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 1–4 of CKD by KDOQI and KDIGO guidelines: stage 1 (GFR ≥ 90 ml/min/1.73 m2); stage 2 (GFR 60–89 ml/min/1.73 m2); stage 3 (GFR 30–59 ml/min/1.73 m2); stage 3a (45–59 ml/min/1.73 m2); stage 3b (GFR 30–44 ml/min/1.73 m2); stage 4 (GFR 15–29 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.

Aims. To estimate the prevalence of type 2 diabetes mellitus (T2DM) in different age groups of the adult population of Novosibirsk, according to epidemiological studies in 2003–2005 and 2013–2016.

Methods. We examined a representative population sample (assessed in 2003–2005) of men and women aged 45–69 years in two administrative districts of Novosibirsk, as a part of the international HAPIEE project. According to the tables of random numbers, representative samples of men and women aged 45–69 years were formed, to which letters were sent, inviting them to pass for examination. During 2013–2016, a second population survey was conducted on a random representative sample of a population of 25–44-year-olds of both sexes. Participants were residents of one of the districts of Novosibirsk. T2DM and impaired fasting glucose (IFG) were diagnosed using fasting plasma glucose (FPG) levels (diabetes: FPG ≥7.0 mmol/l; IFG: FPG 6.1–6.9 mmol/l).

Results. The prevalence of T2DM among residents aged 45–69 years was 11.3%, and overall, no significant difference in prevalence was found between females and males (11.3% vs. 11.0%).

However, the overall prevalence of T2DM among residents aged 25–44 years was 2.2%, and prevalence was higher in men (3.5%) than in women (1.1%), p ≤ 0.05.

High prevalence of IFG was found in the 45–69 age group (18.2%, in 2003–2005), and in the younger age group of 25–44 years (21.6%, in 2013–2016). The high rate among young individuals is particularly alarming.

Less than one half (4.8 out of 11.3%) of participants aged 45–69 tested positive for T2DM, and only one in the age group 25–44 years knew he/she had diabetes. This indicates a lack of knowledge among Siberians about their problem with diabetes.

Conclusion. Approximately one in five adults had IFG. Among the adult population aged 45–69 (in 2003–2005), 18.2% had IFG and 11.3% had T2DM. In individuals aged 25–44 years in 2013–2016, IFG was observed in 21.6%, and 2.2% had T2DM (p≤0.05).

Nonalcoholic fatty liver disease (NAFLD) and type 2 diabetes mellitus (T2DM) are pathological conditions that are co-occurring, and have been reaching epidemic proportions. One of the most significant risk factors for the development of both T2DM and NAFLD is obesity, which increases existing insulin resistance (IR). IR thought to be one of the main pathogenic causes linking T2DM and NAFLD. In recent years, there has been increased interest in obtaining non-invasive methods for assessing fibrosis and determining indications for liver biopsy, such as the NAFLD fibrosis score, extended liver fibrosis panel, and transient elastography. However, liver biopsy remains the gold standard for diagnosing NAFLD. Given that patients with T2DM are at higher risk of NAFLD than the general population, and that the presence of diabetes is a risk factor for the progression of NAFLD, patients with T2DM should be more closely monitored by clinicians. The present review paper is devoted to the search for cause–effect relationships of concurrent diseases such as NAFLD and disorders of carbohydrate metabolism, and priority areas of diagnosis of NAFLD.

Background. Tissue repair processes are impaired in diabetic foot ulcers (DFUs). Previous research has shown that glycaemic control, cytokines and growth factors play an important role in wound healing. Emerging evidence also suggests that genes play a role via their regulation of cell proliferation, collagen synthesis and granulation tissue formation.

Aim. To evaluate collagen genes expression in different stages of wound healing in patients with DFUs.

Materials and methods. Prospective study included four patients with neuropathic DFUs after surgical debridement. Tissue samples were taken for morphological and genetic tests on days 0, 10 and 15 of local treatment to evaluate expression of collagen genes (i.e. COL1A1, COL1A2, COL3A1) and to perform morphological tests.

Results. The present study confirmed that the size of wounds decreased by 8.8 ± 7% after 10 days of local treatment and by 18.3 ± 8% after 15 days of local treatment. According to histological examination of wound biopsies at day 10, all patients showed a tendency for lower levels of inflammatory infiltrate, increased number of fibroblast-like cells, presence of maturing granulation tissue and emergence of connective tissue fibres. After 15 days, we detected inflammatory infiltration in the wounds, despite the formation of mature granulation tissue. According to results of genetic analysis on day 10 of local wound treatment, we found a tendency for increased expression of collagen genes relative to the baseline: COL1A1 increased by 3.2 ± 1.3 times, COL1A2 by 2.0 ± 1.0 times and COL3A1 by 1.25 ± 1.1 times. On day 15 of local treatment, in contrast, we found a tendency for decreased expression of COL1A1, COL1A2 and COL3A1 relative to the baseline (1.7 ± 0.6, 2.5 ± 2 and 20.0 ± 3 times, respectively).

Conclusions. The expression of collagen genes (COL1A1, COL1A2, COL3A1) is more pronounced in proliferation phase and is subsequently reduced towards the end. These data were confirmed by morphological study and clinical pictures.

Nowadays, diabetes mellitus is an important public health problem. Together, population growth, prevalence of obesity, and a sedentary lifestyle has led to an increased number of individuals with diabetes mellitus. Globally, cataracts remain the leading cause of blindness and the second cause of visual impairment among patients with diabetes mellitus.

Phacoemulsification with intraocular lens implantation is the standardised surgical technique to treat cataracts. Advances in cataract surgical techniques have significantly decreased the incidence of complications. However, surgery may not be safe, as the risk of complications increases in patients with diabetes mellitus with pre-existing blood–ocular barrier pathology. Cystoid macular oedema is one of the most severe postoperative complications after cataract surgery. It is considered the most important cause of suboptimal visual acuity and strongly affects early recovery.

The optimal pharmacological therapy for prevention of CME following cataract surgery in patients with diabetes mellitus continues to be debated and needs further investigation.

Type 2 diabetes causes hundred thousand deaths worldwide every year. Though new antidiabetic drugs appear annually and new classes of drugs are invented approximately every ten years still a lot of type 2 diabetic patients remain to be out of the target glycemic levels.

According to most of the guidelines for type 2 diabetes,treatment metformin is the first line therapy for this disease. The choice of second-line antidiabetic drug usually depends on doctors’ preference. That is why defining the correct drug for exact patient is still an urgent question. This review provides data on antidiabetic drugspotential for preventing the progression of micro- and macrovascular complications.The question of the potential of early antidiabetic therapy intensification to activate legacy effect is debated. Early and lasting compensation of diabetes with the use of multiple drugs can become a basis for primary prevention of cardiovascular disease in such patients.

Maintaining glycemic control through intensive clinical management of patients with type 2 diabetes mellitus (T2DM) is well recognized to reduce the risk of diabetes-associated complications. Patients in Russia have high rates of microvascular and macrovascular complications as a result of undiagnosed, untreated, or inadequately treated diabetes, emphasizing the need for better clinical management. The introduction of basal insulin therapy is often necessary for patients with T2DM when oral antihyperglycemic drugs and lifestyle management strategies are no longer effective inmaintaining glycemic targets. However, after initiation of insulin, patients often remain on basal insulin for long periods despite suboptimal glycemic control, and intensification of insulin therapy is frequently necessary. Here, we report on several different insulin intensification strategies available to clinicians and their patients to improve glycemic control and the advantages and disadvantages of each approach. These strategies include the use of short- and long-acting insulins administered either as bolus doses or as premixed insulins. When selecting the most appropriate intensification strategy, clinicians should consider the lifestyle and treatment goals of their patients to help ensure treatment success.

Background. A major meta-analysis has confirmed the ability of statins to exert both diabetogenic and hyperglycaemic effects. To date, practical recommendations for predicting glucose dynamics during lipid-lowering therapy have not been developed.

Aims. Identify the combination of factors that can predict changes in basal glycaemia during 6-month lipid-lowering therapy in patients at high risk of cardiovascular disease.

Methods. This study reports on 50 patients with diabetes or impaired glucose tolerance, and 18 patients with coronary artery disease without disorders of carbohydrate metabolism. Of note, 29 of the 50 diabetic or glucose intolerant patients had documented ischaemic heart disease (stable angina). Patients were randomised into three groups: Gr.1 (n=33, atorvastatin therapy), Gr.2 (n=17, atorvastatin in combination with ezetimibe) and Gr.3 (n=18, rosuvastatin therapy). After treatment for 24 weeks, we assessed lipid profile dynamics, metabolism of glucose/insulin and the HOMA-IR index. Multivariate analysis was then performed to identify factors that predicted increases in basal glycaemia.

Results. All of the included patients completed 24 weeks of treatment (N=68). Lipid-lowering effect was significant in all three groups, and overall, target LDL cholesterol level was achieved in 50% of patients (n=34). In Gr.2, basal glucose level increased from 5.5(5.3–6.6) to 6.3(5.6–7.8) mmol/l (p=0.0014), which was accompanied by an increase in HOMA-IR (p=0.024). No significant change in basal glycaemia was observed in Grs.1 and 3. Moreover, an increase in the basal glycaemia was observed in 48.5% of patients in Gr.1, 70.6% in Gr.2 and 44.4% in Gr.3. Multivariate discriminant analysis across all patient groups revealed a canonical linear discriminant function that included the following factors: baseline basal glucose levels, total cholesterol levels, triglycerides and ratio of LDL/HDL cholesterol. Sensitivity and specificity of the model accounted for 75%; 51 out of the 68 cases were correctly classified when predicting the dynamics of basal glucose during lipid-lowering therapy.

Conclusions. Our data demonstrate the ability to predict the dynamics of the basal glycaemia during lipid-lowering therapy. This may allow for a new way to identify patients at high risk of statin-related increases in glycaemia.

Maturity-onset diabetes of the young (MODY) is a heterogeneous group of disorders characterised by autosomal dominant type of inheritance and caused by genetic defects leading to dysfunction of pancreatic beta-cells. To date, at least 13 subtypes of MODY have been described in the literature, the most frequent of which are MODY types 1–3. MODY2 and MODY3 are the most prevalent subtypes, and were previously described in our country, Russia. Several cases of rare MODY subtypes were subsequently described in the Russian literature. The current report is the first in the Russian literature to present clinical and molecular genetic characteristics of two cases of another rare MODY subtype—MODY9. This type of MODY is associated with mutations in the PAX4 gene, which encodes transcription factor PAX4, one of the factors essential for pancreatic beta-cell differentiation. Molecular genetic analysis was performed using next-generation sequencing, a new method recently applied to verify monogenic diseases and, in particular, MODY. This study reports a novel mutation in the PAX4 gene in MODY patients.