Abstract
Diabetes mellitus (DM) is one of the leading causes of chronic kidney disease (CKD). It is important that besides the increased morbidity of type 2 DM, the frequency of diabetic nephropathies increased too. According to the world data, more than 80% of CKD terminal cases are caused by DM, hypertension, or comorbidity. The most effective strategy to decrease the influence of diabetic nephropathy is the prevention of type 2 DM, as well as diagnosis and treatment of CKD in early stages among those who are already suffering from diabetes. Compensation of carbohydrate metabolism and the control of blood pressure play the leading role in decreasing the risk of diabetic kidney disease or slowing its progression. But on advanced stages of CKD, the compensation of carbohydrate metabolism is complicated due to the high risk of hypoglycemia. The article reviews the publications and guidelines on the safety and opportunities for use of hypoglycemic agents in patients with type 2 DM and CKD. Drugs with proved cardioprotective and nephroprotective properties, namely sodium-glucose transporter protein 2 inhibitors, are not used at glomerular filtration rate (GFR) <45 ml/min/1.73 m2, and glucagon-like peptide‑1 receptor agonists — at GFR <30 ml/min/1.73 m2. Incretin mimetics had proven themselves as drugs for metabolism control in the comprehensive therapy of patients with type 2 DM, including those with CKD. Published data show the efficacy and safety of dipeptidyl peptidase‑4 inhibitors used nowadays in patients with decreased GFR (including people on dialysis). Special attention is paid to vildagliptin, a selective oral dipeptidyl peptidase‑4 inhibitor, which due to its favorable safety profile is used successfully in elderly patients with type 2 DM and CKD, as well as with a history of severe cardiovascular pathology, at all stages of CKD (including uremia), in patients with high hypoglycemia risk. Target glycemic levels in patients with type DM and CKD have to be individualized considering life expectancy, renal function, risk of hypoglycemia, and comorbid pathology.
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