Diabetic Nephropathy
Diabetic nephropathy, or diabetic kidney disease, is a chronic condition characterized by the progressive loss of kidney function due to complications from type 1 or type 2 diabetes. Poorly-controlled blood sugar damages blood vessels in the kidneys, leading to protein leakage in urine, rising blood pressure, and ultimately end-stage renal disease (ESRD).
Health Outcomes
- Activation of Nrf2 Pathway
- Altered Blood Parameters
- Altered Metabolite Profile
- Changed Bicarbonate Level
- Changed Phosphate Level
- Changed Urinary Calcium Creatinine Ratio
- Delayed Disease Progression
- Delayed Onset of Urinary Tract Infections
- Elevated Malondialdehyde Levels
- Enhanced Antioxidant Activity
- Enhanced Antioxidant Capabilities
- Enhanced Antioxidant Levels
- Enhanced Antioxidant Response
- Enhanced Antioxidative Capacity
- Enhanced Cell Viability Under Oxidative Stress
- Enhanced Endoplasmic Reticulum Stress Response
- Enhanced Kidney Antioxidant Capacity
- Enhanced Metabolite Levels
- Enhanced Protein Kinase C Activity
- Enhanced Reactive Oxygen Species Resistance
- Improved Antioxidant Defense
- Improved Antioxidant Function
- Improved Arginine Metabolism
- Improved Blood Glucose Levels
- Improved Chronic Kidney Disease Outcomes
- Improved Clinical Outcomes
- Improved Cytoprotection During Oxidative Stress
- Improved Dialysis Adequacy
- Improved Estimated Glomerular Filtration Rate
- Improved Fibrosis
- Improved Free Radical Scavenging Activity
- Improved Kidney Function
- Improved Mean Arterial Pressure
- Improved Metabolic Regulation
- Improved Metabolome Profile
- Improved Nephropathy
- Improved Oxidative Stress Resistance
- Improved Protein Kinase C Activity
- Improved Renal Function
- Improved Serum Biomarkers
- Improved Symptoms of Chronic Condition
- Improved Total Antioxidant Status
- Improved eGFR
- Increase in Persistent Diseased Sites
- Increased 1,2-Propanediol Concentration
- Increased ACE Inhibitor Activity
- Increased Antioxidant Activity
- Increased Antioxidant Enzyme Levels
- Increased Cell Adhesion
- Increased Collagen Synthesis
- Increased Creatinine Clearance
- Increased ER Stress-Associated Proteins
- Increased Endogenous Acrolein Formation
- Increased Expression of Oxidation-Related Gene
- Increased Hydrogen Peroxide Production
- Increased Hyperkalemia
- Increased Interleukin-6 Production in Macrophages
- Increased Malondialdehyde Levels
- Increased Monocarboxylic Acid Transporter mRNAs
- Increased Nrf2 Protein Content
- Increased Number of Persistent Diseased Sites
- Increased Oxidative Stress Tolerance
- Increased PPAR-γ Activity
- Increased Plasma Phosphorus
- Increased Plasma Protein Levels
- Increased Production of ACE-Inhibitory Peptides
- Increased Production of Bioactive Peptides with Angiotensin Converting Enzyme Inhibitory Activity
- Increased Serum Antioxidant Enzyme Levels
- Increased Serum Glucose Levels
- Increased Soluble Receptor of Advanced Glycation End Products
- Increased Superoxide Dismutase Levels
- Increased Type 1 Collagen Synthesis
- Increased Uric Acid Excretion
- Increased VEGF Level
- Inhibited Absorption of Advanced Glycation End-products (AGEs)
- Inhibited α-Amylase Activity
- Maintained pH Levels
- Modulated Metabolite Profile
- Modulated PPAR/SREBP Pathway
- No Change in Inflammation Markers
- No Significant Acute Effect on Calcium Metabolism
- Protection Against Oxidative Stress
- Reduced ACE Activity
- Reduced Advanced Glycation End Product Level
- Reduced Angiogenesis
- Reduced Apelin Gene Expression
- Reduced Bicarbonate Level
- Reduced Blood Glucose Elevation
- Reduced Carboxymethyl Lysine
- Reduced Contrast-Induced Acute Kidney Injury
- Reduced Contrast-Induced Nephropathy
- Reduced Diabetic Complications
- Reduced Dietary Advanced Glycation End Product Intake
- Reduced Electrolyte Level
- Reduced Enzyme Activity Related to Diabetes
- Reduced Fasting Blood Sugar Levels
- Reduced Glucotoxicity
- Reduced Glutathione Redox Ratio
- Reduced Glycation End Product Accumulation
- Reduced Glycative Stress Marker Level
- Reduced Indoxyl Sulfate Levels
- Reduced Kidney Cell Apoptosis
- Reduced Kidney Damage
- Reduced Kidney Fibrosis
- Reduced Kidney Function
- Reduced Kidney Histological Damage
- Reduced Kidney Injury
- Reduced Kidney Oxidative Stress
- Reduced Kidney Pathological Changes
- Reduced Malonaldehyde Levels
- Reduced Metabolic Function
- Reduced Need for Continuous Renal Replacement Therapy
- Reduced Nitric Oxide Production
- Reduced Organ Failure Severity
- Reduced Oxidative Damage in Serum
- Reduced Oxidative Stress Markers
- Reduced Physiological Impairments
- Reduced Pre-Dialysis Serum Triglyceride Levels
- Reduced Proteinuria
- Reduced Proteinuria Levels
- Reduced Renal FL-furosine Levels
- Reduced Renal Free-CML
- Reduced Renal Hypertrophy
- Reduced Renal Inflammation
- Reduced Renal Pathological Damage
- Reduced Renal Replacement Therapy
- Reduced Renal Sympathetic Activity
- Reduced Serum Carboxymethyl-Lysine Levels
- Reduced Serum Levels of CML
- Reduced Serum MDA Concentrations
- Reduced Stigmasterol Absorption
- Reduced Succinate Levels
- Reduced Urinary Albumin
- Reduced Urinary Calcium Level
- Reduced Urinary Nitrite Level
- Reduction of Diabetes-Induced Organ Damage
- Reproduced Protective Effect via Extracellular Vesicles
- Slower CKD Progression
- Stabilized Amino Acid Metabolism
- Stabilized Hemoglobin A1c Level
- Stable Kidney Function
- Suppressed PPAR/SREBP Pathway Gene Activity
- Unchanged Heat Shock Protein Levels
- Unchanged Monocyte Chemoattractant Protein-1 Levels
- Worsened Acidosis