About this trial
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.
Eligibility criteria
Qualifiers
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)
Disqualifiers
cardiovascular diseases, but hypertension
diabetes
cerebrovascular diseases
peripheral artery disease
Trial design
Treatments tested in this trial
- Not listed
Trial groups
Sponsors and collaborators
Josip Juraj Strossmayer University of Osijek
Lead sponsor
University Hospital Center Osijek
Collaborator