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• W2896753005 abstract "Pediatric-onset chronic kidney disease (CKD) is as relevant to adults as it is to children. Congenital anomalies of the kidney and urinary tract may have a significant impact on health from birth or during childhood or may not manifest until adulthood. Many acquired kidney diseases start to appear in late childhood and adolescence. The propensity for more rapid progression of CKD to end-stage kidney disease in adults of African ancestry, as well as disparities in access to kidney transplantation and allograft longevity, have been well documented for decades. Similar disparate patterns are seen in children, and we now know that there are a range of biological and nonbiological risk factors for the development and progression of CKD in people of African descent that are pertinent to CKD in children. In some cases, it is unclear whether there are effective potential interventions, whereas in other situations, there are opportunities to improve outcomes. Pediatric-onset chronic kidney disease (CKD) is as relevant to adults as it is to children. Congenital anomalies of the kidney and urinary tract may have a significant impact on health from birth or during childhood or may not manifest until adulthood. Many acquired kidney diseases start to appear in late childhood and adolescence. The propensity for more rapid progression of CKD to end-stage kidney disease in adults of African ancestry, as well as disparities in access to kidney transplantation and allograft longevity, have been well documented for decades. Similar disparate patterns are seen in children, and we now know that there are a range of biological and nonbiological risk factors for the development and progression of CKD in people of African descent that are pertinent to CKD in children. In some cases, it is unclear whether there are effective potential interventions, whereas in other situations, there are opportunities to improve outcomes. Pediatric-onset chronic kidney disease (CKD) can affect health along the entire life course. Insults to the kidney during development or childhood can lead to decreased function that starts in the pediatric age range or may not manifest until adulthood. The majority of pediatric CKD results from hereditary or congenital diseases, but as children reach adolescence, we start to see the emergence of acquired diseases more commonly seen in adulthood.1Harambat J. van Stralen K.J. Kim J.J. Tizard E.J. Epidemiology of chronic kidney disease in children.Pediatr Nephrol. 2012; 27: 363-373Crossref PubMed Scopus (571) Google Scholar The propensity for more rapid progression of CKD to end-stage renal disease (ESRD) in adults of African ancestry has been well documented for decades.2Tarver-Carr M.E. Powe N.R. Eberhardt M.S. et al.Excess risk of chronic kidney disease among African-American versus white subjects in the United States: a population-based study of potential explanatory factors.J Am Soc Nephrol. 2002; 13: 2363-2370Crossref PubMed Scopus (235) Google Scholar We now know that there are specific risk factors for the development and progression of CKD in African American children. Some are biological, such as premature birth or low birth weight3Carmody J.B. Charlton J.R. Short-term gestation, long-term risk: prematurity and chronic kidney disease.Pediatrics. 2013; 131: 1168-1179Crossref PubMed Scopus (160) Google Scholar or the presence of the high-risk apolipoprotein L1 (APOL1) genotype,4Foster M.C. Coresh J. Fornage M. et al.APOL1 variants associate with increased risk of CKD among African Americans.J Am Soc Nephrol. 2013; 24: 1484-1491Crossref PubMed Scopus (183) Google Scholar and some are social, such as lack of access to timely health care or differential treatment.5Palmer Alves T. Lewis J. Racial differences in chronic kidney disease (CKD) and end-stage renal disease (ESRD) in the United States: a social and economic dilemma.Clin Nephrol. 2010; 74: S72-S77PubMed Google Scholar, 6Young B.A. The interaction of race, poverty, and CKD.Am J Kidney Dis. 2010; 55: 977-980Abstract Full Text Full Text PDF PubMed Scopus (15) Google Scholar Many theoretical models have been proposed that show the interactions and impact of socioeconomic status (education, employment, and income) on social determinants of health (neighborhood and environment, psychosocial factors, and health care access). These can be amplified by racial biases and interact with biological factors, leading to adverse health outcomes.7Crews D.C. Pfaff T. Powe N.R. Socioeconomic factors and racial disparities in kidney disease outcomes.Semin Nephrol. 2013; 33: 468-475Abstract Full Text Full Text PDF PubMed Scopus (45) Google Scholar, 8Norton J.M. Moxey-Mims M.M. Eggers P.W. et al.Social determinants of racial disparities in CKD.J Am Soc Nephrol. 2016; 27: 2576-2595Crossref PubMed Scopus (144) Google Scholar, 9Hall Y.N. Social determinants of health: addressing unmet needs in nephrology.Am J Kidney Dis. 2018; 72: 582-591Scopus (29) Google Scholar A large portion of this brief review is based on what has been learned from the Chronic Kidney Disease in Children (CKiD) longitudinal study, but it also includes data from other studies addressing aspects of disparities relevant to specific diseases. Over time, analysis of the population participating in the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK)-sponsored CKiD Study has revealed that the progression pattern of CKD in children falls into at least 2 subgroups; glomerular disease and nonglomerular disease.10Warady B.A. Abraham A.G. Schwartz G.J. et al.Predictors of rapid progression of glomerular and nonglomerular kidney disease in children and adolescents: the Chronic Kidney Disease in Children (CKiD) Cohort.Am J Kidney Dis. 2015; 65: 878-888Abstract Full Text Full Text PDF PubMed Scopus (153) Google Scholar While African American children make up 23% of the overall CKiD population, they represent 19% of the nonglomerular-disease group but 36% of the group with glomerular disease. Children with glomerular disease, as a group, progress more rapidly than those with nonglomerular disease. The genetics and associated risks of APOL1 variants with glomerular disease have been discussed in detail elsewhere in this journal supplement.11Freedman B.I. Limou S. Ma L. Kopp J.B. APOL1-associated nephropathy: a key contributor to racial disparities in CKD.Am J Kidney Dis. 2018; 72: S8-S16Abstract Full Text Full Text PDF PubMed Scopus (77) Google Scholar Adults with an APOL1 high-risk genotype have increased risk for focal segmental glomerulosclerosis (FSGS) and CKD compared with those with a low-risk genotype. This knowledge led to a partnership between the CKiD Study and Nephrotic Syndrome Study Network (NEPTUNE) to assess the APOL1 status of the children with glomerular disease.12Ng D.K. Robertson C.C. Woroniecki R.P. et al.APOL1-associated glomerular disease among African American children: a collaboration of the Chronic Kidney Disease in Children (CKiD) and Nephrotic Syndrome Study Network (NEPTUNE) cohorts.Nephrol Dial Transplant. 2017; 32: 983-990PubMed Google Scholar All children in NEPTUNE have a glomerular disease diagnosis as opposed to a subset in CKiD. Children with APOL1 high-risk variants in both studies had an older median age of disease onset, higher likelihood of having FSGS as the diagnosis, and higher likelihood of having been born preterm (Table 1). Additionally, these children had lower initial estimated glomerular filtration rates and a faster decline in estimated glomerular filtration rates over time. Because prematurity is a known risk factor for developing glomerular disease/FSGS,3Carmody J.B. Charlton J.R. Short-term gestation, long-term risk: prematurity and chronic kidney disease.Pediatrics. 2013; 131: 1168-1179Crossref PubMed Scopus (160) Google Scholar the authors theorized that prematurity may be a second hit that facilitates the development of glomerular damage resulting from the high-risk genotype. This need for a second hit makes sense because the majority of individuals who carry the high-risk genotype do not have kidney disease; that is, there are incomplete phenotypic penetrance and differences in expressivity.Table 1Characteristics of African-American Children With Glomerular Disease in the CKiD Study and NEPTUNE, by APOL1 Risk Genotype StatusData Source: Ng et al.12Ng D.K. Robertson C.C. Woroniecki R.P. et al.APOL1-associated glomerular disease among African American children: a collaboration of the Chronic Kidney Disease in Children (CKiD) and Nephrotic Syndrome Study Network (NEPTUNE) cohorts.Nephrol Dial Transplant. 2017; 32: 983-990PubMed Google ScholarCKiDNEPTUNEAPOL1 Low Risk (n = 28)APOL1 High Risk (n = 28)APOL1 Low Risk (n = 27)APOL1 High Risk (n = 21)Focal segmental glomerulosclerosis7 (25%)25 (89%)7 (26%)14 (67%)Premature birth1 (4%)7 (27%)3 (12%)5 (26%)Median age at disease onset, y4.5 [1.5 to 12.5]11.5 [9.5 to 12.5]11 [4 to 14]14 [10.5 to 16.5]Median eGFR at study entry, mL/min/1.73 m269 [46 to 87]53 [44 to 68]94 [78 to 114]74 [66 to 90]Mean eGFR change, mL/min/1.73 m2 per y−8.4% [−16.7% to +0.6%]−18.1% [−25.1% to −10.4%]−3.2% [−12.4% to +7.0%]−13.4% [−22.0% to −3.9%]Note: Data are presented as count (percentage) or median or mean [95% confidence interval].Abbreviations: APOL1, apolipoprotein L1; CKiD, Chronic Kidney Disease in Children; eGFR, estimated glomerular filtration rate; NEPTUNE, Nephrotic Syndrome Study Network. Open table in a new tab Note: Data are presented as count (percentage) or median or mean [95% confidence interval]. Abbreviations: APOL1, apolipoprotein L1; CKiD, Chronic Kidney Disease in Children; eGFR, estimated glomerular filtration rate; NEPTUNE, Nephrotic Syndrome Study Network. Within the CKiD Study, African American children with FSGS and a high-risk APOL1 genotype also had increased odds of several renal and cardiovascular morbidities.13Woroniecki R.P. Ng D.K. Limou S. et al.Renal and cardiovascular morbidities associated with APOL1 status among African-American and non-African-American children with focal segmental glomerulosclerosis.Front Pediatr. 2016; 4 (eCollection 2016): 122Crossref PubMed Scopus (22) Google Scholar Compared with children with low-risk APOL1 and FSGS, children with a high-risk genotype had higher prevalences of uncontrolled hypertension, left ventricular hypertrophy, elevated C-reactive protein levels, and obesity. It is also possible that the increased cardiovascular risk in children with high-risk APOL1 genotype is a consequence of their underlying glomerular disease severity and rate of progression. More aggressive treatment of obesity may be an important component of managing CKD and left ventricular hypertrophy in this high-risk population. The strongest effect of APOL1 renal-risk alleles in adults is manifested in human immunodeficiency virus (HIV)-associated nephropathy (HIVAN).14Kopp J.B. Nelson G.W. Sampath K. et al.APOL1 genetic variants in focal segmental glomerulosclerosis and HIV-associated nephropathy.J Am Soc Nephrol. 2011; 22: 2129-2137Crossref PubMed Scopus (587) Google Scholar Approximately 65% of children with HIV-1 infection or AIDS in the United States are African American, and these children have a unique susceptibility to developing HIVAN.15Ray P.E. Hu C.A. Advances in our understanding of the pathogenesis of HIV-1 associated nephropathy in children.Future Virol. 2011; 6: 883-894Google Scholar The role of APOL1 high-risk alleles in youth with perinatal HIV infection was recently assessed in a nested case-control study of perinatal HIV-infected participants in the Pediatric HIV/AIDS Cohort Study. The investigators found that 27% of CKD cases in the adolescent cohort carried 2 risk alleles, and there was 3.5-fold increased odds of CKD in those with the APOL1 high-risk genotypes.16Purswani M.U. Patel K. Winkler C.A. et al.Pediatric HIVAIDS Cohort StudyBrief report: APOL1 renal risk variants are associated with chronic kidney disease in children and youth with perinatal HIV infection.J Acquir Immune Defic Syndr. 2016; 73: 63-68Crossref PubMed Scopus (23) Google Scholar These findings at least partially explain the increased HIVAN susceptibility seen in African American children. The viral infection is a likely second hit. There are known racial disparities in preterm birth rates,17Shiono P.H. Klebanoff M.A. Ethnic differences in preterm and very preterm delivery.Am J Public Health. 1986; 76: 1317-1321Crossref PubMed Scopus (83) Google Scholar and children born preterm are at higher risk for developing CKD. This is likely due in part to low birth weight and the associated decreased nephron endowment and compounded by the many external stressors to which these infants are exposed in the immediate postnatal period.3Carmody J.B. Charlton J.R. Short-term gestation, long-term risk: prematurity and chronic kidney disease.Pediatrics. 2013; 131: 1168-1179Crossref PubMed Scopus (160) Google Scholar, 18Frey H.A. Klebanoff M.A. The epidemiology, etiology, and costs of preterm birth.Semin Fetal Neonatal Med. 2016; 21: 68-73Abstract Full Text Full Text PDF PubMed Scopus (338) Google Scholar These stressors include nephrotoxic medications, hemodynamic instability, infections, suboptimal nutrition, and episodes of acute kidney injury. Therefore, following the findings from the CKiD Study and NEPTUNE that children with glomerular disease and the high-risk APOL1 genotype were significantly more likely to have been born prematurely, investigators looked at whether the high-risk APOL1 genotype was associated with prematurity in the general African American population.19Robertson C.C. Gillies C.E. Putler R.K. et al.An investigation of APOL1 risk genotypes and preterm birth in African American population cohorts.Nephrol Dial Transplant. 2017; 32: 2051-2058PubMed Google Scholar They analyzed 2 publicly available genetic data sets of preterm birth in African Americans, the Gene Environment Association (GENEVA) Study of preterm delivery and the Boston Medical Center genome-wide association study of preterm birth. Neither study showed an association between maternal high-risk APOL1 and prematurity, gestational age, or birth weight. There was also no association of prematurity, gestational age, or birth weight with the high-risk APOL1 status of infants in the GENEVA Study. Consequently, this can be interpreted as supporting the hypothesis that prematurity may be a second hit for a subset of APOL1-associated kidney disease, rather than prematurity being a direct result of APOL1 high-risk genotype. Alternatively, other stresses may lead to increased risk for prematurity and also function as additional risk factors for the development of APOL1-associated nephropathy, including gene-environment and gene-gene interactions. Despite the study limitations discussed by the authors, these data can serve as a framework for potential prospective studies of the associated risk for the development of glomerular disease even into adulthood in those born prematurely who also carry the high-risk APOL1 genotype. Several studies have demonstrated an association between low birth weight and increased risk for ESRD.20White S.L. Perkovic V. Cass A. et al.Is low birth weight an antecedent of CKD in later life? A systematic review of observational studies.Am J Kidney Dis. 2009; 54: 248-261Abstract Full Text Full Text PDF PubMed Scopus (338) Google Scholar Because both low birth weight and ESRD cluster in families, Ruggajo et al21Ruggajo P. Skrunes R. Svarstad E. Skjærven R. Reisæther A.V. Vikse B.E. Familial factors, low birth weight, and development of ESRD: a nationwide registry study.Am J Kidney Dis. 2016; 67: 601-608Google Scholar conducted a retrospective registry-based cohort study in Norway to evaluate whether familial factors account for the low birth weight–ESRD association. The authors found a graduated increased risk for ESRD in those with a low-birth-weight sibling, those born with low birth weight themselves, and those born with low birth weight who also had a sibling with low birth weight (hazard ratios ranging from 1.20-1.78). There was a similar pattern of increased risk for ESRD when assessing associations for those born small for gestational age. These results were striking because of the significant associations in this primarily white population in a high-income country. This highlights the likely larger influence of maternal, in utero, and environmental factors than genetics in the likelihood of premature birth. One can speculate on the potential higher impact of these risk factors in populations with lower socioeconomic status, more exposures to environmental risks, lower rates of prenatal care, and higher incidences of prematurity, low birth weight, and small for gestational age,22Luyckx V.A. Brenner B.M. Birth weight, malnutrition and kidney-associated outcomes--a global concern.Nat Rev Nephrol. 2015; 11: 135-149Crossref PubMed Scopus (183) Google Scholar, 23Abitbol C.L. Moxey-Mims M. Chronic kidney disease: low birth weight and the global burden of kidney disease.Nat Rev Nephrol. 2016; 12: 199-200Google Scholar which include many African and African American populations. Apart from the increased incidence of FSGS and resultant ESRD in African American children,24Baum M.A. Ho M. Stablein D. Alexander S.R. North American Pediatric Renal Transplant Cooperative StudyOutcome of renal transplantation in adolescents with focal segmental glomerulosclerosis.Pediatr Transplant. 2002; 6: 488-492Crossref PubMed Scopus (59) Google Scholar, 25Hogg R. Middleton J. Vehaskari V.M. Focal segmental glomerulosclerosis--epidemiology aspects in children and adults.Pediatr Nephrol. 2007; 22: 183-186Crossref PubMed Scopus (44) Google Scholar a recent publication compared the outcome of kidney transplants in black and nonblack children with ESRD from FSGS.26Guan I. Singer P. Frank R. Chorny N. Infante L. Sethna C.B. Role of race in kidney transplant outcomes in children with focal segmental glomerulosclerosis.Pediatr Transplant. 2016; 20: 790-797Crossref PubMed Scopus (15) Google Scholar They found that black children were 1.5 times more likely to have graft failure and were more likely to experience acute rejection, as well as delayed graft function. There are conflicting data for FSGS recurrence risk in the allograft. A North American Pediatric Renal Trials and Collaborative Studies (NAPRTCS) report indicated a lower recurrence rate in African American children compared with white or Hispanic children,27Tejani A. Stablein D.H. Recurrence of focal segmental glomerulosclerosis posttransplantation: a special report of the North American Pediatric Renal Transplant Cooperative Study.J Am Soc Nephrol. 1992; 2: S258-S263Google Scholar but Guan et al26Guan I. Singer P. Frank R. Chorny N. Infante L. Sethna C.B. Role of race in kidney transplant outcomes in children with focal segmental glomerulosclerosis.Pediatr Transplant. 2016; 20: 790-797Crossref PubMed Scopus (15) Google Scholar found no difference in their analysis of the Organ Procurement and Transplantation Network database. In this retrospective study, many social and biological variables that could have potentially affected allograft outcomes could not be assessed. For example, the impact of the APOL1 status of donors would have been of great interest. This is something that will be explored prospectively in the newly funded NIDDK study APOLLO (APOL1 Long-term Kidney Transplantation Outcomes Network).28Freedman B.I. Moxey-Mims M. The APOL1 Long-Term Kidney Transplantation Outcomes Network-APOLLO.Clin J Am Soc Nephrol. 2018; 13: 940-942Crossref PubMed Scopus (34) Google Scholar African American adults with CKD have faster progression to ESRD and are less likely to receive a kidney transplant. Many of the same social and economic factors discussed elsewhere in this journal supplement in relation to adults likely affect the rate of CKD progression and likelihood of transplantation in children as well.29Patzer R.E. Amaral S. Klein M. et al.Racial disparities in pediatric access to kidney transplantation: does socioeconomic status play a role?.Am J Transplant. 2012; 12: 369-378Crossref PubMed Scopus (72) Google Scholar The CKiD Study assessed whether African American children reach renal replacement therapy sooner than non–African American children after accounting for socioeconomic status.30Ng D.K. Moxey-Mims M. Warady B.A. Furth S.L. Muñoz A. Racial differences in renal replacement therapy initiation among children with a nonglomerular cause of chronic kidney disease.Ann Epidemiol. 2016; 26: 780-787Crossref PubMed Scopus (29) Google Scholar To eliminate the known biological affect that APOL1 has on glomerular disease, the analysis was limited to children with CKD from nonglomerular diseases. Time to the start of renal replacement therapy after CKD onset was assessed using parametric survival models, and socioeconomic status differences were accounted for by inverse probability weights. Before inverse probability weighting, the data showed that African American children reached the start of renal replacement therapy 3.2 years earlier than non–African American children. When inverse probability weighting accounted for socioeconomic status, this difference was halved to 1.6 years. However, when comparing time to either dialysis therapy or transplantation, the time to dialysis therapy was 37.5% shorter for African American children, but their wait was 53.7% longer for transplantation. These data reflect those in the most recent US Renal Data System report, which show that black/African American children are most likely to have dialysis as their first ESRD modality compared with children of other races.31Saran R. Robinson B. Abbott K.C. et al.US Renal Data System 2017 Annual Data Report: epidemiology of kidney disease in the United States.Am J Kidney Dis. 2018; 71: S1-S672PubMed Google Scholar Although there are likely still biological factors such as organ availability from donors of similar blood types, tissue markers, and genetic characteristics, these findings may reflect sociocultural and institutional differences not captured by socioeconomic status. There are certainly opportunities for public health interventions to increase organ donation and encourage more timely completion of the transplantation evaluation process for earlier activation on the transplant waiting list. Although not the focus of this brief review, there are other contributing factors to racial disparities in children with CKD. One is touched on previously, with regard to potential bias in providing access to kidney transplants. Others include income and parental education, specifically maternal education.32Hildago G. Ng D.K. Moxey-Mims M. et al.Association of income level and kidney disease severity and progression among children and adolescents with CKD: a report from the Chronic Kidney Disease in Children (CKiD) Study.Am J Kidney Dis. 2013; 62: 1087-1094Google Scholar, 33Young B.A. Katz R. Boulware L.E. et al.Risk factors for rapid kidney function decline among African Americans: the Jackson Heart Study (JHS).Am J Kidney Dis. 2016; 68: 229-239Abstract Full Text Full Text PDF PubMed Scopus (50) Google Scholar The impact of early-life socioeconomic status on the development and progression of CKD in children, including gestational determinants, has been well described.34Brophy P.D. Shoham D.A. Early-life course socioeconomic factors and chronic kidney disease.Adv Chronic Kidney Dis. 2015; 22: 16-23Abstract Full Text Full Text PDF PubMed Scopus (27) Google Scholar Many factors, studied primarily in adults but likely to have an effect on offspring, include the size and quality of social networks35Dunkler D. Kohl M. Heinze G. et al.Modifiable lifestyle and social factors affect chronic kidney disease in high-risk individuals with type 2 diabetes mellitus.Kidney Int. 2015; 87: 784-791Abstract Full Text Full Text PDF PubMed Scopus (65) Google Scholar and perceived racial discrimination.36Beydoun M.A. Poggi-Burke A. Zonderman A.B. Rostant O.S. Evans M.K. Crews D.C. Perceived discrimination and longitudinal change in kidney function among urban adults.Psychosom Med. 2017; 79: 824-834Crossref PubMed Scopus (31) Google Scholar Lower income also contributes to minority families being disproportionately exposed to numerous environmental risk factors due to the neighborhoods in which they live, and many environmental toxins (air pollution, water toxins, lead, and others) are known to be nephrotoxic.37Weidemann D.K. Weaver V.M. Fadrowski J.J. Toxic environmental exposures and kidney health in children.Pediatr Nephrol. 2016; 31: 2043-2054Google Scholar Historical and recent data confirm that there are many factors that affect the occurrence, progression, and access to treatment of CKD in children of African descent. These factors include a range of biological differences and societal disparities. Those taking care of these vulnerable children should be mindful of these multiple competing and compounding issues because treatment options are being considered along the continuum from CKD to kidney failure to transplantation." @default.
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• W2896753005 title "Kidney Disease in African American Children: Biological and Nonbiological Disparities" @default.
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