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Diabetic nephropathy (DN) is one of the most serious complications of diabetes mellitus (DM), causing almost half of all cases of endstage renal disease in the United States (de Boer et al., 2011). Kidneys are important for homeostasis of glucose, cause their role in gluoconeogenesis, filtration, re-absorption and secretion of the glucose. Hence, the changes in the kidney function are involved in development of hyperglycaemia and type 2 diabetes (DM2). Direct connection between hyperglycemia and damage of the renal cells has been established in many studies (Rai et al., 2015) (Michishita et al., 2017). Increase in glucose re-absorption as a consequence of the increased blood glucose and renal re-absorption is one of the mechanisms in development of the hyperglycaemia and consequent microvascular complications (Triplitt, 2012). Hyperglycaemia causes renal damage directly and indirectly, by haemodynamic modifications. It is responsible for glomerular hyperfiltration and microalbuminuria, which in turn increase the expression of the pro-fibrotic transforming growth factor-beta (TGFβ) (Schena and Gesualdo, 2005, Kanwar et al., 2008). Hyperglycaemia and the hyperfiltration cause the damage of the glomeruli and consequent proteinuria (Triplitt, 2012) (Sampanis, 2008).

The Influence of the Tannic Acid on the Expression of the Connexins 45 in a Rat Kidney Damaged by the Chronic Hyperglycemia