Diabetes prevalence is increasing worldwide, especially through the increase of type 2 diabetes. Diabetic nephropathy occurs in up to 40% of diabetic patients and is the leading cause of end-stage renal disease. Various factors affect the development and progression of diabetic nephropathy. Hyperglycaemia increases free radical production, resulting in oxidative stress, which plays an important role in the pathogenesis of diabetic nephropathy. Free radicals have a short half-life and are difficult to measure. In contrast, oxidation products, including lipid peroxidation, protein oxidation, and nucleic acid oxidation, have longer lifetimes and are used to evaluate oxidative stress. In recent years, different oxidative stress biomarkers associated with diabetic nephropathy have been found. This review summarises current evidence of oxidative stress biomarkers in patients with diabetic nephropathy. Although some of them are promising, they cannot replace currently used clinical biomarkers (eGFR, proteinuria) in the development and progression of diabetic nephropathy.

Diabetic kidney disease is a frequent microvascular complication of diabetes and is currently the leading cause of chronic kidney disease and end-stage kidney disease worldwide. Although the prevalence of other complications of diabetes is falling, the number of diabetic patients with end-stage kidney disease in need of kidney replacement therapy is rising. In addition, these patients have extremely high cardiovascular risk. It is more than evident that there is a high unmet treatment need in patients with diabetic kidney disease. Finerenone is a novel nonsteroidal mineralocorticoid receptor antagonist used for treating diabetic kidney disease. It has predominant anti-fibrotic and anti-inflammatory effects and exhibits several renal and cardiac protective effects. This review article summarizes the current knowledge and future prospects of finerenone in treating patients with kidney disease.

Diabetes mellitus is a global health issue and main cause of chronic kidney disease. Both diseases are also linked through high cardiovascular morbidity and mortality. Diabetic kidney disease (DKD) is present in up to 40% of diabetic patients; therefore, prevention and treatment of DKD are of utmost importance. Much research has been dedicated to the optimization of DKD treatment. In the last few years, mineralocorticoid receptor antagonists (MRA) have experienced a renaissance in this field with the development of non-steroidal MRA. Steroidal MRA have known cardiorenal benefits, but their use is limited by side effects, especially hyperkalemia. Non-steroidal MRA still block the damaging effects of mineralocorticoid receptor overactivation (extracellular fluid volume expansion, inflammation, fibrosis), but with fewer side effects (hormonal, hyperkalemia) than steroidal MRA. This review article summarizes the current knowledge and newer research conducted on MRA in DKD.

Purpose: Abdominal adipose tissue has important inflammatory properties and is a source of various inflammatory mediators. Given that concentrations of some inflammatory mediators are high among hemodialysis (HD) patients, abdominal obesity may play an important role in the pathogenesis of microinflammation which is known to be associated with accelerated atherosclerosis. The aim of our study was to determine the impact of microinflammation on cardiovascular (CV) mortality in abdominal obese HD patients. Methods: Seventy–one HD patients (mean age 59.3 ± 12.8 years) were included in our study. Waist circumference (WAC) was measured and abdominal obesity was defined according to the International Diabetes Federation. Serum levels of lipids (triglycerides, high density lipoproteins (HDL) cholesterol, low density lipoproteins (LDL) cholesterol) and inflammatory mediators (interleukin–6, tumor necrosis factor–alpha, vascular cellular adhesion molecule–1 (VCAM–1), intercellular adhesion molecule–1 (ICAM–1)) were measured. Patients were observed from the date of measurement (November 2003) of inflammatory mediators until their death or to 10th of November 2009. Results: The mean WAC value for men was 97.6 ± 16.1 cm, and for women 92.2 ± 15.9 cm. Abdominal obesity was found in 62% of the enrolled patients. Cox regression analysis showed that the inflammatory mediators VCAM–1 (p<0.031) and ICAM–1 (p<0.024) were predictors of CV mortality in abdominal obese HD patients. Both inflammatory mediators remained predictors of CV mortality if age and other known risk factors for atherosclerosis (arterial hypertension, smoking, HDL and LDL cholesterol and triglycerides) were included in the analysis. Conclusion: The results of our study indicate that microinflammation is associated with CV mortality in abdominal obese HD patients.