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• W1970070985 abstract "Human immunodeficiency virus (HIV)-associated nephropathy (HIVAN) is the most common finding on renal biopsy in HIV-infected black patients and is also the commonest cause of end-stage renal disease in these patients. Early detection of HIVAN may be beneficial in evaluating early treatment. This study examined the pattern of renal diseases in HIV-infected South Africans and also attempted to diagnose HIVAN at an early stage. In this single-center cross-sectional study, 615 HIV-infected patients were screened for proteinuria. Thirty patients with varying degrees of proteinuria underwent renal biopsy. Patients with diabetes mellitus, uncontrolled hypertension, known causes of chronic kidney disease, and serum creatinine above 250 μmol/l were excluded. Patients in this study were not on antiretroviral therapy. HIVAN was found in 25 (83%) patients. Six of them (24%) had microalbuminuria. Altogether, seven patients with persistent microalbuminuria were biopsied and six (86%) showed HIVAN. Other biopsy findings included membranoproliferative nephropathy in two (7%) and interstitial nephritis in three (10%). Four patients with HIVAN had associated membranous nephropathy. HIVAN is the commonest biopsy finding among our study patients with HIV infection who present with varying degrees of proteinuria. Microalbuminuria is a manifestation of HIVAN in our study patients. Therefore, microalbuminuria may be an early marker of HIVAN, and screening for its presence may be beneficial. Renal biopsy may be considered in seropositive patients who present with persistent microalbuminuria, especially with low CD4 counts irrespective of good renal function. This will allow diagnosis and treatment of HIVAN at an early stage and may prevent further disease progression. Human immunodeficiency virus (HIV)-associated nephropathy (HIVAN) is the most common finding on renal biopsy in HIV-infected black patients and is also the commonest cause of end-stage renal disease in these patients. Early detection of HIVAN may be beneficial in evaluating early treatment. This study examined the pattern of renal diseases in HIV-infected South Africans and also attempted to diagnose HIVAN at an early stage. In this single-center cross-sectional study, 615 HIV-infected patients were screened for proteinuria. Thirty patients with varying degrees of proteinuria underwent renal biopsy. Patients with diabetes mellitus, uncontrolled hypertension, known causes of chronic kidney disease, and serum creatinine above 250 μmol/l were excluded. Patients in this study were not on antiretroviral therapy. HIVAN was found in 25 (83%) patients. Six of them (24%) had microalbuminuria. Altogether, seven patients with persistent microalbuminuria were biopsied and six (86%) showed HIVAN. Other biopsy findings included membranoproliferative nephropathy in two (7%) and interstitial nephritis in three (10%). Four patients with HIVAN had associated membranous nephropathy. HIVAN is the commonest biopsy finding among our study patients with HIV infection who present with varying degrees of proteinuria. Microalbuminuria is a manifestation of HIVAN in our study patients. Therefore, microalbuminuria may be an early marker of HIVAN, and screening for its presence may be beneficial. Renal biopsy may be considered in seropositive patients who present with persistent microalbuminuria, especially with low CD4 counts irrespective of good renal function. This will allow diagnosis and treatment of HIVAN at an early stage and may prevent further disease progression. About 42 million people worldwide have been infected with the human immunodeficiency virus (HIV).1UNAIDS/WHO AIDS epidemic update: December 2004Google Scholar Almost 30 million HIV-infected people live in Africa, especially in sub-Saharan Africa, which is the most affected region in the world.2.Joint United Nation Programme on HIV/AIDS and World Health Organization Report on the Global HIV/AIDS Epidemic. World Health Organization, Geneva1997Google Scholar Sub-Saharan Africa has just over 10% of the world's population, but is home to 60% of the world's population of those living with HIV, approximately 25.4 million people. In South Africa, the estimate of HIV-1 prevalence from the national population-based survey in adults aged 15–49 years was about 16%,3.Shisana O. Simbayi L. Nelson Mandela/HSRC study of HIV/AIDS: South African national HIV prevalence, behavioural risks and mass media – household survey 2002. Human Sciences Research Council, Cape Town2002Google Scholar whereas the UNAIDS/WHO estimate based on antenatal clinic data was 20.1%.4.UNAIDS Report on the global HIV/AIDS epidemic. UNAIDS, Geneva2002Google Scholar It has the highest number of people living with HIV in the world, estimated at 5.3 million, with average life expectancy below the age of 40 years. HIV infection affects multiple organs and the kidney is a common target. A variety of renal syndromes may occur during the course of HIV infection.5.Weiner N.J. Goodman J.W. Kimmel P.L. The HIV-associated renal diseases: current insight into pathogenesis and treatment.Kidney Int. 2003; 63: 1618-1631Abstract Full Text Full Text PDF PubMed Scopus (109) Google Scholar These can be either acute or chronic. HIV-associated nephropathy (HIVAN) is one of the chronic kidney diseases directly caused by HIV infection.6.Herman E.S. Klotman P.E. HIV-associated nephropathy: epidemiology, pathogenesis, and treatment.Semin Nephrol. 2003; 23: 200-208Abstract Full Text Full Text PDF PubMed Scopus (64) Google Scholar Black patients have a relative risk of 51.1 for developing end-stage renal disease from AIDS or an AIDS-defining diagnosis compared with white patients.7.Barisoni L. Pathologic features of HIV-associated nephropathy. In: Kimmel PL, moderator. Pathogenesis and treatment of HIV-associated renal diseases: lessons from clinical and animal studies, molecular pathologic correlations, and genetic investigations.Ann Intern Med. 2003; 139: 218-220Google Scholar HIVAN is reported as the commonest form of chronic renal disease in HIV-infected patients and is the third leading cause of end-stage renal disease in African Americans aged 20–64 in the United States.8.D'Agati V. Appel G.B. HIV infection and the kidney.J Am Soc Nephrol. 1997; 8: 138-152PubMed Google Scholar, 9.Monahan M. Tanji N. Klotman P.E. HIV-associated nephropathy: an urban epidemic.Semin Nephrol. 2001; 21: 394-402Abstract Full Text PDF PubMed Scopus (46) Google Scholar, 10.US Renal Data System (USRDS) USRDS 2001 Annual Data Report. The National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD2001Google Scholar However, the actual incidence and prevalence of renal diseases in HIV infection in general, and that of HIVAN in particular, are unknown; this renders epidemiologic assessments difficult. In Africa, there is also a paucity of data regarding renal involvement in HIV disease. The aim of this study, therefore, was to examine the pattern of renal involvement in HIV-infected patients in South Africa. Early detection of HIVAN may be beneficial in evaluating early treatment in an attempt to protect the kidney from further disease progression. This study, therefore, also attempted to diagnose HIVAN at an early stage. A total of 615 patients were screened between April 2002 and April 2004. The characteristics of the patients are shown in Table 1. Thirty-eight patients (6%) were found to have proteinuria. Microalbuminuria was tested in 90 patients who agreed to participate further in the study and was present in 32 patients (36%). However, persistent microalbuminuria was noted in only seven patients (8%). Of 45 patients (38 with proteinuria and seven with persistent microalbuminuria), only 30 patients underwent renal biopsy. Among the proteinuric patients, 10 were lost to follow-up before the renal biopsy was performed and five refused to have renal biopsy; all seven patients with persistent microalbuminuria agreed to the procedure. All were black Africans except for one patient who was of mixed race of African origin as defined by the registration office, based on the national identification document. Of the 30 patients, 12 (40%) were male and 18 (60%) were female; mean age was 35 (range 17–43) years. The mean CD4 count was 251/mm3 (range 3–641/mm3).Table 1Characteristics of patients evaluated for proteinuriaCharacteristicsProteinuria negativeMicroalbuminuric UP 0.03–0.3 g/24 hMacroalbuminuric (proteinuric) UP>0.3 g/24 hP-valueDemographics Patients tested61590615 Patients classified570738 Patients characterized570723Age (years; mean (range))27 (13–63)32 (21–40)32 (17–55)Sex: M/F139/4312/510/13(%)(24/76)(29/71)(43/57)Race Black559 (98%)7 (100%)22 (96%) Indian9 (1.6%)00 White2 (0.3%)00 Mixed001Clinical Systolic/diastolic BP (mmHg; mean±s.d.)117±14/70±9121±15/81±10120±12/74±11 Peripheral edema (%)0061 CD4/mmł (mean±s.d.)163±35216±33264±46 UP (g/24 h; mean±s.d.)ND0.14±0.16±60.0138 Serum creatinine (μmol/l; mean±s.d.)6066±22125±500.0071 eGFR (ml/min; mean±s.d.)ND133±3177±350.0009HIVAN—6 (86%)19 (83%)BP, blood pressure; eGFR, estimated glomerular filtration rate; F, female; HIVAN, HIV-associated nephropathy; M, male; ND, not done; s.d., standard deviation; UP, urine protein.Only significant P-values (in comparisons between micro- and macro-albuminuric groups) are shown. Open table in a new tab BP, blood pressure; eGFR, estimated glomerular filtration rate; F, female; HIVAN, HIV-associated nephropathy; M, male; ND, not done; s.d., standard deviation; UP, urine protein. Only significant P-values (in comparisons between micro- and macro-albuminuric groups) are shown. HIVAN was present in 25 (83%) patients, their mean CD4 count was 226/mm3 (range 3–586/mm3); six (24%) of these patients had microalbuminuria (Table 2). The seven patients with persistent microalbuminuria who underwent renal biopsy had a mean CD4 count of 216/mm3 (range 114–379/mm3), mean serum creatinine of 66 μmol/l (range 37–111 μmol/l), and mean calculated creatinine clearance of 107 ml/min (estimated glomerular filtration rate of 133 ml/min) (Table 3). The total number of glomeruli present in biopsy samples from microalbuminuric patients varied from 11 to 45. One patient had interstitial inflammation without glomerular or tubular alterations of HIVAN; this was interpreted as interstitial nephritis. One patient showed prominent glomerular basement membrane with spikes and electron-dense subepithelial deposits, indicating concomitant membranous glomerulopathy in addition to features of HIVAN. Detailed morphologic changes of microalbuminuric patients are shown in Table 4. The representative images from the microalbuminuric patients are illustrated in Figures 1, 2, 3, 4, 5 and 6. Histological features of combined HIVAN and membranous nephropathy (Figures 7a, b and 8) were found in four patients, two of whom tested positive for HBsAg (Table 5); the other two were tested negative for both HBsAg and hepatitis B PCR. Anti-nuclear factor, hepatitis C virus antibodies, and Wasserman reaction were negative in all four patients. Other biopsy findings included two (7%) patients with membranoproliferative glomerulonephritis and three (10%) with interstitial nephritis (Table 6).Table 2Characteristics of patients with HIVANHepatitis serologyPatient no.Age (years)SexCD4Serum creatinine (μmol/l)Cr Cl (ml/min)eGFR (ml/min/1.73 m2) (MDRD equation)BCUrine protein (g/24 h) 129F3778899(-)NA0.94 228F1836980113(-)(-)0.9 326F2046563123(-)NA0.06 434F2466295123(-)(-)0.30 540M1991117882(-)(-)0.23 643M1147091137(-)(-)0.04 727F37958104140(-)(-)0.17 821F13761130138(-)(-)0.07 926M58690117114(-)NA6.331017FNA8248102(-)NA2.91143MNA2133938(-)(-)11.641225M39272138148(-)(-)1.141324F3351124966(-)NA3.611438MNA1615554(-)(-)6.831521F1301783140(-)(-)9.211638F1591814535(+)(-)14.01729M3317878131(+)(-)24.751855M4021038992(-)(-)4.921932F1451355051(-)(-)5.752029F1451725639(-)(-)4.472130F2131562243(-)NA1.352226FNA1553145(-)NA5.192342M13088116106(-)(-)2.232429M9011910489(-)(-)1.382524FNA6397129(-)(-)11.15Cr Cl, creatinine clearance; eGFR, estimated glomerular filtration rate; F, female; HIVN, HIV-associated nephropathy; M, male; MDRD, modification of diet in renal disease; NA, not available; (-), negative; (+), positive.All were black Africans. Open table in a new tab Table 3Characteristics of patients with microalbuminuriaHepatitis serologyPatient no.Age (year)SexCD4Serum creatinine (μmol/l)Cr Cl (ml/min)eGFR (ml/min/1.73 m2) (MDRD equation)BCUrine protein (g/24 h)Renal biopsy2630F23937188188(-)(-)0.13IN 326F2046563123(-)NA0.06HIVAN 434F2466295123(-)(-)0.30HIVAN 540M1991117882(-)(-)0.23HIVAN 643M1147091137(-)(-)0.04HIVAN+Mem GN 727F37958104140(-)(-)0.17HIVAN 821F13761130138(-)(-)0.07HIVANCr Cl, creatinine clearance; eGFR, estimated glomerular filtration rate; HIVAN, HIV-associated nephropathy; IN, interstitial nephritis; MDRD, modification of diet in renal disease; Mem GN, membranous glomerulonephritis; NA, not available; (-), negative.All were black Africans. Open table in a new tab Table 4Detailed morphologic changes of microalbuminuric patientsPatient no.Total no. of glomeruliNo. of collapsing glomeruli (%)No. of glomeruli with FSGSMicrocystic tubular dilatation (%)Interstitial inflammation/fibrosis (%)Diagnosis26280 (0)00a30% atrophic tubules present.60IN 3115 (45)52540HIVAN 4116 (55)33030HIVAN 5175 (29)53010HIVAN 6458 (18)82510HIVAN+Mem GNbAlso has prominent glomerular basement membrane with spikes+electron-dense subepithelial deposits. 7236 (26)62510HIVAN 8115 (45)53040HIVANFSGS, focal segmental glomerulosclerosis; HIVAN, HIV-associated nephropathy; IN, interstitial nephritis; Mem GN, membranous glomerulonephritis.a 30% atrophic tubules present.b Also has prominent glomerular basement membrane with spikes+electron-dense subepithelial deposits. Open table in a new tab Figure 2Microalbuminuric patient: high-power view demonstrating dilated tubules lined by flattened epithelium, and containing pale eosinophilic luminal secretions (H+E, original magnification, × 480).View Large Image Figure ViewerDownload (PPT)Figure 3Microalbuminuric patient: low-power view demonstrating hypertrophied and dilated tubules (H+E, original magnification, × 120).View Large Image Figure ViewerDownload (PPT)Figure 4Microalbuminuric patient: high-power view demonstrating hypertrophied tubules lined by swollen epithelial cells with vacuolated or eosinophilic cytoplasm (H+E, original magnification, × 480).View Large Image Figure ViewerDownload (PPT)Figure 5Microalbuminuric patient: medium-power view demonstrating collapsing glomerulopathy with focal segmental glomerulonephritis (H+E, original magnification, × 240).View Large Image Figure ViewerDownload (PPT)Figure 6Microalbuminuric patient: focus of interstitial nephritis containing interstitial lymphocytes and plasma cells with associated tubular atrophy (H+E, original magnification, × 240).View Large Image Figure ViewerDownload (PPT)Figure 7HIVAN combined with membranous glomerulonephritis. (a) HIVAN (collapsing glomerulopathy) (arrow) (Jones' silver stain, original magnification, × 240). (b) High-power view of (a): membranous glomerulonephritis demonstrating spike formation (arrow) (Jones' silver stain, × 1200, oil emersion).View Large Image Figure ViewerDownload (PPT)Figure 8EM of Figure 7: ultrastructural examination demonstrating thickened basement membrane with subepithelial (black arrow) and intramembranous deposits (white arrow), and swollen podocytes and foot process fusion (bold arrow) (original magnification, × 64 000).View Large Image Figure ViewerDownload (PPT)Table 5Characteristics of patients with combined HIVAN and membranous nephropathyHepatitis serologyPatient no.Age (years)SexCD4Se Cr (μmol/l)Cr Cl (ml/min)UP (g/24 h)BC 643M11470910.04(-)(-)1638F1591814514.0(+)(-)1729M331787824.75(+)(-)2524FNA639711.15(-)(-)All patients were black African.Cr Cl, creatinine clearance; NA, not available; (-), negative; (+), positive; Se Cr, serum creatinine; UP, urine protein. Open table in a new tab Table 6Characteristics of patients with renal histology other than HIVANHepatitis serologyPatient no.Age (years)RaceSexCD4Serum creatinine (μmol/l)Cr Cl/eGFR (MDRD equation) (ml/min/1.73 m2)BCUP (g/24 h)Renal biopsy2630BF23937188/188(-)(-)0.13IN2729BM64119848/45(-)(-)12.98MPGN2834BF61173135/102(-)NA0.47IN2942MRM21014725/58(-)(-)5.45MPGN3040BF398580/83(-)(-)0.48INB, black; Cr Cl, creatinine clearance; eGFR, estimated glomerular filtration rate; F, female; IN, interstitial nephritis; M, male; MPGN, membranoproliferative glomerulonephritis; MR, mixed race of African origin; NA, not available; (-), negative; (+), positive. Open table in a new tab Cr Cl, creatinine clearance; eGFR, estimated glomerular filtration rate; F, female; HIVN, HIV-associated nephropathy; M, male; MDRD, modification of diet in renal disease; NA, not available; (-), negative; (+), positive. All were black Africans. Cr Cl, creatinine clearance; eGFR, estimated glomerular filtration rate; HIVAN, HIV-associated nephropathy; IN, interstitial nephritis; MDRD, modification of diet in renal disease; Mem GN, membranous glomerulonephritis; NA, not available; (-), negative. All were black Africans. FSGS, focal segmental glomerulosclerosis; HIVAN, HIV-associated nephropathy; IN, interstitial nephritis; Mem GN, membranous glomerulonephritis. All patients were black African. Cr Cl, creatinine clearance; NA, not available; (-), negative; (+), positive; Se Cr, serum creatinine; UP, urine protein. B, black; Cr Cl, creatinine clearance; eGFR, estimated glomerular filtration rate; F, female; IN, interstitial nephritis; M, male; MPGN, membranoproliferative glomerulonephritis; MR, mixed race of African origin; NA, not available; (-), negative; (+), positive. This study examined a population of HIV-infected subjects, both in an in-patient, and an outpatient ambulatory setting. Of the 615 patients, 15 (2%) were recruited when hospitalized for various reasons and 600 (98%) were asymptomatic outpatients. We performed renal biopsies in 30 patients with variable degrees of proteinuria, and HIVAN was the commonest biopsy finding, present in 25 of 30 patients (83%). Almost all patients presenting with persistent microalbuminuria who underwent renal biopsy (six out of seven patients) showed the presence of HIVAN. This particular patient group constituted 24% of all patients with HIVAN; they had a low mean CD4 count of 216/mm3 and normal renal function with a mean calculated creatinine clearance of 107 ml/min (estimated glomerular filtration rate of 133 ml/min). The prevalence of renal diseases associated with HIV infection in Africa is unknown. There is a lack of surveillance and reporting for renal disease in HIV-positive patients. The true prevalence of HIVAN worldwide is also unclear. Initial studies suggested that about 10% of HIV-infected patients develop HIVAN.11.Pardo V. Aldana M. Colton R. et al.Glomerular lesions in the acquired immunodeficiency syndrome.Ann Intern Med. 1984; 101: 429-434Crossref PubMed Scopus (252) Google Scholar, 12.Gardenswartz M.H. Lerner C.W. Seligson G.R. et al.Renal disease in patients with AIDS: a clinicopathologic study.Clin Nephrol. 1984; 21: 197-204PubMed Google Scholar, 13.Pardo V. Meneses R. Ossa L. et al.AIDS-related glomerulopathy: occurrence in specific risk groups.Kidney Int. 1987; 31: 1167-1173Abstract Full Text PDF PubMed Scopus (137) Google Scholar, 14.Rao T.K.S. Friedman E.A. Nicastri A.D. The types of renal disease in the acquired immunodeficiency syndrome.N Engl J Med. 1987; 316: 1062-1068Crossref PubMed Scopus (272) Google Scholar, 15.Bourgoignie J.J. Menses R. Ortiz C. et al.The clinical spectrum of renal disease associated with human immunodeficiency virus.Am J Kidney Dis. 1988; 12: 131-137Abstract Full Text PDF PubMed Scopus (133) Google Scholar, 16.Valeri A. Neusy A.J. Acute and chronic renal disease in hospitalised patients.Clin Nephrol. 1991; 35: 110-118PubMed Google Scholar However, it appears that it is influenced by the type of study (whether autopsy or biopsy-based) and the demographics of the HIV-infected population. The occurrence of HIVAN in autopsy studies of AIDS patients varies from 1 to 12%.17.Mazbar S.A. Schoenfeld P.Y. Humphreys M.H. Renal involvement in patients infected with HIV: experience at San Francisco General Hospital.Kidney Int. 1990; 37: 1325-1332Abstract Full Text PDF PubMed Scopus (83) Google Scholar, 18.D'Agati V. Suh J. Carbone L. et al.Pathology of HIV-associated nephropathy: a detailed morphologic and comparative study.Kidney Int. 1989; 35: 1358-1370Abstract Full Text PDF PubMed Scopus (343) Google Scholar, 19.Seney F.D.J. Burns D.K. Silva F.G. Acquired immunodeficiency syndrome and the Kidney.Am J Kidney Dis. 1990; 16: 1-13Abstract Full Text PDF PubMed Scopus (109) Google Scholar, 20.Lopes G.S. Marques L.P. Rioja L.S. et al.Glomerular disease and human immunodeficiency virus infection in Brazil.Am J Nephrol. 1992; 12: 281-287Crossref PubMed Scopus (42) Google Scholar, 21.Shahinian V. Rajaraman S. Borucki M. et al.Prevalence of HIV-associated nephropathy in autopsies of HIV-infected patients.Am J Kidney Dis. 2000; 35: 884-888Abstract Full Text Full Text PDF PubMed Scopus (102) Google Scholar However, renal biopsy series showed a higher prevalence of HIVAN when compared with autopsy studies. We have reviewed the renal biopsy-based studies (excluding autopsy series) reported in the literature (Table 7). HIVAN was found to be the commonest form of renal involvement in HIV-positive black patients, ranging from 53 to 79%,22.Connolly J.O. Weston C.E. Hendry B.M. HIV-associated renal disease in London hospitals.Q J Med. 1995; 88: 627-634Google Scholar, 23.Winston J.A. Klotman M.E. Klotman P.E. HIV-associated nephropathy is a late, not early, manifestation of HIV-1 infection.Kidney Int. 1999; 55: 1036-1040Abstract Full Text Full Text PDF PubMed Scopus (159) Google Scholar, 24.Ahuja T.S. Borucki M. Funtanilla M. et al.Is the prevalence of HIV-associated nephropathy decreasing?.Am J Nephrol. 1999; 19: 655-659Crossref PubMed Scopus (82) Google Scholar, 25.Nochy D. Glotz D. Dosquet P. et al.Renal disease associated with HIV infection: a multicentric study of 60 patients from Paris hospitals.Nephrol Dial Transplant. 1993; 8: 11-19PubMed Google Scholar except for a study from the Congo by Assounga et al.,26.Assounga A.G. Yala F. Mongo Y. et al.HIV and nephropathy in Congo: a comparative study of HIV-positive vs HIV-negative patients.Saudi J Kidney Dis Transplant. 1996; 7: S30-S32Google Scholar who reported a lower rate of HIVAN (19%) among black Africans; however, only 32 out of 43 HIV-positive patients underwent kidney biopsy. The literature review by Bourgoignie27.Bourgoignie J.J. Renal complications of human immunodeficiency virus type 1.Kidney Int. 1990; 37: 1571-1584Abstract Full Text PDF PubMed Scopus (135) Google Scholar of renal biopsies in HIV-infected patients reported before 1990 revealed focal segmental glomerulosclerosis in 83%. However, the racial or ethnic origins of these patients were not mentioned in the review, although it is likely that the majority were black.Table 7Renal biopsy seriesStudyCountryNumber of patients biopsiedHIVAN (%)% African descent with HIVANSe Cr (μmol/l)UP (g/24 h)Mean CD4Bourgoignie27.Bourgoignie J.J. Renal complications of human immunodeficiency virus type 1.Kidney Int. 1990; 37: 1571-1584Abstract Full Text PDF PubMed Scopus (135) Google Scholar (1990)Literature review of biopsies reported before 1990176146?———(83%)Nochy et al.25.Nochy D. Glotz D. Dosquet P. et al.Renal disease associated with HIV infection: a multicentric study of 60 patients from Paris hospitals.Nephrol Dial Transplant. 1993; 8: 11-19PubMed Google Scholar (1993)France602679%———(29B+31C)(43%)(23/29)Casanova et al.28.Casanova S. Mazzucco G. Barbiano di Belgiojoso G. et al.Pattern of glomerular involvement in human immuno-deficiency virus-infected patients: an Italian study.Am J Kidney Dis. 1995; 26: 446-453Abstract Full Text PDF PubMed Scopus (102) Google Scholar (1995)Italy2600%61–7350.2–17.6—(all white Italian)(0%)Connolly et al.22.Connolly J.O. Weston C.E. Hendry B.M. HIV-associated renal disease in London hospitals.Q J Med. 1995; 88: 627-634Google Scholar (1995)UK191173%137–14002.6–10.0208(11B+7C+1A)(58%)(8/11)(<10–630)Assounga et al.26.Assounga A.G. Yala F. Mongo Y. et al.HIV and nephropathy in Congo: a comparative study of HIV-positive vs HIV-negative patients.Saudi J Kidney Dis Transplant. 1996; 7: S30-S32Google Scholar (1996)Congo32619%———(all black African)(19%)(6/32)Praditpornsilpa et al.29.Praditpornsilpa K. Napathorn S. Yenrudi S. et al.Renal pathology and HIV infection in Thailand.Am J Kidney Dis. 1999; 33: 282-286Abstract Full Text Full Text PDF PubMed Scopus (57) Google Scholar (1999)Thailand2600%53–29171.5–10.7275(all Asian)(0%)(<133 in 92%)(11–560)Winston et al.23.Winston J.A. Klotman M.E. Klotman P.E. HIV-associated nephropathy is a late, not early, manifestation of HIV-1 infection.Kidney Int. 1999; 55: 1036-1040Abstract Full Text Full Text PDF PubMed Scopus (159) Google Scholar (1999)USA201053%123–4951.1–12.060(17AA+3H)(50%)(9/17)(<133 in 10%)(0–200)Ahuja et al.24.Ahuja T.S. Borucki M. Funtanilla M. et al.Is the prevalence of HIV-associated nephropathy decreasing?.Am J Nephrol. 1999; 19: 655-659Crossref PubMed Scopus (82) Google Scholar 1999)USA14975%59–332All >1.5187(12AA+2C)(64%)(9/12)(<133 in 44%)(6–686)Our studySouth Africa302583%61–2130.04–24.75232(29B+1mixed race)(83%)(25/30)(<133 in 68%)(3–586)A, Asian; AA, African American; B, black; C, caucasian; H, hispanic; HIVAN, HIV-associated nephropathy; Se Cr, serum creatinine; UP, urine protein. Open table in a new tab A, Asian; AA, African American; B, black; C, caucasian; H, hispanic; HIVAN, HIV-associated nephropathy; Se Cr, serum creatinine; UP, urine protein. The prevalence of HIVAN was variable among the different racial groups. Casanova et al.28.Casanova S. Mazzucco G. Barbiano di Belgiojoso G. et al.Pattern of glomerular involvement in human immuno-deficiency virus-infected patients: an Italian study.Am J Kidney Dis. 1995; 26: 446-453Abstract Full Text PDF PubMed Scopus (102) Google Scholar conducted a biopsy study in white Italian HIV-positive patients; however, HIVAN was not demonstrated. The study by Praditpornsilpa et al.29.Praditpornsilpa K. Napathorn S. Yenrudi S. et al.Renal pathology and HIV infection in Thailand.Am J Kidney Dis. 1999; 33: 282-286Abstract Full Text Full Text PDF PubMed Scopus (57) Google Scholar in Thailand also did not demonstrate a single case of HIVAN among 26 HIV-positive patients presenting with varying degrees of proteinuria. However, HIVAN was commonly found among the HIV-infected black patients. Therefore, there may be a role for genetic factors in the development of HIVAN.8.D'Agati V. Appel G.B. HIV infection and the kidney.J Am Soc Nephrol. 1997; 8: 138-152PubMed Google Scholar, 9.Monahan M. Tanji N. Klotman P.E. HIV-associated nephropathy: an urban epidemic.Semin Nephrol. 2001; 21: 394-402Abstract Full Text PDF PubMed Scopus (46) Google Scholar, 10.US Renal Data System (USRDS) USRDS 2001 Annual Data Report. The National Institutes of Health, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, MD2001Google Scholar HIVAN was also found to occur in a high proportion of our patients who were biopsied (83%). The patients we recruited were hospital in-patients as well as asymptomatic outpatients, which we consider to be fairly representative of the population we serve. Twelve of 25 patients with HIVAN (48%) had nephrotic range proteinuria and most of them were in-patients. However, outpatients with microalbuminuria were also included and that group, in fact, constituted 24% of the total number of patients with HIVAN. So this study covered both extremes of proteinuric patients, from in- and outpatient groups. Microalbuminuria has been assessed by various investigators to diagnose subclinical renal involvement in systemic diseases. Valente et al.30.Valente de Almeida R. Rocha de Carvalho J.G. de Azevedo V.F. et al.Microalbuminuria and renal morphology in the evaluation of subclinical lupus nephritis: non-specific mesangial fibrils in sclerosing glomeruli.Clin Nephrol. 1998; 53: 218-229Google Scholar performed renal biopsies in patients with systemic lupus erythematosus who had microalbuminuria but no clinical signs of renal involvement, to evaluate subclinical lupus nephropathy. Fifteen (50%) had mesangial glomerulonephritis type IIb, 12 (40%) had mesangial glomerulonephritis type IIa, and three (10%) showed no changes on light microscopy or immunofluorescence (IMF) (type I). Similarly, microalbuminuric diabetic patients were biopsied to detect the presence of diabetic nephropathy. Typical diabetic nephropathy was found in a significant number of patients.31.Kanauchi M. Dohi K. Predictors of diabetic renal lesions in type 2 diabetes associated with microalbuminuria.Eur J Clin Invest. 2001; 31: 110-112Crossref PubMed Scopus (5) Google Scholar, 32.Fioretto P. Mauer M. Brocco E. et al.Patterns of renal injury in NIDDM patients with microalbuminuria.Diabetologia. 1996; 39: 1569-1576Crossref PubMed Scopus (364) Google Scholar Studies also reported an association between microalbuminuria and hypertension.33.Parving H.H. Mogensen C.E. Jensen H.A. et al.Increased urinary albumin excretion rate in benign essential hypertension.Lancet. 1974; 1: 1190-1192Abstract PubMed Scopus (357) Google Scholar According to these reports, microalbuminuria appears to be an early indicator of renal disease in patients with these systemic diseases. Therefore, microalbuminuria detected in HIV-positive patients may be considered to be an early indicator of the presence of subclinical renal disease that may be due to HIVAN or other renal disease that is not due to HIV nephropathy. Luke et al.34.Luke D.R. Sarnoski T.P. Dennis S. Incidence of microalbuminuria in ambulatory patients with acquired immunodeficiency syndrome.Clin Nephrol. 1992; 38: 69-74PubMed Google Scholar measured microalbuminuria in 72 HIV-seropositive ambulatory patients. There were 14 patients (19%) who had increased urinary microalbumin levels; seven of these patients had proteinuria similar to those values found in diabetic nephrotic syndrome. Two other studies reported the prevalence of microalbuminuria, without clinical evidence of renal disease, as 30 and 25%, respectively in HIV-infected outpatients.35.Kimmel P.L. Umana W.O. Bosch J.P. Abnormal urinary protein excretion in HIV-Infected patients.Clin Nephrol. 1993; 39: 17-21PubMed Google Scholar, 36.Kabanda A. Vandercam B. Bernard A. et al.Low molecular weight proteinuria in human immunodeficiency virus-infected patients.Am J Kidney Dis. 1996; 27: 803-808Abstract Full Text PDF PubMed Scopus (57) Google Scholar However, renal biopsies were not performed in these patients to determine the renal pathology. There have been no renal biopsy studies undertaken in HIV-infected patients with microalbuminuria to date. In our study, seven patients with microalbuminuria underwent renal biopsy and six (86%) patients had HIVAN. Interestingly, the microalbuminuric group constituted 24% of all patients with HIVAN. However, these patients had normal renal function (mean calculated creatinine clearance of 107 ml/min (estimated glomerular filtration rate of 133 ml/min)) and had low CD4 counts (mean of 216 (range 114–379)). The majority of patients with HIVAN had low CD4 counts (<250 in 12 out of 18 patients), in keeping with other reports.23.Winston J.A. Klotman M.E. Klotman P.E. HIV-associated nephropathy is a late, not early, manifestation of HIV-1 infection.Kidney Int. 1999; 55: 1036-1040Abstract Full Text Full Text PDF PubMed Scopus (159) Google Scholar, 37.Winston J.A. Burns G.C. Klotman P.E. The human immunodeficiency virus (HIV) epidemic and HIV-associated nephropathy.Semin Nephrol. 1998; 18: 373-377PubMed Google Scholar Therefore, HIVAN occurs in patients with low CD4 counts in general and can present initially with microalbuminuria. When comparing the characteristics of patients who were evaluated for proteinuria, there were no significant differences in age, sex, race, mean blood pressure, and CD4 count among the three different groups (Table 1). Subclinical renal involvement in the proteinuria-negative group is not excluded, as the majority were not tested for microalbuminuria. As persistent microalbuminuria was found in 8% of those whom we tested, it is likely that we would have detected more patients with microalbuminuria, had they all been tested. Subsequent renal biopsy, if carried out, may have shown the renal abnormalities, as was the case in our study. The finding of combined HIVAN and membranous nephropathy in four patients is somewhat unusual. To our knowledge, this combination has not been previously reported in the literature. Two of these patients had positive hepatitis B serology, which could explain the presence of membranous nephropathy; however, the etiology in the remaining two patients is unclear. HIV infection may be the cause of both histological patterns, and needs further clarification. There were limitations to our study; the study design involved a convenience sample rather than a random sample; there were many more outpatients than in-patients; electron microscopy (EM) and IMF studies could not be carried out in most of the samples, which may have detected more cases of membranous nephropathy, especially with EM, although the diagnosis of HIVAN was obvious on light microscopy. As HIV infection is a risk factor for the development of chronic kidney disease, the recommendations of the HIV Medicine Association of the Infectious Diseases Society of America suggest screening for chronic kidney disease in HIV-infected patients.38.Gupta S.K. Eustace J.A. Winston J.A. et al.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.Clin Infect Dis. 2005; 40: 1559-1585Crossref PubMed Scopus (511) Google Scholar The screening tests for kidney disease in HIV-seropositive patients, in fact, should be considered similar to those carried out in patients with diabetes mellitus, which includes testing for microalbuminuria, to detect early renal involvement In conclusion, microalbuminuria may be an early marker of HIVAN and screening for its presence may be beneficial. Renal biopsy may be considered in seropositive black patients who present with persistent microalbuminuria, especially with low CD4 counts irrespective of the level of renal function. This will allow diagnosis and treatment of HIVAN at an early stage and may prevent further progression of renal disease. This is a single-center, cross-sectional study. Ethical approval for the study was obtained from the Ethics Committee of the University of KwaZulu-Natal. Patients attending HIV Clinic, referrals from Medical OutPatient Departments, and hospital in-patients were screened. Inclusion criteria were: (1) HIV seropositivity (detection of HIV antibodies by enzyme-linked immunosorbent assay test and confirmed by Western blot) and (2) proteinuria ranging from microalbuminuria to severe proteinuria. Microalbuminuric patients were also included in the study in order to detect HIVAN at an early stage before macroalbuminuria developed. Standard urine dipstick testing was by UriCheck 9 (RapiMed Diagnostics, Sekunjalo Health Care, Sandton, South Africa) in all patients. Those with a positive test for proteinuria proceeded to 24-h urine collection to quantify the amount of protein in the urine. Those with normal dipstick tests who agreed to further screening underwent further urinalysis for microalbumin by Micral-Test strips (Roche, Laval, Quebéc, Canada). Patients with two positive tests for microalbumin at least a month apart were selected as having persistent microalbuminuria and were asked to collect 24-h urine for quantification of microalbumin. Microalbuminuria was defined as the presence of urinary protein between 30 and 300 mg/24 h. The confounding factors for microalbuminuria such as fever, heavy exercise, cardiac failure, hyperglycemia, uncontrolled hypertension, acute illness, urinary tract infection, and prostatic disease had been looked for and were excluded. Exclusion criteria were (1) diabetes mellitus; (2) uncontrolled hypertension (systolic blood pressure >160 mmHg); (3) known causes of chronic kidney disease such as chronic pyelonephritis, autosomal dominant polycystic kidney disease, lupus nephritis and (4) serum creatinine >250 μmol/l. A cutoff serum creatinine level of 250 μmol/l was used to exclude those patients with advanced nephropathy. All patients who met the inclusion criteria and agreed to take part in the study underwent percutaneous renal biopsy under ultrasound guidance after informed consent was obtained. Biopsies were reported on by the Anatomical Pathology Department. Light microscopy was carried out in all samples. The stains included hematoxylin and eosin (H+E), periodic acid Schiff, methanamine silver, Jones and Masson's trichrome. Nine patients had IMF studies carried out for immunoglobulin A, immunoglobulin G, immunoglobulin M, complement C1q, C3, and C4. EM was performed in six patients. The policy of the Department of Anatomical Pathology initially was not to undertake IMF studies on tissue samples from HIV-positive patients because of the possible hazard to the laboratory staff. However, with a change in policy, IMF studies were performed and nine subjects had IMF carried out. There were some logistic problems with EM studies initially; an attempt was made later to do EM and IMF studies in the remaining tissue samples from the earlier biopsies. However, it was not possible to retrieve more tissue for further studies, as all the wax blocks were used up in the subjects initially studied. All biopsy samples were reviewed by a single pathologist who was blinded to the degree of proteinuria, but not to the HIV status of the patients. HIVAN was defined as the presence of focal segmental glomerulosclerosis, glomerular collapse, microcystic tubular dilatation, and interstitial inflammation. Using a × 10 objective, a micrometer mounted on an HC PLAN × 10/20 eyepiece was used to quantify the tubular alterations. The tubular alterations were scored by calculating the percentage involved in each core of tissue, in 100 sequential H+E-stained cores. This was then averaged to the closest five. CD4 counts were measured by flow cytometry to assess the stage of HIV disease. In terms of renal function, glomerular filtration rate was estimated by using the Modification of Diet in Renal Diseases equation and creatinine clearance was calculated, based on 24-h urine samples and serum creatinine. Serological tests, including anti-nuclear factor, Wasserman reaction, hepatitis B and C, were carried out. As this study was undertaken before the free and large-scale availability of antiretroviral therapy, the patients in this study were not on antiretroviral therapy; none of the patients were on angiotensin-converting enzyme inhibitors or angiotensin receptor blockers at the time of renal biopsy. None of them had used heroin or any illicit drugs in the past. Results are expressed as mean±s.d. The significance of differences among the groups was determined using analysis of variance. The Bonferroni method was performed to compare individual pairs of group means. Values of P<0.05 were considered significant. We thank the University of KwaZulu-Natal, KwaZulu-Natal Kidney Association, National Kidney Foundation (South Africa), and Servier Laboratories (South Africa) for financial assistance." @default.
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