Sudha K. Iyengar, Jeffrey R. Schelling, John R. Sedor

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Approaches to understanding susceptibility to nephropathy: From genetics to genomics Sudha K. Iyengar, Jeffrey R. Schelling, John R. Sedor Kidney International Volume 61, Issue 1, Pages S61-S67 (January 2002) DOI: 10.1046/j.1523-1755.2002.0610s1061.x Copyright © 2002 International Society of Nephrology Terms and Conditions

Figure 1 A comparison of HCFA 2728 diagnostic categories demonstrated significant differences between CAs and AAs. Hypertensive nephrosclerosis was more common cause of ESRD among AAs, whereas type 2 diabetes was equally frequent in the two ethnic groups. Kidney International 2002 61, S61-S67DOI: (10.1046/j.1523-1755.2002.0610s1061.x) Copyright © 2002 International Society of Nephrology Terms and Conditions

Figure 2 Data from the ESRD genetics project demonstrating that aggregation of family history among AAs is greater than among CAs. We observed that independent of race females demonstrated greater familial clustering. Kidney International 2002 61, S61-S67DOI: (10.1046/j.1523-1755.2002.0610s1061.x) Copyright © 2002 International Society of Nephrology Terms and Conditions

Figure 3 Twenty-five SAGE tags demonstrated differential expression patterns between the ROP-Os/+ and C57-Os/+ renal libraries. Each bar on the x axis corresponds to a tag, whereas the units on the y axis represent that tag frequency. Twelve tags are overexpressed, and thirteen tags are underexpressed in the ROP-Os/+ library. Kidney International 2002 61, S61-S67DOI: (10.1046/j.1523-1755.2002.0610s1061.x) Copyright © 2002 International Society of Nephrology Terms and Conditions