OBJECTIVE Finerenone significantly improved cardiorenal outcomes in patients with chronic kidney disease (CKD) and type 2 diabetes (T2D) in the Finerenone in Reducing Kidney Failure and Disease Progression in Diabetic Kidney Disease trial. We explored whether baseline HbA1c level and insulin treatment influenced outcomes. RESEARCH DESIGN AND METHODS Patients with T2D, urine albumin-to-creatinine ratio (UACR) of 30–5,000 mg/g, estimated glomerular filtration rate (eGFR) of 25 to <75 mL/min/1.73 m2, and treated with optimized renin–angiotensin system blockade were randomly assigned to receive finerenone or placebo. Efficacy outcomes included kidney (kidney failure, sustained decrease ≥40% in eGFR from baseline, or renal death) and cardiovascular (cardiovascular death, nonfatal myocardial infarction, nonfatal stroke, or hospitalization for heart failure) composite endpoints. Patients were analyzed by baseline insulin use and by baseline HbA1c <7.5% (58 mmol/mol) or ≥7.5%. RESULTS Of 5,674 patients, 3,637 (64.1%) received insulin at baseline. Overall, 5,663 patients were included in the analysis for HbA1c; 2,794 (49.3%) had baseline HbA1c <7.5% (58 mmol/mol). Finerenone significantly reduced risk of the kidney composite outcome independent of baseline HbA1c level and insulin use (Pinteraction = 0.41 and 0.56, respectively). Cardiovascular composite outcome incidence was reduced with finerenone irrespective of baseline HbA1c level and insulin use (Pinteraction = 0.70 and 0.33, respectively). Although baseline HbA1c level did not affect kidney event risk, cardiovascular risk increased with higher HbA1c level. UACR reduction was consistent across subgroups. Adverse events were similar between groups regardless of baseline HbA1c level and insulin use; few finerenone-treated patients discontinued treatment because of hyperkalemia. CONCLUSIONS Finerenone reduces kidney and cardiovascular outcome risk in patients with CKD and T2D, and risks appear consistent irrespective of HbA1c levels or insulin use.

The article presents the most relevant data of the world literature on the problem of iodine status. The problem of iodine deficiency still remains unresolved on the territory of the former Soviet Union (the median urinary iodine was 29.1 μg/l in Abkhazia, and almost 30% of the examined had the level of ioduria below standard values in Kazakhstan), although some countries have been successful in dealing with iodine deficiency (the median urinary iodine is 191 μg/l in Belarus, 169 μg/l in Ukraine). On the rest of the Eurasian continent, the picture is also different: among the total mass of countries with normal median urinary iodine, there are territories with both iodine deficiency (the median of ioduria ranges from 80 to 138 μg/l in the UK, the median of ioduria is 63 μg/l in France) and its excessive consumption (the median of ioduria is 330.0 μg/l in China). On the territory of America, in 2016, the elimination of iodine deficiency was announced (the median of ioduria ranged from 123 μg/l (Argentina) to 415 μg/l (Colombia)), and Haiti was the only country with a fixed iodine deficiency – 84 μg/l. Research data from different years in the following regions of the Russian Federation are presented: Moscow (the median of ioduria 67.0 μg/l), St. Petersburg (66.0–86.0 μg/l), Tyumen region (106.9 μg/l), Novosibirsk region (93.0 μg/l), Republic of Bashkortostan (70.3 μg/l), Republic of Dagestan (65.8 μg/l), Kemerovo region (90.0 μg/l), Saratov region (59.0–106.0 μg/l), Tomsk region (94 μg/l), Far Eastern region (58.0–74 μg/l), Chelyabinsk region (92.0–164.5 μg/l), Chuvash Republic (72.0 μg/l), Perm region (100.0 μg/l). Almost throughout the Russian Federation, iodine deficiency of mild severity was noted.

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Полиморфизм 1858 C/T (Arg620Тrp) гена PTPN22 ассоциируется с повышенным риском развития аутоиммунных заболеваний. Цель исследования. Анализ ассоциаций полиморфизма C1858T гена PTPN22 с аутоиммунными заболеваниями ЩЖ в популя ции Новосибирска.

Aim. To study the risk of cardiovascular and all-cause mortality in patients with metabolic syndrome (MS) according to a 14-year prospective cohort study in Siberia.Material and methods. Based on the data from the Russian arm of the HAPIEE project, we assessed all-cause deaths occurred by 2017 in the population cohort examined at baseline in 2003-2005 (n=9273). The baseline examination included the assessment of blood pressure (BP), anthropometry, levels of fasting triglycerides, high density lipoprotein cholesterol (HDL-C), and blood glucose. The fatal cases in the studied cohort were identified from “Medical death certificates” for the period from February 1, 2003 to December 31, 2017, based on data from the Department of Civil Registration of Death Acts. Cardiovascular death was established using the International Classification of Diseases, the 10th revision (ICD-10): I (0-99).Results. The mortality rate in subjects with MS was 16,6% — 751 deaths (25,1% in men and 11,5% in women), and it was 20-30% higher than in those without MS. Cardiovascular mortality in subjects with MS was 12,6% — 572 deaths (20,5% in men and 8,9% in women), and it was nearly 30% higher than in those without MS. Multivariable Cox regression revealed that among the components of MS, the elevated BP level even with BP ≥135/80 mm Hg had the major impact on increasing the risk of all-cause mortality (HR=1,7 (1,4; 2,1) in men; HR=2,2 (1,7; 2,8) in women) and increasing the risk of cardiovascular mortality (HR=2,2 (1,5; 3,0) in men and HR=2,8 (1,8; 4.3) in women). Among men, already 1 component of MS increased the risk of cardiovascular and all-cause mortality by 2,0 or more times; among women, 2-4 components of MS increased the risk of death by 3 times, and 5 components — by 4.Conclusion. In the studied population sample, cardiovascular and all-cause mortality during the 14-year follow-up in individuals with MS was about 25-30% higher compared to those without MS. The risk of cardiovascular and all-cause deaths in subjects with MS is comparable to the risk in case of blood pressure ≥135/80 mm Hg. With an increase in the number of MS components from 1 to 5, the risk of all-cause and cardiovascular death increases.