobulin A. Acute •Sepsis•Rhabdomyolysis•Drug toxicity ◊Rifampicin◊Co-trimoxazole◊Aminoglycosides•GN•Pyelonephritis•Renal tuberculosis Acute-on-chronic •HIVAN (± immune complex disease) with ◊ATN◊Nephrotoxic drug◊Granulomatous disease◊Malignant hypertension◊Lymphoma Chronic •HIVAN•HIVAN + other GN ◊Membranous GN◊Mesangiocapillary GN◊IgA nephropathy◊Mesangioproliferative GN•Idiopathic FSGS•Hypertensive nephrosclerosis•Diabetic nephropathy Abbreviations: ATN, acute tubular necrosis; FSGS, focal segmental glomerulosclerosis; GN, glomerulonephritis; HIVAN, human immunodeficiency virus–associated nephropathy; IgA, immunoglobulin A. The social and economic impact of the HIV epidemic in Africa, in particular HIV/AIDS-related poverty and the increasing number of orphans (giving rise to families with children parenting children), perhaps has reached its devastating climax on the continent. The present period of abatement has been brought about by the eventual rollout of cART to an ever increasing number of HIV-positive patients. President Thabo Mbeki of South Africa (immediate past president) and other leaders in Africa had denied that HIV was the only cause of the wasting and destructive disease (initially called “slimmer's disease”) that was seen in the community. Instead, these denialists blamed poverty and consequent malnourishment as the driving force behind the disease process. Dr “Manto” Tshabalala-Msimang served as Minister of Health under Mbeki, and her emphasis on treating South Africa's AIDS epidemic with garlic, beetroot, lemons, and potatoes rather than with antiretroviral medicines set back the public sector rollout of cART by years. This almost certainly caused many thousands to die and perpetuated the ongoing epidemic (new infections and mother-to-baby transmission). She was ridiculed in the local press, and an example of this is shown in a cartoon (Fig 7),28ZapiroLemon is not a vegetable.http://www.zapiro.com/cartoon/123054-040215stGoogle Scholar which originally appeared in the national newspaper, the Sunday Times, on February 15, 2004. Following pressure from activists, notably the Treatment Action Campaign and health care workers, South Africa started providing cART drugs only in 2004. Aside from the denialists, several governments in SSA (except Uganda, Zaire, Zambia, and Senegal) often refuted that there was an epidemic of HIV/AIDS in Africa and showed a cynical skepticism, in which they were willing to accept international aid but were unwilling to combat the virus.29Caraël M. Twenty years of intervention and controversy.in: Denis P. Becker C. The HIV/AIDS Epidemic in Sub-Saharan Africa in a Historical Perspective. Online edition. October 2006: 29-40http://rds.refer.sn/IMG/pdf/AIDSHISTORYALL.pdfGoogle Scholar Also, a study done in Burkina Faso, West Africa, provided interesting data.30Lachaud J.-P. HIV prevalence and poverty in Africa: micro- and macroeconomic evidences applied to Burkina Faso.J Health Econ. 2007; 26: 483-504Crossref PubMed Scopus (41) Google Scholar The results showed that the “treat poverty, treat HIV” theory was flawed. The authors demonstrated that fighting poverty did not necessarily decrease the prevalence of HIV/AIDS. They found that the predicted probability of having HIV was highest in the rich, and the growth of HIV in countries in conflict had been known to be slower than in surrounding countries at peace.31Gisselquist D. Impact of long-term civil disorders and wars on the trajectory of HIV epidemics in sub-Saharan Africa.Sahara J. 2004; 1: 114-127Crossref PubMed Scopus (18) Google Scholar In studies in South Africa, black women have been found to have the highest incidence of HIV infection. This disproportionate increase of females over males is a direct result of the sociocultural differences and economic constraints.32Smith D.J. Premarital sex, procreation, and HIV risk in Nigeria.Stud Fam Plann. 2004; 35: 223-235Crossref PubMed Scopus (52) Google Scholar These factors may have compelled women to initiate sexual partnerships for favors and financial gain (eg, “sugar daddy” relationships).33Luke N. Exchange and condom use in informal sexual relationships in urban Kenya.Econ Dev Cultural Change. 2006; 54: 319-348Crossref Scopus (61) Google Scholar Black females have little bargaining power in this society, which leaves them with limited control over their own sexual behavior.34Clark S. Judith B. Dude A. Protecting girls from HIV/AIDS: the case against child and adolescent marriage.Int Fam Plann Perspect. 2006; 32: 79-88Crossref PubMed Google Scholar The low gross domestic product of most African countries, as well as the burden of communicable diseases, has elevated health care costs above what many African countries are able to afford. The price for urgent or long-term dialysis is far too high for most African countries and dialysis is offered to only those who are able to afford to pay privately (eg, in Nigeria). Alternatively, when governments offer dialysis to their populace, as in South Africa, the finances for dialysis are limited. This restriction in funding has necessitated the development of exclusion criteria by hospital authorities/physicians. These exclusion criteria are artificial and merely serve to act as a gatekeeper to prevent patients from being accepted for dialysis when funding is unavailable. A good example is the development of categories for acceptance that has been in use in Groote Schuur Hospital (Box 3). Category 1 patients will always be treated, category 2 patients will be placed on a waiting list, and category 3 patients will not be accepted into the dialysis program. In reality, category 2 patients seldom “make it” onto the program. As shown in Box 3, HIV-positive status relegates the patient to a category 2 or 3 level.Box 3Assessment Tool for RRT Rationing in Western Cape, South AfricaCategory 1Patients in this category must be accepted for treatment. •Age <50 y•BMI <30 kg/m2•HIV negative•HBsAg negative•South African citizenCategory 2Patients in this category will be accepted depending on availability of space on the program and the number of factors in this category. •Age 50-60 y•BMI 30-35 kg/m2•Hypertension with target-organ damage•Diabetes mellitus•Smoking•HBsAg/HCV positive (no cirrhosis)•HIV positive (CD4 >200 cells/μL, undetectable viral load, on cART)•Late presentation needing urgent dialysis•Comorbid disease (eg, stable IHD)•Previous kidney transplant•Poor home circumstances•Poor social network/support•No proximity to dialysis unitCategory 3Patients in this category will be excluded. •Age >60 y•BMI >35 kg/m2•Transplant contraindicated or associated with unacceptable risk•HIV infection other than described in category 2•Active substance abuse•HBeAg positive or cirrhosis•Diabetes mellitus and age >50 y•Active uncontrollable malignancy with short life expectancy•Non–South African citizen•Advanced irreversible progressive vital organ disease (cardiac/cerebrovascular/liver/lung/unresponsive infections)•Mental illness resulting in diminished capacity to take responsibility for actions•Habitual nonadherence to any medical treatmentAbbreviations: BMI, body mass index; cART, combination antiretroviral therapy; HBeAg, hepatitis B e antigen; HBsAg, hepatitis B surface antigen; HCV, hepatitis C virus; HIV, human immunodeficiency virus; IHD, ischemic heart disease; RRT, renal replacement therapy. Category 1 Patients in this category must be accepted for treatment. •Age <50 y•BMI <30 kg/m2•HIV negative•HBsAg negative•South African citizen Category 2 Patients in this category will be accepted depending on availability of space on the program and the number of factors in this category. •Age 50-60 y•BMI 30-35 kg/m2•Hypertension with target-organ damage•Diabetes mellitus•Smoking•HBsAg/HCV positive (no cirrhosis)•HIV positive (CD4 >200 cells/μL, undetectable viral load, on cART)•Late presentation needing urgent dialysis•Comorbid disease (eg, stable IHD)•Previous kidney transplant•Poor home circumstances•Poor social network/support•No proximity to dialysis unit Category 3 Patients in this category will be excluded. •Age >60 y•BMI >35 kg/m2•Transplant contraindicated or associated with unacceptable risk•HIV infection other than described in category 2•Active substance abuse•HBeAg positive or cirrhosis•Diabetes mellitus and age >50 y•Active uncontrollable malignancy with short life expectancy•Non–South African citizen•Advanced irreversible progressive vital organ disease (cardiac/cerebrovascular/liver/lung/unresponsive infections)•Mental illness resulting in diminished capacity to take responsibility for actions•Habitual nonad" @default.
• W2065835830 created "2016-06-24" @default.
• W2065835830 creator A5024515107 @default.
• W2065835830 creator A5037126701 @default.
• W2065835830 creator A5041398465 @default.
• W2065835830 creator A5085475763 @default.
• W2065835830 date "2012-10-01" @default.
• W2065835830 modified "2023-09-23" @default.
• W2065835830 title "The Evolution of Our Knowledge of HIV-Associated Kidney Disease in Africa" @default.
• W2065835830 cites W1925884511 @default.
• W2065835830 cites W1970070985 @default.
• W2065835830 cites W2007156520 @default.
• W2065835830 cites W2010807875 @default.
• W2065835830 cites W2024610906 @default.
• W2065835830 cites W2027577186 @default.
• W2065835830 cites W2029353650 @default.
• W2065835830 cites W2030803259 @default.
• W2065835830 cites W2037565950 @default.
• W2065835830 cites W2037898843 @default.
• W2065835830 cites W2063711086 @default.
• W2065835830 cites W2073521730 @default.
• W2065835830 cites W2094372310 @default.
• W2065835830 cites W2112311783 @default.
• W2065835830 cites W2115052886 @default.
• W2065835830 cites W2117705817 @default.
• W2065835830 cites W2121965895 @default.
• W2065835830 cites W2126835755 @default.
• W2065835830 cites W2127624109 @default.
• W2065835830 cites W2134127271 @default.
• W2065835830 cites W2135241380 @default.
• W2065835830 cites W2140665904 @default.
• W2065835830 cites W2149136254 @default.
• W2065835830 cites W2151568839 @default.
• W2065835830 cites W2158639804 @default.
• W2065835830 cites W2162606276 @default.
• W2065835830 cites W2168035113 @default.
• W2065835830 cites W2169623461 @default.
• W2065835830 cites W2171628048 @default.
• W2065835830 cites W2172138555 @default.
• W2065835830 cites W2322256416 @default.
• W2065835830 cites W2335458399 @default.
• W2065835830 cites W287569154 @default.
• W2065835830 cites W3121199369 @default.
• W2065835830 cites W4378951505 @default.
• W2065835830 doi "https://doi.org/10.1053/j.ajkd.2012.04.034" @default.
• W2065835830 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/22901595" @default.
• W2065835830 hasPublicationYear "2012" @default.
• W2065835830 type Work @default.
• W2065835830 sameAs 2065835830 @default.
• W2065835830 citedByCount "12" @default.
• W2065835830 countsByYear W20658358302013 @default.
• W2065835830 countsByYear W20658358302015 @default.
• W2065835830 countsByYear W20658358302016 @default.
• W2065835830 countsByYear W20658358302017 @default.
• W2065835830 countsByYear W20658358302018 @default.
• W2065835830 countsByYear W20658358302019 @default.
• W2065835830 countsByYear W20658358302020 @default.
• W2065835830 crossrefType "journal-article" @default.
• W2065835830 hasAuthorship W2065835830A5024515107 @default.
• W2065835830 hasAuthorship W2065835830A5037126701 @default.
• W2065835830 hasAuthorship W2065835830A5041398465 @default.
• W2065835830 hasAuthorship W2065835830A5085475763 @default.
• W2065835830 hasConcept C126322002 @default.
• W2065835830 hasConcept C159047783 @default.
• W2065835830 hasConcept C177713679 @default.
• W2065835830 hasConcept C2778653478 @default.
• W2065835830 hasConcept C2779134260 @default.
• W2065835830 hasConcept C3013748606 @default.
• W2065835830 hasConcept C71924100 @default.
• W2065835830 hasConceptScore W2065835830C126322002 @default.
• W2065835830 hasConceptScore W2065835830C159047783 @default.
• W2065835830 hasConceptScore W2065835830C177713679 @default.
• W2065835830 hasConceptScore W2065835830C2778653478 @default.
• W2065835830 hasConceptScore W2065835830C2779134260 @default.
• W2065835830 hasConceptScore W2065835830C3013748606 @default.
• W2065835830 hasConceptScore W2065835830C71924100 @default.
• W2065835830 hasIssue "4" @default.
• W2065835830 hasLocation W20658358301 @default.
• W2065835830 hasLocation W20658358302 @default.
• W2065835830 hasOpenAccess W2065835830 @default.
• W2065835830 hasPrimaryLocation W20658358301 @default.
• W2065835830 hasRelatedWork W1540807578 @default.
• W2065835830 hasRelatedWork W1588968920 @default.
• W2065835830 hasRelatedWork W2016976166 @default.
• W2065835830 hasRelatedWork W2114905932 @default.
• W2065835830 hasRelatedWork W2471594942 @default.
• W2065835830 hasRelatedWork W2554424493 @default.
• W2065835830 hasRelatedWork W2888428943 @default.
• W2065835830 hasRelatedWork W2919291229 @default.
• W2065835830 hasRelatedWork W2920090081 @default.
• W2065835830 hasRelatedWork W1556208436 @default.
• W2065835830 hasVolume "60" @default.
• W2065835830 isParatext "false" @default.
• W2065835830 isRetracted "false" @default.
• W2065835830 magId "2065835830" @default.
• W2065835830 workType "article" @default.