Clin J Am Soc Nephrol 2: S20-S24, 2007
© 2007 American Society of Nephrology
doi: 10.2215/CJN.03561006
Viruses and Diseases of the Kidney
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HIV-1 and HIV-Associated Nephropathy 25 Years Later
Christina M. Wyatt, and
Paul E. Klotman
Department of Medicine, Division of Nephrology, Mount Sinai School of Medicine, New York, New York
Address correspondence to: Dr. Christina Wyatt, Mount Sinai School of Medicine, Box 1243, One Gustave L. Levy Place, New York, NY 10029. Phone: 212-241-6689; Fax: 212-987-0389; E-mail: christina.wyatt{at}mssm.edu
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Abstract
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Twenty-five years after the first published description of AIDS, HIV-associated nephropathy (HIVAN) remains an important cause of kidney disease in HIV-infected patients. The pathogenesis of HIVAN involves direct HIV infection of the kidney, with both viral and host genetic factors playing an important role. The widespread use of antiretroviral therapy has influenced the epidemiology of HIV-related kidney disease, and the nephrology community should support efforts to improve access to therapy and limit HIV transmission in susceptible minority populations. This article reviews the history of HIV and HIVAN, focusing on advances in the understanding of pathogenesis, epidemiology, and treatment.
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The Early Years: AIDS and AIDS Nephropathy in the Early 1980s
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This year marks the 25th anniversary of the first published report of AIDS, a series of five cases of Pneumocystis carinii pneumonia in healthy young men with male sexual partners (1). In the subsequent year, more than 450 cases were reported to the Centers for Disease Control (2), and the recognized population at risk was expanded to include injection drug users (3) and hemophiliacs (4). The syndrome was formally defined as AIDS by the Centers for Disease Control in September 1982 (5), although the pathogenesis remained unclear. Reports of transfusion-related (6) and maternal-fetal transmission (7) supported an infectious etiology, and the identification of cases in female sexual partners of men with AIDS suggested a role for heterosexual transmission (8). In early 1983, investigators at the Pasteur Institute reported the isolation of a new retrovirus from a patient with early signs of AIDS (9). The next year, researchers at the National Cancer Institute confirmed the presence of a previously isolated human T cell leukemia virus (HTLV-III) in peripheral lymphocytes from patients with AIDS (10,11) and subsequently cloned the retrovirus that now is known as HIV-1 (12).
In 1984, there were several reports of a unique and rapidly progressive form of focal sclerosing glomerulosclerosis (FSGS) in patients with AIDS (13–15). The characteristic glomerular "collapse" was actually first described in uninfected patients (16), but the collapsing FSGS that is associated with HIV is distinguished by the presence of microcystic tubular dilation and interstitial inflammation (17). Although "HIV-associated nephropathy" (HIVAN) was initially described in the setting of advanced AIDS, it was soon recognized that FSGS could also precede the clinical symptoms of AIDS (18). As more cases were reported, it also became apparent that HIVAN primarily affected patients of African descent (18,19). Studies suggested that HIV-1 might infect the kidney or cells within the kidney in HIVAN (20,21), but definitive evidence for renal epithelial infection by HIV-1 did not come until 2000 (Figure 1) (22). Despite the rapid progression to ESRD and death among patients with HIVAN (18), kidney disease received relatively little attention compared with AIDS-defining opportunistic infections and malignancies in the first 10 yr of the epidemic.
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Figure 1. In situ hybridization for HIV-1 mRNA in kidney biopsies. (A and B) Kidney biopsy from an HIV-negative patient demonstrating no HIV-1 mRNA in the sense control (A) or the antisense (B) hybridization of a serial section. (C and D) Kidney biopsy from an HIV-positive patient with kidney disease. No hybridization was observed in the sense control (C). Antisense hybridization (D) demonstrates HIV-1 mRNA in the cytoplasm of tubular epithelial cells and in cellular casts (CC) in the tubular lumen (TL) but not in protein casts (PC). Magnifications: x125 in A and B; x60 in C and D.
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A Period of Progress: Scientific Advances in HIV-1 and HIVAN, 1985 to 2006
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The late 1980s and 1990s were marked by rapid progress in the field of HIV. The US Food and Drug Administration approved the first commercial test for HIV-1 infection in 1985 and the first antiretroviral agent, zidovudine, in 1987. Two additional nucleoside reverse transcriptase inhibitors were approved by the Food and Drug Administration in 1991, prompting discussion of combination therapy. With the approval of the first protease inhibitor in 1995, combination regimens, or highly active antiretroviral therapy (HAART), quickly became the standard of care, with dramatic reductions in AIDS-related mortality (23). Despite the optimism prompted by these improvements in survival, scientists began to consider the implications of possible reservoirs for HIV-1 replication in the central nervous system and in mononuclear cells (24–26). In 1997, scientists identified a viral reservoir in memory T cells (27) and demonstrated HIV-1 replication in lymph nodes in the setting of undetectable plasma viral load (28). The recognition that HIV infection could not be eradicated with available therapy prompted new interest in long-term complications of HIV infection and antiretroviral therapy, including metabolic disorders and liver and kidney diseases.
During this period of progress, optimism, and disappointment in the study of HIV, laboratory investigators also gained significant insights into the pathogenesis of HIVAN. In 1991, investigators at the National Institutes of Health described a transgenic mouse model of HIV-1 infection (Tg26) that developed kidney disease that was identical to human HIVAN (29). The Tg26 mouse model expresses a gag/pol-deleted HIV-1 transgene and is the basis for much of our current understanding of HIVAN pathogenesis. Reciprocal transplantation of kidneys between Tg26 and wild-type mice demonstrated that viral gene expression in the kidney is required for the development of HIVAN (30). Serial deletion of HIV genes from the Tg26 model identified specific viral genes, nef and vpr, which are involved in the pathogenesis of HIVAN (31,32). An HIV-1 transgenic rat model also develops kidney disease that resembles HIVAN and may provide another resource for future studies (33,34).
Targeted expression of viral genes in lymphocytes and lymphoid tissue has been shown to recapitulate some but not all of the pathologic findings that are observed in the Tg26 mouse model and in human HIVAN, suggesting that HIV-1 gene expression in both renal and nonrenal tissues may play a role in the development of HIVAN (32,35). More recently, the development of HIVAN in a mouse model with podocyte-selective expression of HIV-1 suggests that expression in the glomerular epithelium is sufficient (36) but does not exclude a synergistic role for HIV gene expression in nonrenal tissues. In this model, murine genetic background also affects the development of kidney disease. Similar observations in the Tg26 mouse model, which demonstrates significant variability in renal phenotype when bred onto different genetic backgrounds, led to the identification of a genetic susceptibility locus on mouse chromosome 3 (37). These animal data are consistent with the clinical observation that host genetic factors clearly play an important role. HIVAN occurs almost exclusively in patients of African descent (18,19,38,39), and patients with ESRD secondary to HIVAN are more likely to have a family history of ESRD (40).
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A Global Epidemic of AIDS-Related Renal Disease: Epidemiology of HIV-1 and HIVAN in the HAART Era
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With the widespread introduction of HAART in 1996, there was a dramatic decline in AIDS-related deaths in the United States (23). The proportion of deaths that are attributable to AIDS-defining conditions has continued to decline, with chronic complications such as liver and kidney disease becoming increasingly important contributors to mortality in the HAART era (41). At the same time, there has been a more subtle decrease in the incidence of ESRD related to HIV, which reached a plateau at approximately 800 to 900 new cases per year in the United States (Figure 2) (42). Survival among HIV-infected dialysis patients has also improved in the HAART era, approaching survival rates in the general ESRD population (43). On the basis of these data and the increasing prevalence of HIV infection among susceptible black individuals, the pool of patients who are at risk for developing HIVAN has expanded dramatically. Mathematical models that take into account both the expanding population and the impact of HAART in decreasing the incidence of HIVAN in susceptible individuals predict a substantial increase in the number of HIV-positive ESRD patients in the United States (Figure 2) (42).
In sub-Saharan Africa, where an estimated 25 million people are living with HIV/AIDS (44), expanding access to antiretroviral therapy will improve survival and may also be accompanied by an epidemic of HIVAN. Cross-sectional data from South Africa demonstrate albuminuria in 7% of patients, with a surprisingly high prevalence of biopsy-proven HIVAN in patients with microalbuminuria (45). In a series of 99 consecutive kidney biopsies in HIV-infected black South Africans, 27% were diagnostic of HIVAN (46). Cross-sectional data from 195 HAART-naïve Ugandans revealed that 43% had a creatinine clearance <50 ml/min, and 21% had dipstick proteinuria (47), whereas the median creatinine clearance in 90 HAART-naïve Nigerian patients was <60 ml/min (48). In a cohort of 740 HAART-naïve Rwandan women, the prevalence of proteinuria was as high as 13% in women with a CD4 cell count <200 (49). Preliminary data from 3313 patients who are enrolled in a randomized antiretroviral trial in Uganda and Zimbabwe demonstrate stabilization or slight improvement in kidney function after the initiation of HAART (50). These studies suggest that antiretroviral therapy improves renal function, possibly because of underlying HIVAN. Of note, all of these studies used the Cockcroft-Gault equation to estimate GFR, raising the possibility that malnutrition and low body weight may have biased the estimates. Neither of the currently accepted estimation equations has been well validated in HIV-positive patients, and neither has been evaluated in an African population. With expanding access to HAART, including potentially nephrotoxic agents, the accurate estimation of kidney function in this population will be an important challenge.
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Treatment and Prevention of HIVAN in 2006
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Despite remarkable scientific progress in elucidating the pathogenesis of HIVAN, current recommendations for treatment are largely based on observational data and uncontrolled trials. The decline in the incidence of HIV-related ESRD after the introduction of HAART strongly suggests a role for antiretroviral therapy in the treatment of HIVAN (42), which is further supported by reports of clinical and histologic improvement after the initiation of HAART (51,52) and by retrospective cohort studies (53,54). The efficacy of HAART is also consistent with the pathogenic role of direct HIV infection in the development of HIVAN (22). Until recently, the adjunctive use of corticosteroids was not supported by known pathogenic mechanisms, although uncontrolled studies have suggested some improvement in the clinical course of HIVAN (55–57). Recent in vitro data demonstrate a potential role for inflammatory mediators in the tubulointerstitial compartment (58), providing some scientific rationale for the use of corticosteroids in active disease. Support for the use of angiotensin-converting enzyme inhibitors and angiotensin receptor blockers is extrapolated from evidence of benefit in other proteinuric kidney diseases, with limited data in HIVAN (59,60).
Although the introduction of HAART has had a significant impact on the epidemiology of HIV-related kidney disease, antiretroviral therapy seem to be only partially protective (42). This may reflect a combination of incomplete efficacy, suboptimal adherence, and lack of universal access to HAART. In addition, long-term HAART may be complicated by direct nephrotoxicity or by metabolic disorders that are associated with the development of kidney disease, such as hypertension and diabetes (61,62). With the potential for a global epidemic of HIVAN, nephrologists must look beyond antiretroviral therapy for opportunities to have an impact on the epidemiology of HIV-related kidney disease. The nephrology community should support efforts to prevent the spread of HIV infection in susceptible minority populations, including educational campaigns, condom distribution, and harm reduction programs for injection drug users. After more than two decades of investigation into the pathogenesis of HIVAN, nephrologists should join the fight against the known causative agent: HIV itself. This should be done through political and social activism that supports better access to therapy, state and federally supported medical care for HIV-infected patients, and strategies to limit HIV transmission.
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Disclosures
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None.
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References
|
|---|
- Centers for Disease Control (CDC): Pneumocystis pneumonia—Los Angeles.
MMWR Morb Mortal Wkly Rep30
:250
–252,1981[Medline]
- Centers for Disease Control (CDC): Update on Kaposi's sarcoma and opportunistic infections in previously healthy persons—United States.
MMWR Morb Mortal Wkly Rep31
: 294,300
–301,1982
- Masur H, Michelis MA, Greene JB, Onorato I, Stouwe RA, Holzman RS, Wormser G, Brettman L, Lange M, Murray HW, Cunningham-Rundles S: An outbreak of community acquired Pneumocystis carinii pneumonia: Initial manifestation of cellular immune dysfunction.
N Engl J Med305
:1431
–1438,1982
- Centers for Disease Control (CDC): Pneumocystis carinii pneumonia among persons with hemophilia A.
MMWR Morb Mortal Wkly Rep31
:365
–367,1982[Medline]
- Centers for Disease Control (CDC): Update on acquired immune deficiency syndrome (AIDS)—United States.
MMWR Morb Mortal Wkly Rep31
:507
–514,1982[Medline]
- Centers for Disease Control (CDC): Possible transfusion-associated acquired immune deficiency syndrome, AIDS—California.
MMWR Morb Mortal Wkly Rep31
:652
–654,1982[Medline]
- Centers for Disease Control (CDC): Unexplained immunodeficiency and opportunistic infections in infants—New York, New Jersey, California.
MMWR Morb Mortal Wkly Rep31
:665
–667,1982[Medline]
- Centers for Disease Control (CDC): Immunodeficiency among female sexual partners of males with acquired immune deficiency syndrome (AIDS)—New York.
MMWR Morb Mortal Wkly Rep31
:697
–698,1983[Medline]
- Barre-Sinoussi F, Chermann JC, Rey F, Nugeyre MT, Chamaret S, Gruest J, Dauguet C, Axler-Blin C, Brun-Vezinet F, Rouzioux C, Rozenbaum W, Montagnier L: Isolation of a T-lymphotropic retrovirus from a patient at risk for acquired immune deficiency syndrome (AIDS).
Science220
:868
–871,1983[Abstract/Free Full Text]
- Gallo RC, Sarin PS, Gelmann EP, Robert-Guroff M, Richardson E, Kalyanaraman VS, Mann D, Sidhu GD, Stahl RE, Zolla-Pazner S, Leibowitch J, Popovic M: Isolation of human T-cell leukemia virus in acquired immune deficiency syndrome (AIDS).
Science220
:865
–867,1983[Abstract/Free Full Text]
- Gallo RC, Salahuddin SZ, Popovic M, Shearer GM, Kaplan M, Haynes BF, Palker TJ, Redfield R, Oleske J, Safai B, et al.: Frequent detection and isolation of cytopathic retroviruses (HTLV-III) from patients with AIDS and at risk for AIDS.
Science224
:500
–503,1984[Abstract/Free Full Text]
- Hahn BH, Shaw GM, Popovic M, Lo Monico A, Gallo RC, Wong-Staal F: Molecular cloning and characterization of the HTLV-III virus associated with AIDS.
Nature312
:166
–169,1984[CrossRef][Medline]
- Rao TK, Filippone EJ, Nicastri AD, Landesman SH, Frank E, Chen CK, Friedmann EA: Associated FSGS in AIDS.
N Engl J Med310
:669
–673,1984[Abstract]
- Gardenschwartz MH, Lerner CW, Seligson GR, Zabetakis PM, Rotterdam H, Tapper ML, Michelis MF, Bruno MS: Renal disease in patients with AIDS: A clinicopathologic study.
Clin Nephrol21
:197
–204,1984[Medline]
- Pardo V, Aldana M, Colton RM, Fischl MA, Jaffe D, Moskowitz L, Hensley GT, Bourgoignie JJ: Glomerular lesions in the acquired immunodeficiency syndrome.
Ann Intern Med101
:429
–434,1984[Abstract/Free Full Text]
- Weiss MA, Daquioag E, Margolin EG, Pollak VE: Nephrotic syndrome, progressive irreversible renal failure, and glomerular "collapse": A new clinicopathologic entity.
Am J Kidney Dis7
:20
–28,1986[Medline]
- D'Agati V, Suh JI, Carbone L, Cheng JT, Appel G: Pathology of HIV-associated nephropathy: A detailed morphologic and comparative study.
Kidney Int35
:1358
–1370,1989[Medline]
- Carbone L, D'Agati V, Cheng JT, Appel GB: Course and prognosis of human immunodeficiency virus-associated nephropathy.
Am J Med87
:389
–395,1989[Medline]
- Cantor ES, Kimmel PL, Bosch JP: Effect of race on expression of acquired immunodeficiency syndrome-associated nephropathy.
Arch Intern Med151
:125
–128,1991[Abstract/Free Full Text]
- Cohen AH, Sun NC, Shapshak P, Imagawa DT: Demonstration of human immunodeficiency virus in renal epithelium in HIV-associated nephropathy.
Mod Pathol2
:125
–128,1989[Medline]
- Kimmel PL, Ferreira-Centeno A, Farkas-Szallasi T, Abraham AA, Garrett CT: Viral DNA in microdissected renal biopsy tissue from HIV infected patients with nephrotic syndrome.
Kidney Int43
:1347
–1352,1993[Medline]
- Bruggeman LA, Ross MD, Tanji N, Cara A, Dikman S, Gordon RE, Burns GC, D'Agati VD, Winston JA, Klotman ME, Klotman PE: Renal epithelium is a previously unrecognized site of HIV-1 infection.
J Am Soc Nephrol11
:2079
–2087,2000[Abstract/Free Full Text]
- Palella FJ, Delaney KM, Moorman AC, Loveless MO, Fuhrer J, Satten GA, Aschman DJ, Holmberg SD: Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection. HIV Outpatient Study Investigators.
N Engl J Med26
:853
–860,1998
- Koenig S, Gendelman HE, Orenstein JM, Dal Canto MC, Pezeshkpour GH, Yungbluth M, Janotta F, Aksamit A, Martin MA, Fauci AS: Detection of AIDS virus in macrophages in brain tissue from AIDS patients with encephalopathy.
Science233
:1089
–1093,1996
- Stoler MH, Eskin TA, Benn S, Angerer RC, Angerer LM: Human T-cell lymphotropic virus type III infection of the central nervous system. A preliminary in situ analysis.
JAMA256
:2360
–2364,1986[Abstract/Free Full Text]
- McElrath MJ, Pruett JE, Cohn ZA: Mononuclear phagocytes of blood and bone marrow: Comparative roles as viral reservoirs in human immunodeficiency virus type 1 infections.
Proc Natl Acad Sci U S A86
:675
–679,1989[Abstract/Free Full Text]
- Finzi D, Hermankova M, Pierson T, Carruth LM, Buck C, Chaisson RE, Quinn TC, Chadwick K, Margolick J, Brookmeyer R, Gallant J, Markowitz M, Ho DD, Richman DD, Siliciano RF: Identification of a reservoir for HIV-1 in patients on highly active antiretroviral therapy.
Science278
:1295
–1300,1997[Abstract/Free Full Text]
- Wong JK, Gunthard HF, Havlir DV, Zhang ZQ, Haase AT, Ignacio CC, Kwok S, Emini E, Richman DD: Reduction of HIV-1 in blood and lymph nodes following potent antiretroviral therapy and the virologic correlates of treatment failure.
Proc Natl Acad Sci U S A94
:12574
–12579,1997[Abstract/Free Full Text]
- Dickie P, Felser J, Eckhaus M, Bryant J, Silver J, Marinos N, Notkins AL: HIV-associated nephropathy in transgenic mice expressing HIV-1 genes.
Virology185
:109
–119,1991[CrossRef][Medline]
- Bruggeman LA, Dikman S, Meng C, Quaggin SE, Coffman TM, Klotman PE: Nephropathy in human immunodeficiency virus-1 transgenic mice is due to renal transgene expression.
J Clin Invest100
:84
–92,1997[Medline]
- Kajiyama W, Kopp JB, Marinos NJ, Klotman PE, Dickie P: HIV-transgenic mice lacking gag-pol-nef develop glomerulosclerosis and express viral RNA and protein in glomerular epithelial and tubular cells.
Kidney Int58
:1148
–1159,2000[CrossRef][Medline]
- Dickie P, Roberts A, Uwiera R, Witmer J, Sharma K, Kopp JB: Focal glomerulosclerosis in proviral and c-fms transgenic mice links Vpr expression to HIV-associated nephropathy.
Virology322
:69
–81,2004[CrossRef][Medline]
- Reid W, Sadowska M, Denaro F, Rao S, Foulke J, Hayes N, Jones O, Doodnauth D, Davis H, Sill A, O'Driscoll P, Huso D, Fouts T, Lewis G, Hill M, Kamin-Lewis R, Wei C, Ray P, Gallo RC, Reitz M, Bryant J: An HIV-1 transgenic rat that develops HIV-related pathology and immunologic dysfunction.
Proc Natl Acad Sci U S A98
:9271
–9276,2001[Abstract/Free Full Text]
- Ray PE, Liu X, Robinson LR, Reid W, Xu L, Owens JW, Jones OD, Denaro F, Davis HG, Bryant JL: A novel HIV-1 transgenic rat model of childhood HIV-1 associated nephropathy.
Kidney Int6
:2242
–2251,2003
- Hanna Z, Kay DG, Cool M, Jothy S, Rebai N, Jolicoeur P: Transgenic mice expressing human immunodeficiency virus type 1 in immune cells develop a severe AIDS-like syndrome.
J Virology72
:121
–132,1998[Abstract/Free Full Text]
- Zhong J, Zuo Y, Ma J, Fogo AB, Jolicoeur P, Ichikawa I, Matsusaka T: Expression of HIV-1 genes in podocytes alone can lead to the full spectrum of HIV-1-associated nephropathy.
Kidney Int68
:1048
–1060,2005[CrossRef][Medline]
- Gharavi AG, Ahmad T, Wong RD, Hooshyar R, Vaughn J, Oller S, Frankel RZ, Bruggeman LA, D'Agati VD, Klotman PE, Lifton RP: Mapping a locus for susceptibility to HIV-1-associated nephropathy to mouse chromosome 3.
Proc Natl Acad Sci U S A101
:2488
–2493,2004[Abstract/Free Full Text]
- Lucas GM, Eustace JA, Sozio S, Mentari EK, Appiah KA, Moore RD: Highly active antiretroviral therapy and the incidence of HIV-1-associated nephropathy: A 12-year cohort study.
AIDS18
:541
–546,2004[CrossRef][Medline]
- Kopp JB, Winkler C: HIV-associated nephropathy in African Americans.
Kidney Int63
:43
–49,2003[Medline]
- Freedman BI, Soucie JM, Stone SM, Pegram S: Familial clustering of end-stage renal disease in blacks with HIV-associated nephropathy.
Am J Kidney Dis34
:254
–258,1999[Medline]
- Selik RM, Byers RH Jr, Dworkin MS: Trends in diseases reported on US death certificates that mentioned HIV infection, 1987–1999.
J Acquir Immune Defic Syndr29
:378
–387,2002[Medline]
- Schwartz EJ, Szczech LA, Ross MJ, Klotman ME, Winston JA, Klotman PE: HAART and the epidemic of HIV+ end stage renal disease.
J Am Soc Nephrol16
:2412
–2420,2005[Abstract/Free Full Text]
- Abbott KC, Hypolite I, Welch PG, Agodoa LY: Human immunodeficiency virus/acquired immunodeficiency syndrome-associated nephropathy at end-stage renal disease in the United States: Patient characteristics and survival in the pre highly active antiretroviral therapy era.
J Nephrol14
:377
–383,2001[Medline]
- UNAIDS 2006 Global Report. Available at: http://www.unaids.org/en/HIV_data/2006GlobalReport. Accessed September 27, 2006
- Han TM, Naicker S, Ramdial PK, Assounga AG: A cross-sectional study of HIV-seropositive patients with varying degrees of proteinuria in South Africa.
Kidney Int69
:2243
–2250,2006[CrossRef][Medline]
- Gerntholtz TE, Goetsch SJW, Katz I: HIV-related nephropathy: A South African perspective.
Kidney Int69
:1885
–1891,2006[CrossRef][Medline]
- Olson D, Thomas E, Allheimen M, Balkan S, Szumilin E, Humblet P: Impaired renal function of patients initiating HAART in two developing countries [Abstract]. 13th Conference on Retroviruses and Opportunistic Infections, Denver, Colorado, February 5 to 8, 2006
- Agbaji O, Gwanzhi N, Idoko J: Factors affecting the GFR of ARV-naïve HIV-1-infected patients at the Jos Teaching Hospital, Nigeria [Abstract]. XVI International AIDS Conference, Toronto, Canada, August 13 to 18, 2006
- Mugabo JS, Lu J, Binagwaho A, Cohen M, Munyakazi L, Ndamage F, d'Adesky AC, Szczech L: Proteinuria, hematuria, and creatinine clearance in Rwandan women with and without HIV infection [Abstract]. XVI International AIDS Conference, Toronto, Canada, August 13 to 18, 2006
- Reid A, Stohr W, Walker S, Ssali F, Munderi P, Gilks C, on behalf of the DART Trial: Glomerular dysfunction and associated risk factors following initiation of ART in adults with HIV infection in Africa [Abstract]. XVI International AIDS Conference, Toronto, Canada, August 13 to 18, 2006
- Wali RK, Drachenberg CI, Papadimitriou JC, Keay S, Ramos E: HIV-1-associated nephropathy and response to highly-active antiretroviral therapy.
Lancet352
:783
–784,1998[CrossRef][Medline]
- Winston JA, Bruggeman LA, Ross MD, Jacobson J, Ross L, D'Agati VD, Klotman PE, Klotman ME: Nephropathy and establishment of a renal reservoir of HIV type 1 during primary infection.
N Engl J Med344
:1979
–1984,2001[Free Full Text]
- Szczech LA, Edwards LJ, Sanders LL, van der Horst C, Bartlett JA, Heald AE, Svetky LP: Protease inhibitors are associated with a slowed progression of HIV-related renal diseases.
Clin Nephrol57
:336
–341,2002[Medline]
- Atta MG, Gallant JE, Rahman MH, Nagajothi N, Racusen LC, Scheel PJ, Fine DM: Antiretroviral therapy in the treatment of HIV-associated nephropathy.
Nephrol Dial Transplant21
:2809
–2813,2006[Abstract/Free Full Text]
- Eustace JA, Nuermberger E, Choi M, Scheel PJ, Moore R, Briggs WA: Cohort study of the treatment of severe HIV-associated nephropathy with corticosteroids.
Kidney Int58
:1253
–1260,2000[CrossRef][Medline]
- Smith MC, Austen JL, Carey JT, Emancipator SN, Herbener T, Gripshover B, Mbanefo C, Phinney M, Rahman M, Salata RA, Weigel K, Kalayjian RC: Prednisone improves renal function and proteinuria in human immunodeficiency virus-associated nephropathy.
Am J Med101
:41
–48,1996[CrossRef][Medline]
- Watterson MK, Detwiler RK, Bolin P: Clinical response to prolonged corticosteroids in a patient with human immunodeficiency virus-associated nephropathy.
Am J Kidney Dis29
:624
–626,1997
- Ross MJ, Fan C, Ross MD, Chu TT, Shi Y, Kaufman L, Zhang W, Klotman ME, Klotman PE: HIV-1 infection initiates an inflammatory cascade in human renal tubular epithelial cells.
J Acquir Immune Defic Syndr42
:1
–11,2006[CrossRef][Medline]
- Kimmel PL, Mishkin GJ, Umana WO: Captopril and renal survival in patients with human immunodeficiency virus nephropathy.
Am J Kidney Dis28
:202
–208,1996[Medline]
- Wei A, Burns GC, Williams BA, Mohammed NB, Visintainer P, Sivak SL: Long-term renal survival in HIV-associated nephropathy with angiotensin-converting enzyme inhibition.
Kidney Int64
:1462
–1471,2003[CrossRef][Medline]
- Izzedine H, Launay-Vacher V, Deray G: Antiviral drug-induced nephrotoxicity.
Am J Kidney Dis45
:804
–817,2005[CrossRef][Medline]
- Wyatt CM, Klotman PE: Antiretroviral therapy and the kidney: Balancing benefit and risk in patients with HIV infection.
Expert Opin Drug Saf5
:275
–287,2006[CrossRef][Medline]
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Abstract
The Early Years: AIDS...
