ascorbic-acid and Glomerulonephritis

Acute kidney injury (AKI) is common among hospitalized patients with Coronavirus Infectious Disease 2019 (COVID-19), with the occurrence of AKI ranging from 0.5% to 80%. The variability in the occurrence of AKI has been attributed to the difference in geographic locations, race/ethnicity, and severity of illness. AKI among hospitalized patients is associated with increased length of stay and in-hospital deaths. Even patients with AKI who survive to hospital discharge are at risk of developing chronic kidney disease or end-stage kidney disease. An improved knowledge of the pathophysiology of AKI in COVID-19 is crucial to mitigate and manage AKI and to improve the survival of patients who developed AKI during COVID-19. The goal of this article is to provide our current understanding of the etiology and the pathophysiology of AKI in the setting of COVID-19.

Topics: Acute Kidney Injury; Anti-Bacterial Agents; Antiviral Agents; Apolipoprotein L1; Ascorbic Acid; Azotemia; COVID-19; COVID-19 Drug Treatment; Cytokines; Disease Progression; Glomerulonephritis; Glomerulonephritis, Membranous; Hospital Mortality; Humans; Kidney Tubules, Proximal; Length of Stay; Myoglobin; Nephritis, Interstitial; Nephrosis, Lipoid; Renal Insufficiency, Chronic; Rhabdomyolysis; SARS-CoV-2; Severity of Illness Index; Thrombotic Microangiopathies; Vitamins

Pathogenic organism can be considered as pro-oxidant agents because they produce cell death and tissue damage. In addition organism can be eliminated by specific cell defense mechanism which utilize in part, reactive oxygen radicals formed by oxidative stress responses. The cause of the necessarily defense process results in cell damage thereby leading to development of inflammation, a characteristic oxidative stress situation. This fact shows the duality of oxidative stress in infections and inflammation: oxygen free radicals protect against microorganism attack and can produce tissue damage during this protection to trigger inflammation. Iron, a transition metal which participates generating oxygen free radicals, displays also this duality in infection. We suggest also that different infectious pathologies, such as sickle cell anemia/malaria and AIDS, may display in part this duality. In addition, it should be noted that oxidative damage observed in infectious diseases is mostly due the inflammatory response than to the oxidative potential of the pathogenic agent, this last point is exemplified in cases of respiratory distress and in glomerulonephritis. This review analyzes these controversial facts of infectious pathology in relation with oxidative stress.

Topics: Acquired Immunodeficiency Syndrome; Adult; Anemia, Sickle Cell; Animals; Antioxidants; Arachidonic Acid; Ascorbic Acid; Cells, Cultured; Child; Endotoxins; Fetus; Free Radicals; Glomerulonephritis; Humans; Infections; Inflammation; Iron; Malaria; Mice; Oxidative Stress; Phagocytosis; Rabbits; Respiratory Distress Syndrome; Sheep

Plasma and erythrocyte samples from acute post-streptococcal glomerulonephritis (APSGN) children and control children were enrolled in this study. Lipid peroxidation (LPO), measured in terms of thiobarbituric acid-reactive substances (TBARS) was found to be significantly increased in plasma and RBCs of APSGN children (P<0.05) than in control children. Osmotic fragility of erythrocytes was examined. RBCs of APSGN patients were found to be osmotically more sensitive towards hypotonic saline (50% hemolysis at 7 g/l saline) when compared to control RBCs (50% hemolysis at 4 g/l saline). The activities of antioxidant enzymes superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and glutathione S-transferase (GST) were significantly lowered (P<0.05) in APSGN RBCs when compared to control RBCs. Plasma ascorbic acid, reduced glutathione (GSH), RBC ascorbic acid, GSH and RBC total sulphydryl content (TSH) were significantly depleted in APSGN children relative to controls. The susceptibility of RBCs of APSGN children to lipid peroxidation was confirmed in this study.

Topics: Antioxidants; Ascorbic Acid; Catalase; Child; Child, Preschool; Erythrocytes; Female; Glomerulonephritis; Glutathione; Glutathione Peroxidase; Glutathione Transferase; Humans; Lipid Peroxidation; Male; Osmotic Fragility; Oxidative Stress; Plasma; Reference Values; Streptococcaceae; Streptococcal Infections; Superoxide Dismutase

Topics: Ascorbic Acid; Bioethical Issues; Child; Child Health Services; Clinical Trials as Topic; Common Cold; Compensation and Redress; Control Groups; Coronary Care Units; Coronary Disease; Disclosure; Epidemiologic Methods; Ethics Committees, Clinical; Ethics Committees, Research; Ethics, Medical; Federal Government; Female; Glomerulonephritis; Government Regulation; Human Experimentation; Humans; Informed Consent; Insurance, Liability; Jurisprudence; Male; Maternal Health Services; Moral Obligations; Nontherapeutic Human Experimentation; Penicillin G Benzathine; Placebos; Professional Staff Committees; Respiratory Tract Infections; Rheumatic Fever; Risk Assessment; Streptococcal Infections; Therapeutic Human Experimentation; United States; Withholding Treatment

We studied the spontaneous and metal induced oxidation of lipids and proteins in in vitro modeling ways of lipid peroxidation and blood proteins in the formation of malondialdehyde (MDA) and protein carbonyl groups (PCG) in 86 patients with chronic pyelonephritis (cPN) and 64 patients chronic glomerulonephritis(cGN) without prejudice excretory function of the kidneys. Installed the increase in the blood of patients with cPN MDAs 2 times, MDAe--14%, PCG 1.5 times; and cGN--MDAs 2.3 times, MDAe--29%, PCG--2 times. Found increased MDA content and PCG in the blood of patients with cPN and more expressive when cGN. Stimulation of in vitro peroxidation processes contributed significantly increased of production of MDA comparedwith baseline. In the modeling in vitro ascorbate-dependent and NADPH-dependent lipid peroxidation ways and the increase in protein production of MDA and PCG in both groups of patients, especially in the NADPH-dependent way, which must be considered in the correction of oxidative processes and antioxidant therapy appointment.

Topics: Ascorbic Acid; Case-Control Studies; Chronic Disease; Erythrocytes; Ferrous Compounds; Glomerulonephritis; Humans; Lipid Peroxidation; Malondialdehyde; Primary Cell Culture; Protein Carbonylation; Pyelonephritis

Oxalic acid (OA) is thought to be a uremic toxin that participates in the pathogenesis of uremic syndrome. The objectives of this study were to: (1) evaluate the plasma levels of OA in patients with chronic renal disease with various levels of glomerular filtration rate and after renal transplantation; (2) investigate the salivary secretion of OA and ascorbic acid in healthy subjects and in patients with chronic renal failure (CRF); (3) examine the influence of water and sodium diuresis and furosemide administration on the urinary excretion of OA and ascorbic acid in healthy subjects and in CRF patients without dialysis treatment; and (4) evaluate the influence of renal replacement therapy (RRT) on secondary hyperoxalemia in hemodialysis patients.. This study was conducted at the Nephrological Department of P.J. Safárik University. Sixty-one patients with chronic renal disease, 64 CRF patients, 32 continuous ambulatory peritoneal dialysis (CAPD) patients, 15 hemodialysis patients, 21 patients after renal transplantation, and 15 healthy subjects were examined. Maximal water diuresis, diets with low (2 g/day) and high (15 g/day) sodium intake, administration of intravenous furosemide (20 mg), and renal replacement therapy (CAPD, hemodialysis, hemofiltration, and postdilution hemodiafiltration) were utilized in the study.. In patients with chronic renal disease and those after renal transplantation, direct relationships between plasma OA and serum creatinine were found (r = 0.904 and 0.9431, respectively, P < .01). Despite a high level of plasma OA in uremic patients (23.1 +/- 10 micromol/L), there was no significant difference in salivary OA between control subjects (128 +/- 19 micromol/L) and CRF patients (135 +/- 24 micromol/L). The urinary excretion of OA during maximal water diuresis (from 37.5 to 110.3 micromol/4 hours) and after intravenous furosemide (from 34.5 to 66.7 micromol/3 hours) increased significantly, but was not affected by high intake of NaCl. The most significant decrease of plasma OA was observed during postdilution hemodiafiltration (63.3%).. Our study indicates that renal replacement therapy is not effective for a permanent reduction of elevated plasma levels of OA.

Topics: Adult; Ascorbic Acid; Atherosclerosis; Creatinine; Female; Glomerulonephritis; Humans; Kidney Diseases; Kidney Failure, Chronic; Kidney Transplantation; Male; Middle Aged; Oxalic Acid; Peritoneal Dialysis, Continuous Ambulatory; Renal Dialysis; Uremia; Vitamin B 6

Endothelial dysfunction has been found to be linked to and predictive of cardiovascular events. Whether endothelial function of the renal vasculature is impaired in patients with chronic glomerular disease and whether oxidative stress is of importance in this setting has not yet been determined. In this study, endothelial function of the renal vasculature was investigated in 25 patients with chronic glomerular disease and 50 control subjects matched for age and blood pressure. Renal plasma flow (RPF) and glomerular filtration rate were measured by constant infusion input clearance technique at baseline and following infusions of the nitric oxide synthase (NOS) inhibitor N(G)-monomethyl-L-arginine (L-NMMA, 4.25 mg/kg), the substrate of NOS L-arginine (100 mg/kg) and the antioxidant vitamin C (3 g co-infused with L-arginine 100 mg/kg). At baseline, RPF was similar in the two groups. The reduction in RPF in response to L-NMMA was less pronounced in patients with chronic glomerular disease compared to control subjects (-4.6+/-12 vs -9.8+/-9%; P=0.040), indicating reduced basal nitric oxide (NO) activity in chronic glomerular disease. Co-infusion of the antioxidant vitamin C on top of L-arginine induced a more pronounced increase in RPF in patients with chronic glomerular disease than in control subjects (21.7+/-17 vs 10.9+/-22%; P=0.036). Our findings suggest that basal NO activity of the renal vasculature is reduced in patients with chronic glomerular disease compared to age- and blood pressure-matched control subjects. This might be in part related to increased oxidative stress.

Topics: Adult; Antioxidants; Arginine; Ascorbic Acid; Case-Control Studies; Chronic Disease; Drug Combinations; Endothelium, Vascular; Enzyme Inhibitors; Fasting; Female; Glomerular Filtration Rate; Glomerulonephritis; Heart Rate; Hemodynamics; Humans; Infusions, Intravenous; Male; Middle Aged; NG-Nitroarginine Methyl Ester; Nitric Oxide; Nitric Oxide Synthase Type III; Oxidative Stress; Reference Values; Regional Blood Flow; Vasodilation

Hemodynamic maladjustment is a unique observation in chronically severe glomerulonephritides. It is characterized by a markedly elevated efferent arteriolar resistance (RE), an elevated intraglomerular hydrostatic pressure (PG) and a markedly decreased renal plasma flow (RPF), and peritubular capillary flow (PTCF). A correction of such hemodynamic maladjustment can be accomplished by administering a combination of vasodilators (angiotensin receptor antagonist, angiotensin converting enzyme inhibitor, and calcium channel blocker) in 14 chronic glomerulonephritides with severe renal function impairment (mean serum creatinine 3.6 + 1.3 mg/dL). Doses titration aim for maximal renal perfusion effect (increased RPF, PTCF) or maximal renal function improvement (increased CCr, reduced FE Mg) usually higher than needed for maximal blood pressure reduction. Evidence of oxidative stress is also corrected with high doses of vitamins C and E. After a mean period of treatment for 13.5 months, improvements in CCr (pre R(x) 22 +/- 10 vs. post R(x) 32 +/- 13 mL/min/1.73 m2), and FE Mg (pre R(x) 11.9 +/- 4% vs. post R(x) 10 +/- 3%) were observed in conjunction with the improvement in intrarenal hemodynamics namely RPF (pre R(x) 201 +/- 71 vs. post R(x) 288 +/- 99 mL/min/1.73 m2), PTCF (pre R(x) 161 +/- 57 vs. post R(x) 242 +/- 90 mL/ min/1.73 m2), PG (pre R(x) 56.7 +/- 0.5 vs. post R(x) 51 +/- 0.1 mm Hg), and RE (pre R(x) 12085 +/- 6503 vs. post R(x) 6550 +/- 1872 dyne.s.cm(-5)).

Topics: Adult; Angiotensin Receptor Antagonists; Angiotensin-Converting Enzyme Inhibitors; Antioxidants; Ascorbic Acid; Calcium Channel Blockers; Chronic Disease; Disease Progression; Glomerulonephritis; Hemodynamics; Humans; Oxidative Stress; Renal Insufficiency; Vasodilator Agents; Vitamin E

Topics: Adolescent; Ascorbic Acid; Child; Child, Preschool; Combined Modality Therapy; Drug Combinations; Drug Evaluation; Fatty Acids, Unsaturated; Glomerulonephritis; Humans; Lipids; Nephrotic Syndrome; Niacin

Topics: Adult; Ascorbic Acid; Chronic Disease; Glomerulonephritis; Glycoproteins; Humans; Middle Aged

The study deals with investigations on anaemia due to iron or protein calorie deficiency and that associating acute glomerulonephritis, nephrosis and schistosoma haematobium. The rate of intestinal iron absorption using an oral dose of ferrous sulphate equivalent to 4 mg clemental iron/kg body weight was studied. The supplementing action of ascorbic acid in iron absorption in these cases was also investigated. The rate of intestinal iron absorption was enhanced in pure iron deficiency anaemia, acute glomerulonephritis and schistosoma haematobium, retarded in kwashiorkor, marasmus and nephrosis. Ascorbic acid markedly promoted iron absorption in normal subjects but slightly in pure iron deficiency anaemia. It improved iron absorption in acute glomerulonephritis and schistosoma haematobium but not in kwashiorkor, marasmus and nephrotic cases. It is concluded that ascorbic acid supplementation is of certain beneficial effect in alleviating the state of anaemia when intestinal iron absorption is not impaired. Also, it may prove to be of value to be given along with protein rehabilitation in anaemias associating protein deficiency.

Topics: Anemia; Anemia, Hypochromic; Ascorbic Acid; Child, Preschool; Egypt; Female; Glomerulonephritis; Humans; Infant; Intestinal Absorption; Iron; Male; Protein-Energy Malnutrition; Schistosomiasis

Topics: Anemia, Hemolytic; Anemia, Hypochromic; Ascorbic Acid; Bilirubin; Blood Transfusion; Catalase; Chronic Disease; Glomerulonephritis; Gout; Hemoglobinometry; Humans; Iron; Kidney Diseases; Liver Diseases; Nephritis; Nitrogen; Rheumatic Fever; Surgical Procedures, Operative

Topics: Acute Disease; Age Factors; Ascorbic Acid; Calcium; Cerebral Hemorrhage; Cortisone; Diet Therapy; Glomerulonephritis; Gluconates; Humans; Male; Middle Aged; Purpura; Rheumatic Diseases; Rutin; Vitamin K

Topics: Aged; Angiomatosis; Arteriosclerosis; Ascorbic Acid; Glomerulonephritis; Humans; Hypertension; Keratosis; Male; Nails; Pressure; Purpura

Topics: Acute Disease; Ascorbic Acid; Flavonoids; Glomerulonephritis; Humans; Vitamins