Nefro - 27-3 - MIOLO.indd
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133 As we sit down to write this Editorial, the last issue of the Journal of the American Society of Nephrology stands in front of us. Its cover displays an add that publicizes canagliflozin, the first SGLT2i (Sodium GLucose Transporter 2 inhibitor) approved, earlier this year, by the U.S. Food and Drug Administration (FDA) for the treatment of Type 2 Diabetes Mellitus (T2DM). This follows last year approval by the European Medicines Agency (EMA) of the first compound of its class, dapagliflozin. More than a century has elapsed since the original description of glucosuria induced by phlorizin, the parental compound from which all SGLT2i got their inspiration. During this period many insights on the homeostasis of sodium and glucose were unravelled. These two solutes are crucial for the survival of all organisms, higher vertebrates in particular, which have developed elaborate pathways to preserve them. However, in face of the high caloric and salt content of western diets, these phylogenetically conserved pathways have now turned against us and we try desperately to overrun them. They have become “therapeutic targets”. The story behind SGLT2 inhibition is not only the story of sodium and glucose conservation by complex organisms, but also, and for the interested nephrologist, on how the proximal tubule supports and integrates the “functioning logic of the kidney”. GLUCOSE TRANSPORT
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Nefro - 27-1 - MIOLO.indd
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تاریخ انتشار 2013