Effect of kidney disease on glucose handling (including genetic defects)  Joaquim Calado, René Santer, José Rueff  Kidney International  Volume 79, Pages S7-S13 (March 2011) DOI: 10.1038/ki.2010.510 Copyright © 2011 International Society of Nephrology Terms and Conditions

Figure 1 Correlation between tubular glucose load and tubular glucose reabsorption (TG) in various types of renal glucosuria. GFR, glomerular filtration rate; PG, plasma glucose concentration; TmG, maximum of tubular glucose reabsorption. The hatched area is the splay, the difference between actual and ideal reabsorption that is exhibited when the reabsorption curve shows a nonlinear transition as the TmG is reached.6 Copyright 1987, Int Pediatr Nephrol Assoc. Kidney International 2011 79, S7-S13DOI: (10.1038/ki.2010.510) Copyright © 2011 International Society of Nephrology Terms and Conditions

Figure 2 Comparison of the genomic structure of sodium–glucose cotransporter (SGLT)1 and SGLT2. There is a high degree of similarity both in the sequence and in the intron–exon organization. Exon sizes are to scale.14 Copyright 2003, Am Soc Nephrol. Kidney International 2011 79, S7-S13DOI: (10.1038/ki.2010.510) Copyright © 2011 International Society of Nephrology Terms and Conditions

Figure 3 Results of mutation analyses of the human Na+–glucose cotransporter gene SLC5A2 (SGLT2). Coded transmembrane domains 1–14 are shown as dark gray boxes.16 The figure has been updated with five novel mutations presented by Yu et al.,57 at the World Congress of Nephrology, Milan, 22–26 May 2009. Adapted with permission from Calado et al.16 Copyright 2008, published by Oxford University Press on behalf of ERA-EDTA. Kidney International 2011 79, S7-S13DOI: (10.1038/ki.2010.510) Copyright © 2011 International Society of Nephrology Terms and Conditions