|Year : 2014 | Volume
| Issue : 2 | Page : 69-75
Prevalence, risk factors, and histological pattern of kidney disease in patients with Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome at Aminu Kano Teaching Hospital: A clinicopathologic study
Aminu M Sakajiki1, Bappa Adamu2, Fatiu A Arogundade3, Aliyu Abdu2, AT Atanda4, Bilkisu I Garba5
1 Department of Medicine, Yariman Bakura Specialist Hospital, Gusau, Zamfara, Nigeria
2 Department of Medicine, Aminu Kano Teaching Hospital, Bayero University, Kano, Nigeria
3 Department of Medicine, Obafemi Awolowo University Teaching Hospital, Ile-Ife, Nigeria
4 Department of Histopathology, Aminu Kano Teaching Hospital, Bayero University, Kano, Nigeria
5 Department of Paediatrics, Yariman Bakura Specialist Hospital, Gusau, Zamfara, Nigeria
|Date of Web Publication||16-Mar-2015|
Aminu M Sakajiki
Department of Medicine, Yariman Bakura Specialist Hospital, PMB 1010, Gusau, Zamfara
Source of Support: None, Conflict of Interest: None
| Abstract|| |
Background: Renal disease in Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome (HIV/AIDS) contributes significantly to morbidity and mortality associated with HIV infection worldwide.
Aim: To determine the prevalence, risk factors, and histological pattern of kidney disease in HIV-positive patients in Kano, Nigeria.
Materials and Methods: Four hundred consecutive treatment naοve HIV-positive patients with no other condition known to cause kidney disease were screened for proteinuria and reduced glomerular filtration rate (GFR). Kidney disease was defined as the presence of persistent microalbuminuria/proteinuria or decreased GFR (<60 ml/min/1.73 m 2 ). Kidney biopsy was performed on 20 patients. Data were analyzed using SPSS version 17.
Results: The mean ± standard deviation age of the study population was 34.03 ± 10.23 years with 240 (60%) being females. Kidney disease was found in 227 patients (56.8%), with a higher prevalence seen in males (odds ratio = 1.9305, 95% confidence interval = 1.2760-2.9207, P = 0.0018). Proteinuria including persistent microalbuminuria was found in 211 (52.8%) and reduced GFR was found in 64 (16.0%). The risk factors for developing kidney disease were age >40 years, male gender, low CD4 cell count, cigarette smoking, low body mass index, and low serum cholesterol. Logistic regression identified low CD4 cell count as an independent risk factor for kidney disease. Collapsing focal segmental glomerulosclerosis (FSGS) was the predominant histological pattern seen.
Conclusion: The prevalence of renal disease in HIV-positive patients was high in Kano, Nigeria; and microalbuminuria was a manifestation of collapsing FSGS.
Keywords: Histological pattern, Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome patients, kidney disease, prevalence, risk factors
|How to cite this article:|
Sakajiki AM, Adamu B, Arogundade FA, Abdu A, Atanda A T, Garba BI. Prevalence, risk factors, and histological pattern of kidney disease in patients with Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome at Aminu Kano Teaching Hospital: A clinicopathologic study. Ann Nigerian Med 2014;8:69-75
|How to cite this URL:|
Sakajiki AM, Adamu B, Arogundade FA, Abdu A, Atanda A T, Garba BI. Prevalence, risk factors, and histological pattern of kidney disease in patients with Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome at Aminu Kano Teaching Hospital: A clinicopathologic study. Ann Nigerian Med [serial online] 2014 [cited 2021 Feb 26];8:69-75. Available from: https://www.anmjournal.com/text.asp?2014/8/2/69/153356
| Introduction|| |
Kidney disease contributes significantly to morbidity and mortality in patients with Human Immunodeficiency Virus/Acquired Immunodeficiency Syndrome (HIV/AIDS). , HIV-associated nephropathy (HIVAN) is the most common form of chronic kidney disease (CKD) in African-Americans aged 20-64 years.  Screening for CKD in HIV-infected patients is recommended, similar to screening carried out in patients with diabetes mellitus. , There is a wide variability in the prevalence of kidney disease in HIV/AIDS patients, depending on the racial composition of the studied population.  In the USA, 3-10% was reported  and in Europe, a prevalence of 5.3% was reported.  In Africa, the prevalence varies widely depending on the country. It was reported as 11.5% in western Kenya,  50% in Uganda,  and 6% in South Africa.  Studies from Nigeria showed rates of 38% in Ile-Ife  and 31% in Zaria.  To our knowledge, this is the first study with information on kidney disease in HIV/AIDS, from Kano state, the most populous state in the northwest geopolitical zone of Nigeria.
This study was aimed at providing information on the prevalence, risk factors, and histological pattern of kidney disease in HIV/AIDS patients attending the HIV clinic of Aminu Kano Teaching Hospital, Kano, Nigeria.
| Materials and Methods|| |
This was a cross-sectional study conducted at the HIV clinic of Aminu Kano Teaching Hospital, Kano. The study was conducted between May and December 2010. Sample size was determined using Kish's formula and the findings from the previous Nigerian study. 
Four hundred consecutive HIV/AIDS patients who were treatment naïve, aged 18 years and above, and had consented to participate in the study were recruited. Excluded were those with; pregnancy, congestive cardiac failure, adult polycystic kidney disease, diabetes mellitus, hypertension, sickle cell disease, hepatitis B surface antigen positivity, hepatitis C virus antibodies positivity, and active urinary tract infection. Ethical approval was obtained from the ethics research committee of Aminu Kano Teaching Hospital, Kano.
An interviewer-administered questionnaire was used to document the sociodemographic and clinical data of the patients. Blood pressure measurements were taken using standard protocols, with the aid of a standard mercury sphygmomanometer (Accusson, Germany), using appropriate cuff size for the patient after resting for 5 min.
Weight was recorded in kilograms using a weighing scale. Measurement of height was carried out in a standing position, using a stadiometer; and was recorded in meters. Body mass index (BMI) was calculated as the ratio of measured weight to that of the square of the measured height (kg/m 2 ). Spot urine was collected for urinalysis using COMBI-9 (Medi-Test Combi 9 R , Macherey-Nagel, Duren Germany) and urine protein-creatinine ratio according to the National Kidney Foundation Kidney Disease Outcomes Quality Initiative guidelines on assessment of proteinuria.  Urine protein and creatinine were determined using an automated analyzer (VITRO R -350, USA); with the same sample centrifuged for the sediment microscopy. Tests for urine protein were repeated after 4 weeks for samples that were positive for urine protein. Complete blood count was carried out using an automated hematology analyzer (Sysmex R USA), while serum electrolytes, urea, creatinine, lipids, and glucose were carried out using an automated analyzer (VITRO R -350, USA). CD4 cell count was performed using a commercial kit (Dynal R T4 quadrant kit-Dynal Biotech ASA, Oslo Norway). Percutaneous kidney biopsy under ultrasound guidance was performed on 20 patients who had estimated glomerular filtration rate (eGFR) of 15-59 ml/min or proteinuria more than 1 g/day or persistent microalbuminuria; after giving consent. Histopathological slides were prepared from the biopsied tissues, and these were examined with light microscopy; as immunofluorescent microscopy (IM) and electron microscopy (EM) were unavailable. The stains used included hematoxylin and eosin a routine stain for general histological studies, periodic acid Schiff for basement membrane, Jones silver stain to highlight mesangial matrix, and Masson's trichrome for both glomerular and interstitial sclerosis. Underweight and obese were defined according to the WHO criteria. Proteinuria was defined as any detectable proteinuria on dipstick on a urine sample, which is confirmed on repeat tests after 4 weeks. Microalbuminuria was defined as urinary albumin-to-creatinine ratio of ≥30 mg/g but ≤300 mg/g. Hyperlipidemia was defined according to the National Cholesterol Education Program Adult Treatment Panel III 56 guidelines. BMI <18.5 was considered as malnutrition, and anemia was defined as hemoglobin <13.0 g/dl in males and <11.5 g/dl in females, respectively. Kidney disease was defined using either persistent microalbuminuria/proteinuria or reduced GFR (<60 ml/min/1.73 m 2 ) or the presence of both in a patient.
All the data obtained were analyzed using the SPSS version 17 (SPSS Inc., Chicago, IL, USA). All quantitative values were expressed as means ± standard deviation (SD) and qualitative data as percentages. Student's t-test, Chi-square, and Fisher's exact tests were used to assess the relationship between the various groups as appropriate. Odds ratio (OR) was used to determine risk factors for the development of kidney disease and to estimate the magnitude of this relationship. Logistic regression was used to determine independent risk factors for kidney disease. Pearson's test of correlation was used to check for the association between kidney disease and some clinical variables. A P < 0.05 was taken as statistically significant, and confidence intervals (CIs) were reported at 95%.
| Results|| |
There were 240 (60%) females and 160 (40%) males, with a female:male ratio of 1.5:1. Their age ranged from 18 to 70 years, with a mean ± SD of 34.03 ± 10.23 years. Peripheral edema was found in 15 (6.6%), malnutrition in 64 (28.2%) and anemia in 89 (39.2%). Kidney disease defined by the presence of microalbuminuria/proteinuria or decreased GFR (<60 ml/min/1.73 m 3 ) or both was found in 227 (56.8%) of the 400 patients studied. There were 121 females and 106 males with kidney disease, with males having higher prevalence (OR = 1.93, 95% CI = 1.28-2.92, P = 0.0018). The mean age ± SD of the patients with kidney disease was 35.94 ± 10.98 with a range of 18-70 years. The 30-39 years age group accounted for 75 (33.8%) of patients with kidney disease in this study. Proteinuria was found in 141 (35.3%), persistent microalbuminuria was seen in 70 (17.5%), and hematuria in 44 (11%). Reduced GFR was found in 64 (16.0%) of the study participants. One hundred and twenty-two of the proteinuric patients (84.4%) had 24 h protein excretion of <1 g, 14 (10.6%) had 24 h protein excretion of 1-3.49 g, while 5 of the proteinuric patients (4.9%) had nephrotic range proteinuria (3.5-9.6 g/day). Fifty-three of the patients with reduced GFR (82.8%) had stage 3 kidney disease (eGFR 30-59 ml/min); 8 (12.5%) had stage 4 kidney disease (eGFR 15-29 ml/min), while 3 (4.7%) had stage 5 kidney disease (eGFR <15 ml/min). [Table 1] shows clinical characteristics of the study population. Packed cell volume (PCV) and CD4 cell counts showed a significant difference between the two groups.
Factors significantly associated with the development of kidney disease among the study population are shown in [Table 2]. However, to address for confounding factors, multivariate analysis using logistic regression was carried out to identify independent risk factors for kidney disease among the study population as shown in [Table 3]. Low CD4 cell count was identified as an independent risk factor for kidney disease.
|Table 2: Risk factors for developing kidney disease among the study population|
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Kidney biopsy was done on 20 patients who satisfied biopsy criteria and consented. Seven (35%) of the biopsied patients were females. Eleven (55%) of the biopsied patients with kidney disease had histological findings consistent with collapsing form of focal segmental glomerulosclerosis (FSGS), 5 (25%) had interstitial nephritis (IN), while 1 (5%) had a normal histology, despite proteinuria of 2.7 g/day, which is suggestive of minimal change disease. Three patients with persistent microalbuminuria had normal histology, while two had collapsing FSGS. Four (20%) of the patients with FSGS had nephrotic range proteinuria, while 5 (40%) had subnephrotic proteinuria. All the patients with IN and minimal change disease had subnephrotic proteinuria. The clinical and histological characteristics of the biopsied patients are as shown in [Table 4]. Various histological findings were observed as shown in [Figure 1], [Figure 2], [Figure 3] and [Figure 4].
|Figure 1: Glomerulus exhibiting hypercellularity, increased mesangial thickness and adhesions to the Bowman's capsule in a human immunodeficiency virus-positive patient with proteinuria of 9.6 g/day and CD4 count of 59 cells/μl, (H and E, ×40)|
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|Figure 2: Glomerulus showing collapse of the glomerular tuft in a human immunodeficiency virus patient with stage 3 chronic kidney disease and CD4 of 55 cells/μl, (H and E, ×40)|
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|Figure 3: Slide showing microcysts containing casts in a human immunodefi ciency virus patient with stage 3 chronic kidney disease and CD4 count of 55 cells/μl, (H and E, ×40)|
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|Figure 4: Focus of intense interstitial infl ammation containing lymphocytes and plasma cells in a HIV-positive patient with stage IV CKD and CD4 count of 153 cells/μl. (H and E, x10)|
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| Discussion|| |
This study examined 400 HIV-infected treatment naïve adults. The prevalence of kidney disease in this study is similar to what was reported by Agaba et al.  in Jos, and Pepper  in Uganda, in which they found 51.8% and 50%, respectively. This is higher than what was reported by Emem et al. in Ile-Ife and Kwaifa and Bosan  in Zaria where they found the prevalence of 38% and 31%, respectively, but lower than what was reported by Han et al.  in South Africa (83%). This high prevalence could be due to the fact that all the studied patients were blacks, a racial group known to have higher predisposition to HIV-related kidney diseases, ,, as well as the criteria used to define kidney disease. In this study, persistent microalbuminuria was a definition criterion for kidney disease, similar to what Han et al.  utilized, in addition to overt proteinuria and reduced GFR. This could explain the higher prevalence in these two studies, as compared to the Ile-Ife and Zaria studies, in which only overt proteinuria with or without reduced GFR were used to define kidney disease. Although, Agaba et al.  and Pepper  used overt proteinuria with or without reduced GFR to define kidney disease, they got a prevalence that was similar to was found in this study and the South African study. This could be explained by other unidentified factors, since the racial composition of the studied populations were similar. The mean age of 35.9 years for patients with kidney disease in this study was similar to what was reported in other studies. , The finding of high prevalence of kidney disease in males as reported by Rao et al. (80%) and Seifu  (60%), is similar to this study, contrary to the report by Emem et al. in Nigeria, in which a higher prevalence among females (53.5%) was found. The higher proportion of males with renal disease here may be explained by other factors like immunolologic or virologic characteristics, which this study did not address.
Peripheral edema was seen in a small percentage of these patients despite advanced renal disease, low serum albumin and proteinuria, of which some were in the nephrotic range. This agrees with results of other studies. ,, This could be due to hypoadrenalism, salt wasting, volume depletion from recurrent vomiting and diarrhea, which is common in patients with HIV infection. , Malnutrition was seen in 28.2% of patients, which was similar to what was reported by D'Agati and Appel  and Emem et al.  Malnutrition may result from impaired oral intake, malabsorption, impaired metabolism, endocrine dysfunction, and cytokines. Impaired oral intake could result from systemic illnesses, oropharyngeal or esophageal diseases. A number of endocrine dysfunctions have been reported to occur in HIV patients including adrenal dysfunction, thyroid dysfunction, and low testosterone levels, all contributing to the malnutrition occurring in these patients.  Microscopic hematuria was seen in 19.4% of HIV patients with kidney disease in this study. Similar observations were made by Valeri and Neusy in which they found subnephrotic proteinuria and microscopic hematuria at presentation in their series.  Anemia was seen in 39.2%. Other studies reported similar findings, and the degree of anemia varied depending on the stage of kidney disease, CD4 cell count and renal function.  Anemia could result from several causes, including chronic inflammation associated with HIV infection, autoimmune destruction of red blood cells, decreased production of erythropoietin, Vitamin B12 malabsorption, opportunistic and fungal infections as well as bleeding.  Serum total cholesterol was also significantly different among the two groups with lower levels seen in the kidney disease patients, despite some having nephrotic range proteinuria and hypoalbuminemia. This could be in part due to malnutrition prevalent in these patients. The hematological profile showed a significant difference in the two groups of patients; those with kidney disease had lower PCV and CD4 cell count. This is not in agreement with Emem et al. and Kwaifa and Bosan.  Low PCV in these patients could be due to kidney disease as well as advanced HIV infection, as shown by the generally low CD4 cell count; although kidney disease has been reported to occur with high CD4 cell count and even during acute seroconversion. The three patients with stage 5 kidney disease were recruited from the antiretroviral clinic with significant wasting as the only presenting symptoms. The prevalence of microalbuminuria of 17.5% found in this study is lower than that reported by Aderibigbe et al.  in Ilorin, who reported a prevalence of 70.8%, but higher than what was reported by Han et al.  in South Africa.
At bivariate analysis, the risk factors for the development of kidney disease among the study population were older age, male gender, low CD4 count, low BMI, cigarette smoking, and low serum cholesterol. However, after multivariate analysis using logistic regression, only low CD4 cell count remained statistically significant as an independent risk factor for the development of kidney disease.
The result from this study shows involvement of all the components of the nephron, tubules, and the interstitium similar to what was reported by other studies. ,,, The characteristic pathological features of HIVAN, collapsing FSGS, microcystic dilatation and tubular casts were seen in 55% of our patients with kidney disease.
Emem et al. and Kwaifa and Bosan  reported these typical features of HIVAN in their series. Similar reports were made by Laurinavicius et al. and Wrone et al. The prevalence of HIVAN in these biopsies agrees with what was reported by van der Reijden et al. in their autopsy series, however, it was lower than that reported by Emem et al. and D'Agati and Appel. 
Interstitial inflammation reported in previous studies , was found in very high percentage in our patients, and this is in agreement with Han et al.,  Emem et al. and Kwaifa and Bosan  but not in agreement with the findings from other studies. 
Reports from South Africa on the histological diagnosis of kidney disease in HIV-positive patients show great variations. Twahir et al. found collapsing FSGS in as low as 30% of his patients, with the remaining accounted for by other glomerular and tubular lesions, such as mesangioproliferative glomerulonephritis (GN), mesangiocapillary GN, postinfectious GN, acute tubular necrosis, and malignant hypertension. On the other hand, Pantanowitz et al. reported FSGS in 60%; while Han et al.  reported it in 86.2%; with membranous GN and MPGN accounting for 7% each. Our result showing 55% collapsing form of FSGS is comparable to the Pantanowitz et al.  study, but is lower to what was reported by Han et al.  Immune complex GN (ICGN) related to HIV infection has been reported by Haas et al. in 18% of their patients. This study is limited by lack of facilities of both IM and EM studies and as such could not report on ICGN. HIVAN is seen across the spectrum of proteinuria; from microalbuminuria to nephrotic range proteinuria in our study, with similar findings being reported in other studies. ,
| Conclusion|| |
The prevalence of kidney disease was high among patients with HIV/AIDS in Kano. Logistic regression showed low CD4 cell count as an independent risk factor for kidney disease. The histological features of kidney disease seen in these patients were similar to what was reported elsewhere in blacks, with collapsing FSGS predominating. The findings of HIV-FSGS among patients with microalbuminuria in this study provided further evidence that HIVAN can be asymptomatic and routine dipstick would miss such cases.
| References|| |
D'Agati V, Appel GB. HIV infection and the kidney. J Am Soc Nephrol 1997;8:138-52.
Kimmel PL, Barisoni L, Kopp JB. Pathogenesis and treatment of HIV-associated renal diseases: Lessons from clinical and animal studies, molecular pathologic correlations, and genetic investigations. Ann Intern Med 2003;139:214-26.
Gupta SK, Eustace JA, Winston JA, Boydstun II, Ahuja TS, Rodriguez RA, 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;40:1559-85.
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 Int 2006;69:2243-50.
Eggers PW, Kimmel PL. Is there an epidemic of HIV Infection in the US ESRD program? J Am Soc Nephrol 2004;15:2477-85.
Nochy D, Glotz D, Dosquet P, Pruna A, Guettier C, Weiss L, et al.
Renal disease associated with HIV infection: A multicentric study of 60 patients from Paris hospitals. Nephrol Dial Transplant 1993;8:11-9.
Wools-Kaloustian K, Gupta SK, Muloma E, Owino-Ong'or W, Sidle J, Aubrey RW, et al.
Renal disease in an antiretroviral-naïve HIV-infected outpatient population in Western Kenya. Nephrol Dial Transplant 2007;22:2208-12.
Pepper L, Andia I, Matheison P. Prevalence of renal disease in patients attending the HIV/AIDS clinic at Mbarara University Teaching Hospital. In: Program and abstracts of the Third International AIDS society conference on HIV pathogenesis and treatment. Rio de Janeiro, Brazil: Abstract Tupe 15.3C02; 2005.
Emem CP, Arogundade F, Sanusi A, Adelusola K, Wokoma F, Akinsola A. Renal disease in HIV-seropositive patients in Nigeria: An assessment of prevalence, clinical features and risk factors. Nephrol Dial Transplant 2008;23:741-6.
Kwaifa SI, Bosan IB. Chronic kidney disease in HIV infected patients in North Western Nigeria. Trop J Nephrol 2008;3:23-8.
National Kidney Foundation. K/DOQI clinical practice guidelines for chronic kidney disease: Evaluation, classification, and stratification. Am J Kidney Dis 2002;39:S1-266.
Agaba EI, Agaba PA, Sirisena ND, Anteyi EA, Idoko JA. Renal disease in the acquired immunodeficiency syndrome in north central Nigeria. Niger J Med 2003;12:120-5.
Rao TK, Filippone EJ, Nicastri AD, Landesman SH, Frank E, Chen CK, et al.
Associated focal and segmental glomerulosclerosis in the acquired immunodeficiency syndrome. N Engl J Med 1984;310:669-73.
Renal disease in HIV positive patients in Ethiopia. Ethiop J Health Dev 2004;18:203-7.
Glassock RJ, Cohen AH, Danovitch G, Parsa KP. Human immunodeficiency virus (HIV) infection and the kidney. Ann Intern Med 1990;112:35-49.
Valeri A, Neusy AJ. Acute and chronic renal disease in hospitalized AIDS patients. Clin Nephrol 1991;35:110-8.
Mocroft A, Kirk O, Gatell J, Reiss P, Gargalianos P, Zilmer K, et al.
Chronic renal failure among HIV-1-infected patients. AIDS 2007;21:1119-27.
Spivak JL, Barnes DC, Fuchs E, Quinn TC. Serum immunoreactive erythropoietin in HIV-infected patients. JAMA 1989;261:3104-7.
Aderibigbe A, Olanrewaju TO, Chijioke A. Microalbuminuria in HAART-Naïve Patients in Nigeria. Abstract Presented at the 22 nd
Congress of the Nigerian Association of Nephrology; February, 2010 in Zaria Nigeria.
Laurinavicius A, Hurwitz S, Rennke HG. Collapsing glomerulopathy in HIV and non-HIV patients: A clinicopathological and follow-up study. Kidney Int 1999;56:2203-13.
Wrone EM, Carey H, Reilly RF. Glomerular lesions in HIV-infected patients: A Yale University Department of Medicine Residency Peer-Teaching Conference. Yale J Biol Med 1997;70:161-73.
van der Reijden HJ, Schipper ME, Danner SA, Arisz L. Glomerular lesions and opportunistic infections of the kidney in AIDS: An autopsy study of 47 cases. Adv Exp Med Biol 1989;252:181-8.
Hymes KB, Karpatkin S. Human immunodeficiency virus infection and thrombotic microangiopathy. Semin Hematol 1997;34:117-25.
Twahir M, Pascoe MD, Halkett J. Groote Schuur HIV Biopsy Study. SARS; 2000. [Abstract].
Pantanowitz L, Goetsch S, Katz I. Renal Biopsy on HIV Positive Patients at Bara 1989-97 JHB. AFRAN/SARS; 1997. [Abstract].
Haas M, Kaul S, Eustace JA. HIV-associated immune complex glomerulonephritis with "lupus-like" features: A clinicopathologic study of 14 cases. Kidney Int 2005;67:1381-90.
[Figure 1], [Figure 2], [Figure 3], [Figure 4]
[Table 1], [Table 2], [Table 3], [Table 4]
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