However, reduced insulin secretion is mainly responsible for the clinical picture of hyperglycemia. However, the clinical picture, characterized by deficient insulin secretion, worsens, thus exacerbating the loss of glycemic control.
In addition to the pancreas, adipocytes, liver, and intestines, the kidneys also play an important role in glycemic control, particularly due to renal contribution to gluconeogenesis and tubular reabsorption of glucose.
In this review article, based on a report of discussions from an interdisciplinary group of experts in the areas of endocrinology, diabetology and nephrology, we detail the relationship between diabetes and kidney disease, addressing the care in the diagnosis, the difficulties in achieving glycemic control and possible treatments that can be applied according to the different degrees of impairment.
Insulin resistance (IR) is one of the pillars dictating the pathogenesis of DM2 and may differ according to body tissues. Some authors argue it starts in the liver, others in the muscle, and others in the brain.
What we know is that IR is present in various body tissues (liver, peripheral muscle, central nervous system, adipocytes, etc.) of patients with DM2, preventing glucose to entry into the cell and causing hyperglycemia.
DM2 is a disease characterized by persistent hyperglycemia, resulting from partial or complete insulin deficiency, and it is associated with a clinical picture of insulin resistance.
Recently, other organs have been recognized as being involved in the pathogenesis of hyperglycemia in DM2, and it now known that not only dysfunction of the pancreas, but also of the liver, adipose tissue, intestine, kidneys, and central nervous system may contribute to this hyperglycemic state .
Type 2 DM globally affects 18–20 % of adults over the age of 65 years.
It is estimated that approximately 285 million people, between 20 and 79 years old, currently have DM, 70 % of whom live in middle- and low-income countries.
When hyperinsulinemia can no longer compensate for IR and insulin secretion begins to decline, the disruption of these variables results in hyperglycemia and a diagnosis of DM.
In the early stages of DM2, the clinical picture of hyperinsulinemia persists.
Glucose homeostasis is extremely altered in patients with DKD, who are exposed to a high risk of both hyperglycemia and hypoglycemia.