Oxidative stress and endoplasmic reticulum (ER) stress play a key role in tubular damage in both acute kidney injury and chronic kidney disease (CKD). Oxidative stress in the kidneys promotes renal vascular remodeling and increases preglomerular resistance. These are key elements in hypertension, acute and chronic kidney injury, as well as diabetic nephropathy. Chronic renal hypoxia is highlighted as the final common pathway to end-stage renal disease (ESRD). MicroRNA molecules (miRNA) also play an important role in these processes. MicroRNAs (miRNAs) are regulators of gene expression and play a role in the progression of renal ischemia-reperfusion injury. Although the pathophysiological contribution of microRNAs (miRNAs) to kidney damage has also been highlighted, the effect of miRNAs on kidney damage under conditions of oxidative and ER stress remains understudied.

Inclusion Criteria:

• healthy normotensive adults (eGFR CKD-EPI >90 mL/min/1.73 m2, BP <140/90 mmHg)
• hypertensive adults (eGFR CKD-EPI >90 mL/min/1.73 m2, BP >140/90 mmHg)
• patients with chronic kidney disease stage 3-5 (eGFR CKD-EPI< 60 mL/min/1.73 m2)

Exclusion Criteria:

• cardiovascular diseases, but hypertension
• diabetes
• cerebrovascular diseases
• peripheral artery disease

Patients with CKD and healthy controls, i.e. patients with hypertension without kidney damage (eGFR CKD-EPI > 90 mL/min/1.73 m2). Subjects and controls will be age- and gender-matched. Inclusion criteria for patients with CKD: the study will include patients having chronic kidney disease of the 3rd - 5th degree (eGFR CKD-EPI< 60 mL/min/1.73 m2).