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Type 2 diabetes mellitus (DM) globally affects 18–20 % of adults over the age of 65 years.

Diabetic kidney disease (DKD) is one of the most frequent and dangerous complications of DM2, affecting about one-third of the patients with DM2.

Factors that are associated with an increased risk of hypoglycemia in DKD patients include decreased renal gluconeogenesis, deranged metabolic pathways (including altered metabolism of medications) and decreased insulin clearance.

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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.

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.

The gold standard to evaluate insulin resistance is the euglycemic insulin clamp technique.

Appropriate glycaemic monitoring and control tailored for diabetic patients is required to avoid hypoglycaemia and other glycaemic disarrays in patients with DM2 and kidney disease.

Understanding the renal physiology and pathophysiology of DKD has become essential to all specialties treating diabetic patients.

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.

There are several factors involved in the process of insulin secretion, and incretins are one of the most important.

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