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Molecular basis of genetic renal diseases 2
Published on December 28, 2016 25 min
Other Talks in the Series: The Kidney in Health and Disease
Molecular basis of genetic renal diseases 1
- Dr. Paul Jennings
- Medical University of Innsbruck, Austria
What’s new for IgA nephropathy part 2: clinical presentation, diagnosis, prognosis, treatment
- Prof. Maurizio Salvadori
- University of Florence, Italy
Now we'll move along to the proximal tubule, and there's a number of inherited proximal tubular diseases.
The first of these we will discuss are diseases of glucose reabsorption.
Under normal conditions, all of the glucose is removed as it passes through the proximal tubule, and this is achieved due to different apical and basolateral glucose transporters, the first of which is the sodium-glucose transporter type 2, which is encoded by the SLC5A2; This is a low affinity, high capacity transporter present on the apical side of the cells, and it's present in the S1 segment. The second transporter is the sodium-glucose transporter type 1, which is a high affinity, low capacity transporter. It is not only responsible for glucose and sodium transport but can also transport galactose, and this is present in the S3 segment of the proximal tubule also on the apical side. Glucose that's brought into the proximal tubule is removed on the basolateral side through GLUT2, which is also a sodium-glucose and galactose co-transporter, and it's encoded by the SLC2A2. Now SGLT2 has recently become a target to try and alleviate the symptoms of diabetes by blocking this protein and allowing glucose and sodium to continue the journey through the rest of the nephron.