Abstract
Various pathological conditions may alter the participation of the kidney in glucose metabolism. This article focuses on pathophysiology of renal glucose reabsorption and on pathophysiology of renal gluconeogenesis.
As for the former, mechanisms associated with complete deficit of SGLT2, the main transport protein of glucose, are described. Familial renal glucosuria, a hereditary disease mostly manifesting by an isolated glucosuria, is also discussed.
Attention in then given to reabsorption of glucose in diabetes. The second part of the text focuses on changes in the regulation of renal gluconeogenesis in diabetics and on causes and consequences of glycogen deposition in the kidney.