The dramatic increase in the number of patients with diabetes mellitus (DM) and chronic renal disease (CRD) in the recent years emphasizes the closeassociation between the two conditions and the leading role of DM in the development of renal pathology. Diabetology and nephrology are highly costlybranches of public health, and the burden of substitution renal therapy in DM patients continues to grow. The necessity of a renoprotection programat the early stages of DM for the prevention or delay of terminal renal insufficiency becomes increasingly clear. Such program should be based on theconceptual model of the evolvement of diabetic nephropathy as a consequence of combined action of metabolic and hemodynamic factors modulatedby genetic ones.

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Background. Diabetes mellitus (DM) is a non-infectious disease with a high prevalence worldwide and is one of the most common causes of diabetic kidney disease (DKD). Anaemia is a well-known complication of chronic kidney disease (CKD) and has been estimated to affect one in three adults with DM. Aims. To evaluate the prevalence and severity of anaemia among patients with DKD and to compare the distribution of anaemia among patients with diabetic and non-diabetic CKD. Methods. A total of 2,015 patients with DM [n = 807 with type 1 DM (T1DM); n = 1,208 with type 2 DM (T2DM)] and 244 patients with biopsy-proven chronic glomerulonephritis (CGN) were selected. Patients with glomerular filtration rate (GFR) of 15 ml/min/1,73 m2 (stage 5 CKD) and treated by erythropoietin-stimulating agents and/or iron medication were not included. The presence of anaemia was defined as haemoglobin (Hb) of 130 g/l in men and 120 g/l in woman. GFR was calculated using the MDRD formula. CKD stages were defined based on stages 14 of CKD by KDOQI and KDIGO guidelines: stage 1 (GFR 90 ml/min/1.73 m2); stage 2 (GFR 6089 ml/min/1.73 m2); stage 3 (GFR 3059 ml/min/1.73 m2); stage 3a (4559 ml/min/1.73 m2); stage 3b (GFR 3044 ml/min/1.73 m2); stage 4 (GFR 1529 ml/min/1.73 m2). Results. Rates of anaemia were higher among patients with DM and DKD (38.8% and 22.6% for T1DM and T2DM, respectively) than diabetic patients without DKD (16.6% and 11.5%, respectively. Prevalence of anaemia by CKD stage increased from 23.3% in stage 1 to 80% in stage 4 among patients with T1DM, and from 16.9% to 81 % among patients with T2DM. The prevalence of anaemia was also higher among protoeinuric patients (53.9% and 34.4% for T1DM and T2DM, respectively) relative to microalbuminuric patients (29.4% and 17.6%, respectively). Anaemia prevalence was significantly greater in DKD due to T1DM (53.9%) than in CGN (19.7), and the rates did not differ based on stages of CKD. Conclusions. We found a two-fold higher rate of anaemia among patients with DM and CKD than patients with DM and non-DKD. In addition, we found that the frequency of anaemia depends on renal function (i.e., stage of CKD) and degree of albuminuria. Taken together, anaemia is highly prevalent among patients with T1DM and DKD compared with patients with chronic CGN, without differences in its severity.

Frequency of the diabetes mellitus (DM) and chronic kidney disease (CKD) steadily increases around the world. Compensation of a carbohydrate metabolism plays a key role in prevention of development and progressing of CKD in patients with DM, that was proved in the largest researches. However at later stages of CKD compensation of a carbohydrate metabolism is extremely complicated because of high risk of hypoglycemia due to decrease in a renal gluconeogenesis, insulin and anti-hyperglycemic agents cumulation, inadequate level of glycated hemoglobin due to nephrogenic anemia. Thus, great care and an individual approach in choosing and intensification of hypoglycemic therapy are required in patients with diabetes. Incretin drugs have taken a worthy place in the international and national guidelines for the treatment of patients with type 2 diabetes mellitus (DM2). Inhibitors of dipeptidyl peptidase-4 (DPP-4) showed a favorable efficacy and safety profile in patients with normal renal function and patients with CKD.

Cardiovascular complications, a major cause for disability and morbidity in diabetes mellitus (DM), constitute the greatest threat of the diabetes epidemic. Glycemic stability within the therapeutic targets is a prerequisite to prevention of micro- and macrovascular complications of DM. Traditional therapies are aimed at cardinal defects determining development of type 2 diabetes mellitus (T2DM). Unfortunately even in combination they fail to deliver long-term glycemic control without stimulation of weight gain and increase in hypoglycemic risks with negative cardial, renal and hepatic impact. Preservation of beta-cell secretion capacity is also hardly attainable. Incretin-based therapy is a novel, actively developed approach that influences gut hormone physiology for better glycemic control. So far research efforts have yielded two classes of drugs: GLP-1 mimetics and DPP-4 inhibitors. Both are regarded nowadays for a number of important benefits, including beta-cell function improvement, adjusted to human physiology (i.e. stimulation of insulin secretion ?as needed? by the body, - hence low hypoglycemic risk). They also feature positive cardiovascular and body weight effects, thereby taking an important position in complex DM treatment.