The initiation and progression of sickle cell nephropathy

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Presentation transcript:

The initiation and progression of sickle cell nephropathy Donald E. Wesson Kidney International Volume 61, Issue 6, Pages 2277-2286 (June 2002) DOI: 10.1046/j.1523-1755.2002.00363.x Copyright © 2002 International Society of Nephrology Terms and Conditions

Figure 1 (A) Glomerulus from a patient with sickle cell disease (right) is much larger than one from an age-matched control (left) at the same magnification. (B) Glomerular area indicated on the ordinate is significantly larger in sickle cell patients than control. From Ref. 13. Kidney International 2002 61, 2277-2286DOI: (10.1046/j.1523-1755.2002.00363.x) Copyright © 2002 International Society of Nephrology Terms and Conditions

Figure 2 Compared to normal, the transgenic mouse model of sickle cell disease produces higher levels of ethane, a measure of the production of reactive oxygen species. This increase is most evident after the animals are reoxygenated (▪) following hypoxia; () the baseline period. From Ref. 67. Kidney International 2002 61, 2277-2286DOI: (10.1046/j.1523-1755.2002.00363.x) Copyright © 2002 International Society of Nephrology Terms and Conditions

Figure 3 Emigration of leukocytes is greater following hypoxia/reoxygenation in the transgenic mouse model of sickle cell disease () than in controls (▪). From Ref. 14. Kidney International 2002 61, 2277-2286DOI: (10.1046/j.1523-1755.2002.00363.x) Copyright © 2002 International Society of Nephrology Terms and Conditions

Kidney International 2002 61, 2277-2286DOI: (10. 1046/j. 1523-1755 Kidney International 2002 61, 2277-2286DOI: (10.1046/j.1523-1755.2002.00363.x) Copyright © 2002 International Society of Nephrology Terms and Conditions