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• W2044010802 abstract "Genetics of progressive renal failure in diabetic kidney disease Diabetic kidney disease is a microvascular complication that is observed in a minority of patients with long-standing hyperglycemia. Diabetic nephropathy (DN) is associated with shortened patient survival, severe morbidity, and increased health care costs. Unfortunately, the incidence rates of DN continue to increase in Western societies, and DN is now the most common reported cause of end-stage renal disease in developed nations. DN results from a complex interplay between inherited and environmental factors. This article reviews the data that support an inherited basis for susceptibility to DN by summarizing familial aggregation studies, genome-wide linkage, and population-based association analyses in diabetic and nondiabetic kidney disease. Recent evidence linking genes involved in the regulation of endothelial function with genetic predisposition to albuminuria is presented. The integration of carefully designed genetic linkage and association studies with gene expression experiments in human and animal models of diabetic kidney disease appear to offer great promise for detecting the molecular mechanisms underlying susceptibility to DN. Genetics of progressive renal failure in diabetic kidney disease Diabetic kidney disease is a microvascular complication that is observed in a minority of patients with long-standing hyperglycemia. Diabetic nephropathy (DN) is associated with shortened patient survival, severe morbidity, and increased health care costs. Unfortunately, the incidence rates of DN continue to increase in Western societies, and DN is now the most common reported cause of end-stage renal disease in developed nations. DN results from a complex interplay between inherited and environmental factors. This article reviews the data that support an inherited basis for susceptibility to DN by summarizing familial aggregation studies, genome-wide linkage, and population-based association analyses in diabetic and nondiabetic kidney disease. Recent evidence linking genes involved in the regulation of endothelial function with genetic predisposition to albuminuria is presented. The integration of carefully designed genetic linkage and association studies with gene expression experiments in human and animal models of diabetic kidney disease appear to offer great promise for detecting the molecular mechanisms underlying susceptibility to DN. One third of white patients with diabetes mellitus (DM) will develop overt proteinuria, reduced glomerular filtration rate (GFR), and end-stage renal disease (ESRD). The proportion of individuals developing severe nephropathy is higher among diabetic African Americans, Hispanic Americans, and Native Americans1U.S. Renal Data System, Usrds 2003 Annual Report Atlas of End-Stage Renal Disease in the United States. National Institutes of Health, National Institutes of Diabetes and Digestive and Kidney Diseases, Bethesda, MD2003Google Scholar. Although microalbuminuria is recognized as a major risk factor for premature cardiovascular disease and progressive chronic kidney disease in type 1 and type 2 diabetic individuals, it also signifies endothelial dysfunction with a heightened risk for cardiovascular disease in nondiabetic hypertensive patients and in normotensives. Diabetic retinopathy, another microvascular complication, develops over time in the vast majority of diabetic patients. In contrast, renal complications only develop in a subset of diabetic patients despite chronically elevated blood sugar, blood pressure, and serum lipids. The poor correlation between glycemic and hypertension control with development of diabetic nephropathy (DN) suggests that environmental factors are not the sole cause. Mounting evidence supports the role of genetic factors in the pathogenesis of DN. Familial aggregation of overt DN and diabetic ESRD has been widely observed. Seaquist et al demonstrated that 83% of the type 1 diabetic siblings of white probands with DN had overt nephropathy. In contrast, only 17% of the diabetic siblings of probands without nephropathy (despite long durations of DM) developed overt DN2Seaquist E.R. Goetz F.C. Rich S.S. et al.Familial clustering of diabetic kidney disease: Evidence for genetic susceptibility to diabetic nephropathy.N Engl J Med. 1989; 320:: 1161-1165Crossref PubMed Scopus (881) Google Scholar. Similarly, Quinn et al3Quinn M. Angelico M.C. Warram J.H. et al.Familial factors determine the development of diabetic nephropathy in patients with IDDM.Diabetologia. 1996; 39: 940-945Crossref PubMed Scopus (400) Google Scholar reported that the presence of nephropathy in a diabetic was strongly influenced by the degree of proteinuria in their diabetic sibling. A 72% cumulative risk of nephropathy was observed in those whose diabetic siblings had proteinuria, compared with a 25% cumulative risk in those having normoalbuminuric siblings. The large difference observed in nephropathy risk based on familial aggregation strongly suggests that inherited factors are causative. Familial aggregation of DN in type 1 DM and type 2 DM has been reported in every study that has assessed for this risk factor, including European4Borch-Johnsen K. Norgaard K. Hommel E. et al.Is diabetic nephropathy an inherited complication?.Kidney Int. 1992; 41: 719-722Abstract Full Text PDF PubMed Scopus (290) Google Scholar,5Strojek K. Grzeszczak W. Morawin E. et al.Nephropathy of type II diabetes: Evidence for hereditary factors?.Kidney Int. 1997; 51: 1602-1607Abstract Full Text PDF PubMed Scopus (58) Google Scholar, Pima Indian6Pettitt D.J. Saad M.F. Bennett P.H. et al.Familial predisposition to renal disease in two generations of Pima Indians with type 2 (non–insulin-dependent) diabetes mellitus.Diabetologia. 1990; 33: 438-443Crossref PubMed Scopus (358) Google Scholar, African American7Satko S.G. Langefeld C.D. Daeihagh P.D. et al.Nephropathy in siblings of African-Americans with overt type 2 diabetic nephropathy.Am J Kidney Dis. 2002; 40: 489-494Abstract Full Text Full Text PDF PubMed Scopus (31) Google Scholar, South American8Canani L.H. Gerchman F. Gross J.L. Familial clustering of diabetic nephropathy in Brazilian type 2 diabetic patients.Diabetes. 1999; 48: 909-913Crossref PubMed Scopus (84) Google Scholar, Southeast Asian9Ramirez S.P.B. Mcclellan W. Port F.K. et al.Risk factors for proteinuria in a large, multiracial, Southeast Asian population.J Am Soc Nephrol. 2002; 13: 1907-1917Crossref PubMed Scopus (129) Google Scholar, and Indian populations10Vijay V. Snehalatha C. Shina K. et al.Familial aggregation of diabetic kidney disease in type 2 diabetes in south India.Diabetes Res Clin Pract. 1999; 43: 167-171Abstract Full Text Full Text PDF PubMed Scopus (48) Google Scholar. Familial aggregation of nondiabetic ESRD has also been repeatedly observed11Freedman B.I. Familial aggregation of end-stage renal failure: Aetiological implications.Nephrol Dial Transplant. 1999; 14: 295-297Crossref PubMed Scopus (17) Google Scholar, as has the clustering of diabetic and nondiabetic nephropathy within single families12Freedman B.I. End-stage renal failure in African Americans: Insights in kidney disease susceptibility.Nephrol Dial Transplant. 2002; 17: 198-200Crossref PubMed Scopus (45) Google Scholar. Few topics in the renal literature demonstrate such consistent results. The heritability of urinary albumin excretion was evaluated in type 2 diabetic Pima Indian and white families. A heritability of 0.21 was observed for urine albumin:creatinine ratio (ACR) in a segregation analysis in 715 diabetic Pima families. This work supported the existence of a major (Mendelian) gene contributing to albuminuria13Imperatore G. Knowler W.C. Pettitt D.J. et al.Segregation analysis of diabetic nephropathy in Pima Indians.Diabetes. 2000; 49: 1049-1056Crossref PubMed Scopus (75) Google Scholar. Similar results were reported in white diabetic patients at the Joslin Diabetes Center14Fogarty D. Hanna L.S. Wantman M. et al.Segregation analysis of urinary albumin excretion in families with type 2 diabetes.Diabetes. 2000; 49: 1057-1063Crossref PubMed Scopus (58) Google Scholar. The familial aggregation of urine ACR was again confirmed in white type 2 DM concordant siblings in the Diabetes Heart Study (DHS)15Langefeld C.D. Beck S.R. Bowden D.W. et al.Heritability of GFR and albuminuria in Caucasians with type 2 diabetes mellitus.Am J Kidney Dis. 2004; 5: 796-800Abstract Full Text Full Text PDF Scopus (95) Google Scholar. The heritability of urine ACR was 0.46 in 662 diabetic individuals from 310 DHS families (comprising 422 DM-concordant sibling pairs)15Langefeld C.D. Beck S.R. Bowden D.W. et al.Heritability of GFR and albuminuria in Caucasians with type 2 diabetes mellitus.Am J Kidney Dis. 2004; 5: 796-800Abstract Full Text Full Text PDF Scopus (95) Google Scholar. Age, gender, use of medicines affecting ACR, and blood pressure contributed to less than 10% of the variation in urine ACR. The heritability of renal function in the DHS (calculated with the Modification of Diet in Renal Disease GFR equation) was 0.7515Langefeld C.D. Beck S.R. Bowden D.W. et al.Heritability of GFR and albuminuria in Caucasians with type 2 diabetes mellitus.Am J Kidney Dis. 2004; 5: 796-800Abstract Full Text Full Text PDF Scopus (95) Google Scholar. The proportion of the variance in GFR that was attributable to mean blood pressure, medication effect, and hemoglobin A1C was 2%. Together, these reports strongly support the presence of genes influencing albuminuria and renal function in diabetic families. Genome-wide scans in appropriate family collections offer great hope for identifying the major genetic components of DN. The advantage of the genome screen strategy is the comprehensive evaluation of the entire genome, because there is no a priori knowledge of the location of putative DN susceptibility genes. The first genome scan searching for nephropathy and retinopathy loci was performed in 98 Pima Indian sibling pairs concordant for DN16Imperatore G. Hanson R.L. Pettitt D.J. et al.Sib-pair linkage analysis for susceptibility genes for microvascular complications among Pima Indians with type 2 diabetes. Pima Diabetes Genes Group.Diabetes. 1998; 47: 821-830Crossref PubMed Scopus (293) Google Scholar. The strongest evidence for linkage was observed on chromosome 7q (maximum log of the odds [LOD] score 2.7 at genetic marker D7S500), with additional evidence for linkage on chromosomes 3 and 9 (also linked to retinopathy) and chromosome 20. A discordant sibling-pair analysis in type 1 diabetes families17Moczulski D.K. Rogus J.J. Antonellis A. et al.Major susceptibility locus for nephropathy in type 1 diabetes on chromosome 3q: Results of novel discordant sib-pair analysis.Diabetes. 1998; 47: 1164-1169Crossref PubMed Scopus (157) Google Scholar reported a nephropathy linkage on chromosome 3 in the region containing the angiotensin II type-1 receptor gene. A detailed evaluation of the angiotensin II type-1 receptor gene excluded a role for this gene in the 3q linkage peak. A genome scan of 18 large Turkish kindreds containing multiple individuals with type 2 DN has been reported18Vardarli I. Baier L. Hanson J.A. et al.Gene for susceptibility to diabetic nephropathy in type 2 diabetes maps to 18q22.3–23.Kidney Int. 2002; 62: 2176-2183Abstract Full Text Full Text PDF PubMed Scopus (142) Google Scholar. A major linkage peak was observed on chromosome 18q using an autosomal dominant model for inheritance of DN (LOD score 6.6 between markers D18S43 and D18S50). Evaluation of these loci in Pima Indian families confirmed evidence of linkage, despite the fact that the original genome wide scan was not sensitive enough to detect it. We recently reported a genome scan for DN in 206 African American type 2 diabetic sibling pairs concordant for severe diabetic kidney failure (ESRD or advanced DN) from 166 families19Bowden D.W. Colicigno C.J. Langefeld C.D. et al.A genome scan for diabetes associated end-stage renal disease in African Americans.Kidney Int. 2004; 66: 1517-1526Abstract Full Text Full Text PDF PubMed Scopus (151) Google Scholar. In an initial analysis, no LOD scores above 2.0 were detected. Multilocus interaction analysis detected 6 additional loci (on chromosomes 7p, 12p, 14q, 16p, 18q, and 21q) with LOD scores between 1.15 and 1.63. Ordered subset analyses were performed to identify potentially homogeneous families for detection of genetic linkage. Using ordered subset analyses, African American families with the earliest mean age at development of diabetes had evidence for a DN susceptibility locus on chromosome 18q (LOD 3.72 in 64% of families). The linkage peaks for DN observed on chromosomes 3q, 7q, and 18q overlap despite the genome scans being performed in diverse populations, using different study designs and methodologies. Linkage was identified on chromosome 3q in white families with type 1 DN17Moczulski D.K. Rogus J.J. Antonellis A. et al.Major susceptibility locus for nephropathy in type 1 diabetes on chromosome 3q: Results of novel discordant sib-pair analysis.Diabetes. 1998; 47: 1164-1169Crossref PubMed Scopus (157) Google Scholar, and type 2 DN in Pima Indians16Imperatore G. Hanson R.L. Pettitt D.J. et al.Sib-pair linkage analysis for susceptibility genes for microvascular complications among Pima Indians with type 2 diabetes. Pima Diabetes Genes Group.Diabetes. 1998; 47: 821-830Crossref PubMed Scopus (293) Google Scholar and African Americans19Bowden D.W. Colicigno C.J. Langefeld C.D. et al.A genome scan for diabetes associated end-stage renal disease in African Americans.Kidney Int. 2004; 66: 1517-1526Abstract Full Text Full Text PDF PubMed Scopus (151) Google Scholar. The 18q linkage to DN was observed in Turkish18Vardarli I. Baier L. Hanson J.A. et al.Gene for susceptibility to diabetic nephropathy in type 2 diabetes maps to 18q22.3–23.Kidney Int. 2002; 62: 2176-2183Abstract Full Text Full Text PDF PubMed Scopus (142) Google Scholar and African American families and in an association analysis in Pima Indians. The replication of results increases the likelihood that these chromosomal locations harbor DN genes. The National Institutes of Health-sponsored Family Investigation of Nephropathy and Diabetes (FIND) study will soon complete a genome scan using single nucleotide polymorphisms in more than 6000 individuals from multiply-affected DM families enriched for the presence of overt DN or diabetic ESRD20Knowler W.C. Coresh J. Elston R.C. et al.The Family Investigation of Nephrology and Diabetes (FIND): Design and methods.J Diabetes Complications. 2005; 19: 1-9Abstract Full Text Full Text PDF PubMed Scopus (80) Google Scholar. African American, white, Hispanic American, and American Indian families are being recruited. The final FIND genome scan will be performed with associated quantitative traits (albuminuria, proteinuria, and GFR) as well as for the presence or absence of overt DN. The FIND study should have adequate power to determine whether DN susceptibility alleles are consistent between ethnic groups. The clustering of diabetic and nondiabetic ESRD in families suggested that these diverse disorders might share common susceptibility loci (i.e., renal failure genes might exist that were independent of the presence of hyperglycemia or hypertension). However, genome scans in large numbers of African American families with predominantly nondiabetic etiologies of ESRD21Freedman B.I. Langefeld C.D. Rich S.S. et al.A genome wide scan for end-stage renal disease in African Americans enriched for non-diabetic nephropathy.J Am Soc Nephol. 2004; 15: 2719-2727Crossref PubMed Scopus (42) Google Scholar and all-cause ESRD22Freedman B.I. Bowden D.W. Rich S.S. et al.A genome scan for all-cause end-stage renal disease in African Americans.Nephrol Dial Transplant. 2005; 20: 712-718Crossref PubMed Scopus (36) Google Scholar failed to replicate the linked regions observed in the diabetic ESRD genome scan19Bowden D.W. Colicigno C.J. Langefeld C.D. et al.A genome scan for diabetes associated end-stage renal disease in African Americans.Kidney Int. 2004; 66: 1517-1526Abstract Full Text Full Text PDF PubMed Scopus (151) Google Scholar. Evidence for linkage was observed on chromosomes 13q33.3 and 1q25.1 in both the nondiabetic ESRD and the all-cause ESRD genome scans. Our current understanding of the pathophysiology of DN suggests that complex interactions exist between multiple pathways. These have been previously reviewed23Baynes J.W. Thorpe S.R. Role of oxidative stress in diabetic complications: A new perspective on an old paradigm.Diabetes. 1999; 48: 1-9Crossref PubMed Scopus (2068) Google Scholar, 24Flyvbjerg A. Putative pathophysiological role of growth factors and cytokines in experimental diabetic kidney disease.Diabetologia. 2000; 43: 1205-1223Crossref PubMed Scopus (192) Google Scholar, 25Caramori M.L. Mauer M. Pathophysiology of renal complications.in: Porte JR, D. Sherwin R.S. Baron A. Ellenberg and Rifkin's Diabetes Mellitus. McGraw-Hill, New York2003: 697-722Google Scholar, 26Caramori M.L. Mauer M. Diabetes and nephropathy.Curr Opin Nephrol Hypertens. 2003; 12: 273-282Crossref PubMed Scopus (127) Google Scholar, 27Brownlee M. Livingston J.N. Biochemical mechanisms of microvascular disease.in: Porte JR, D. Sherwin R.S. Baron A. Ellenberg and Rifkin's Diabetes Mellitus. McGraw-Hill, New York2003: 181-196Google Scholar and include increased activity of a variety of growth factors and cytokines (i.e., transforming growth factor β, growth hormone, insulin-like growth factor 1, vascular endothelial growth factor, and epidermal growth factor); activation of protein kinase C isoforms; increased release of renin, angiotensin, endothelin, and bradykinin; formation of reactive oxygen species; increased formation of advanced glycation end-products; increased activity of the aldose reductase pathway; and abnormalities in glucose transport mechanisms. These pathways likely interact to cause DN. Based on underlying biology, researchers have studied functional candidate gene polymorphisms that alter levels or activities within these pathways. At present, little consistent evidence exists for the contribution of these candidate genes to risk for DN. The majority of candidate gene classes evaluated in DN have been implicated in inflammatory processes. This reflects the general impression that inflammation plays a key role in the genesis of diabetic complications. Microalbuminuria is a hallmark of endothelial dysfunction, and it represents a “pro-inflammatory” state. Therefore, we recently examined the roles of two endothelial dysfunction-related genes, endothelial nitric oxide synthase (NOS3) and P-selectin, in predisposition to diabetic albuminuria. The NOS3 gene is expressed by vascular endothelial cells and variation in the NOS3 gene encoding endothelial nitric oxide synthase alters nitric oxide production. Endothelial dysfunction contributes to the development of DN as a result of a decrease in production of active nitric oxide. Therefore, the NOS3 gene on chromosome 7q35-36 would appear to be a strong candidate gene for susceptibility to DN. NOS3 was also in the chromosome region that was found to be linked with nephropathy in type 2 diabetic Pima Indian families16Imperatore G. Hanson R.L. Pettitt D.J. et al.Sib-pair linkage analysis for susceptibility genes for microvascular complications among Pima Indians with type 2 diabetes. Pima Diabetes Genes Group.Diabetes. 1998; 47: 821-830Crossref PubMed Scopus (293) Google Scholar. Only a single polymorphism, T-786C in the promoter region, has been reported to affect transcription by reducing promoter activity28Nakayama M. Yasue H. Yoshimura M. et al.T-786→ mutation in the 5′-flanking region of the endothelial nitric oxide synthase gene is associated with coronary spasm.Circulation. 1999; 99: 2864-2870Crossref PubMed Scopus (663) Google Scholar. In a case-control study of 347 type 1 DM patients, the -789C allele was more frequent in the 78 cases with advanced diabetic nephropathy than in the 74 cases with proteinuria or 195 control subjects free of DN29Zanchi A. Moczulski D.K. Hanna L.S. et al.Risk of advanced diabetic nephropathy in type 1 diabetes is associated with endothelial nitric oxide synthase gene polymorphism.Kidney Int. 2000; 57: 405-413Abstract Full Text Full Text PDF PubMed Scopus (179) Google Scholar. Another case control study demonstrated that the frequency of the C allele was significantly increased in hemodialysis patients with nondiabetic nephropathy (N = 168) and with DN (N = 84), compared with healthy controls (N = 187)30Asakimori Y. Yorioka N. Taniguchi Y. et al.T(-786)→C polymorphism of the endothelial nitric oxide synthase gene influences the progression of renal disease.Nephron. 2002; 91: 747-751Crossref PubMed Scopus (39) Google Scholar. These two studies suggested that the progression of renal disease was influenced by the T-786C polymorphism. We examined the role of the T-786C polymorphism in susceptibility to albuminuria in 590 white siblings from 230 type 2 DM families in the DHS31Liu Y. Burdon K.P. Langefeld C.D. et al.T-786C polymorphism of the endothelial nitric oxide synthase gene is associated with albuminuria in the Diabetes Heart Study.J Am Soc Nephrol. 2005; 16: 1085-1090Crossref PubMed Scopus (43) Google Scholar. This study demonstrated that the -786C allele was associated with increased ACR (31% increase in absolute level of ACR for each additional copy of the -786C allele; P < 0.0001) in a co-dominant inheritance mode. In support of this finding, quantitative pedigree disequilibrium test analyses revealed an excess transmission of the C allele to those with higher levels of ACR (P = 6.25e-05). P-selectin, an adhesion molecule, is expressed on the surface of activated platelets and vascular endothelial cells. This adhesion molecule might play an important role in the pathogenesis of atherosclerosis by mediating leukocyte “rolling” on the endothelium, promoting the inflammatory process, and contributing to plaque initiation and progression. Therefore, variation in the P-selectin gene may account for a portion of one's predisposition to endothelial dysfunction and subsequent microalbuminuria. Prior association studies suggested that P-selectin gene polymorphisms impacted the risk of myocardial infarction32Tregouet D.A. Barbaux S. Escolano S. et al.Specific hapoltypes of the P-selectin gene are associated with myocardial infarction.Hum Mol Genet. 2002; 11: 2015-2023Crossref PubMed Scopus (161) Google Scholar. A role for the P-selectin gene in DN and albuminuria was heretofore unknown. We determined that Ser290Asn (S290N), a non-synonymous polymorphism in exon 7 of the P-selectin gene, was associated with an increased risk for the presence of albuminuria in DHS families (odds ratio, 1.71 for each 290Asn allele; P = 0.002)33Liu Y. Burdon K.P. Langefeld C.D. et al.P-selectin gene haplotype associations with albuminuria in the Diabetes Heart Study.Kidney Int. 2005; 68: 741-746Abstract Full Text Full Text PDF PubMed Scopus (10) Google Scholar. This association appeared to be in a co-dominant inheritance mode. Haplotype analyses revealed that haplotypes containing an asparagine (N) codon trended toward association with increasing degrees of albuminuria. Biologic mechanisms underlying the associations of these haplotypes with the risk of albuminuria have not yet been elucidated. The evaluation of candidate genes underlying susceptibility to DN has been a difficult task with inconsistent results. This lack of replication was likely due to small sample sizes, incomplete genetic dissection of the polymorphisms in candidate genes, moderate effect sizes, and extensive genetic and phenotypic heterogeneity. Multicenter initiatives, such as the FIND and Genetics of Kidney Disease in Diabetes, will soon provide renewable sources of DNA from large numbers of diabetic families. Continued sequencing and analysis of the human genome by the Human Genome Project34Collins F.S. Morgan M. Patrinos A. The Human Genome Project: Lessons from large-scale biology.Science. 2003; 300: 286-290Crossref PubMed Scopus (694) Google Scholar,35Collins F.S. Green E.D. Guttmacher A.E. et al.A vision for the future of genomics research.Nature. 2003; 442: 835-847Crossref Scopus (1335) Google Scholar, the HapMap project36The International HapMap Consortium: The International HapMap Project.Nature. 2003; 426: 789-796Crossref PubMed Scopus (4688) Google Scholar, and the Programs for Genomic Applications project will allow better exploitation of genetic variation. The technology for carrying out large-scale molecular genetic studies is rapidly improving, which will soon enable the performance of whole genome association studies. Combining in vitro and in vivo functional studies in DN with the results from population-based genetic analyses is likely to further our understanding of the genetic basis of DN. These analyses will have the potential to identify genes producing susceptibility to DN and may lead to novel treatment strategies to slow or prevent this devastating complication of diabetes mellitus." @default.
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