ascorbic-acid and Uremia

Uraemic patients are exposed either to iron deficiency due to impaired digestive n associated with various blood losses (particularly in dialysis patients) or iron verload related to blood transfusions in the pre-erythropoetin era or excessive intravenous iron supplementation. The central role of hepcidin in the regulation of oral iron absorption d its effects in uraemia have been recently evidenced. The increased haemoglobin synthesis induced by erythropoiesis stimulating agents (ESA) enhances iron requirements. In case of exhaustion of tissue reserves and/or insufficient exogenous supply, iron deficiency develops which is the major limiting factor for ESA efficacy. Careful biological follow-up is mandatory to detect early iron deficiency or overload, the latter being considered as possibly increasing the uraemic patients' susceptibility to bacterial or viral infections. Intravenous administration of Vitamin C, by enhancing the release of iron from the reticuloendothelial system towards transferrin increases the circulating iron available for erythropoiesis and contributes to the optimisation of ESA efficacy.

Topics: Anemia, Iron-Deficiency; Antimicrobial Cationic Peptides; Ascorbic Acid; Erythropoietin; Hepcidins; Humans; Intestinal Absorption; Iron; Iron Deficiencies; Uremia

Topics: Animals; Ascorbic Acid; Carbohydrate Metabolism; Glycation End Products, Advanced; Humans; Lipid Metabolism; Oxidation-Reduction; Oxidative Stress; Uremia

Topics: Abdomen; Abdominal Muscles; Ascorbic Acid; Female; Hernia; Humans; Jaundice; Laparotomy; Male; Methods; Microscopy, Electron, Scanning; Middle Aged; Postoperative Complications; Pressure; Risk; Surgical Wound Dehiscence; Surgical Wound Infection; Suture Techniques; Sutures; Uremia; Wound Healing

Topics: Ascorbic Acid; Ascorbic Acid Deficiency; Chlorine; Erythrocyte Aging; Erythrocytes; Glucosephosphate Dehydrogenase Deficiency; Hexosephosphates; Humans; Minnesota; Pentosephosphates; Renal Dialysis; Uremia; Water

Topics: Adolescent; Ascorbic Acid; Biochemical Phenomena; Biochemistry; Child; Classification; Diet; Genetics, Medical; Glycine; Glycolates; Humans; Hyperoxaluria, Primary; Infant; Kidney Calculi; Metabolic Diseases; Metabolism; Nephrocalcinosis; Oxalates; Pathology; Terminology as Topic; Uremia; Urine; Vitamin B 6 Deficiency

Vitamin C (ascorbate) deficiency and symptoms consistent with deficiency (fatigue, myalgia, dyspnoea, gingivitis, cardiovascular instability and depression) are common in patients with renal failure. This study aimed to determine if supplementation with ascorbate in patients with severe renal failure improved symptoms or cardiovascular stability, or was associated with adverse effects.. The study was a 3-month, double-blind, randomized trial of ascorbic acid 250 mg or matching placebo given thrice weekly. Subjects were clinically stable and either received conventional dialysis or had an estimated glomerular filtration rate of <20 mL/min. Symptoms were measured using the Kidney Dialysis Quality of Life-Short Form (KDQOL-SF™) symptom subscale, and the study was 80% powered to detect a change of 10 in the KDQOL-SF™.. Ninety-nine subjects were randomized, and ascorbate deficiency was present in 40% at baseline. Mean symptom scores at follow-up were similar in the two groups (P-value=0.19). There was a trend to slightly worse nausea scores in the ascorbate group after controlling for the level of baseline nausea (P=0.09), and there was no impact on cardiovascular stability. Compliance appeared adequate at 91%, and deficiency was corrected in most (85%) of the subjects in the active treatment group.. This study indicates that ascorbate supplementation does not improve symptoms or cardiovascular stability in those with severe renal impairment, but is associated with a trend towards worse nausea.

Topics: Ascorbic Acid; Ascorbic Acid Deficiency; Dietary Supplements; Double-Blind Method; Humans; Prospective Studies; Renal Insufficiency; Uremia

The effect of ascorbate treatment on apheresis-induced oxidative stress in uremic and dyslipidemic patients was evaluated.. We developed a chemiluminescence-emission spectrum and high-performance liquid chromatography analysis to assess the effect of ascorbate supplement on plasma reactive oxygen species (ROS) scavenging activity and oxidized lipid/protein production in hyperlipidemic and uremic patients undergoing apheresis. Apheresis was efficient in reduction of atherogenic lipoproteins, complement, fibrinogen, soluble intercellular adhesion molecule-1, and oxidative parameters including phosphatidylcholine hydroperoxide (PCOOH), malonaldehyde, methylguanidine, and diotyrosine. Apheresis itself, however, activated leukocytes to increase ROS activity and reduced the plasma ROS scavenging activity. Ascorbate administration selectively diminished apheresis-enhanced H2O2 and inflammatory mediators such as tumor necrosis factor alpha (TNF-alpha) and monocyte chemoattractant protein-1. Chronically dyslipidemic and uremic patients undergoing biweekly apheresis plus ascorbate treatment had lower levels of C-reactive protein and PCOOH than did those without ascorbate treatment during a 6-month follow-up study period.. We demonstrate that apheresis with ascorbate treatment provides a therapeutic potential in reducing atherosclerotic risk via inhibition of H2O2-induced oxidative stress in patients with uremia or dyslipidemia.

Topics: Adult; Antioxidants; Ascorbic Acid; Biomarkers; C-Reactive Protein; Combined Modality Therapy; Drug Therapy, Combination; Female; Humans; Hyperlipidemias; Hypolipidemic Agents; Lipid Peroxidation; Luminescent Measurements; Male; Malondialdehyde; Methylguanidine; Middle Aged; Neutrophils; Oxidative Stress; Plasmapheresis; Reactive Oxygen Species; Respiratory Burst; Treatment Outcome; Tyrosine; Uremia; Vitamin E

The aim of this study was to evaluate the probable protective effect of vitamin C and vitamin E on diclofenac-induced acute nephrotoxicity using biochemical, molecular and histopathological examination in rats following administration of diclofenac sodium (50mg/kg, I.M).. Ninety male Wister rats were allotted in six equal groups. Rats in the 1st group (control group) were injected with physiological saline, while rats in the 2nd group (C-group) were given vitamin C (100mg/kg orally via stomach tube) for 5 successive days. The 3rd group (E-group) was given vitamin E (250mg/kg orally in diet) for 5 successive days. Rats in the 4th group (D-group) were injected by diclofenac sodium (50mg/kg, I.M) for 5 successive days. The 5th group (DvC-group) was given diclofenac sodium (50mg/kg, I.M) and vitamin C (100mg/kg orally via stomach tube) for 5 successive days. Rats in the 6th group (DvE-group) were given diclofenac sodium (50mg/kg, I.M) and vitamin E (250mg/kg orally in diet) for 5 successive days. Blood samples were collected two days post treatment (1st week of experiment), 2nd and 4th week of the experiment for assessment of urea, creatinine, malondialdehyde, nitric oxide and superoxide dismutase activities. At the end of 4th week, rats were sacrificed and kidneys were excised for biochemical analyses, histopathological evaluation and determination of kidney interleukin-1β, interleukin-18, demsin and nepherin expressions in by reverse transcriptase-polymerase chain reaction (RT-PCR).. The results showed that, diclofenac induced severe kidney damage as indicated by histopathological changes and increased serum oxidative stress parameters. Behavioral changes were monitored; a significant increase in uremia in intoxicated animals was also noted indicating that diclofenac sodium provoked kidney damage in rats. Application of vitamin C (DvC-group) and vitamin E (DvE-group) were found to improve the abovementioned abnormalities.. The present data suggest that, vitamin C and vitamin E might play an important role in reducing oxidative stress and kidney damage induced by diclofenac sodium.

Topics: Acute Kidney Injury; Animals; Antioxidants; Ascorbic Acid; Biomarkers; Cytoprotection; Diclofenac; Disease Models, Animal; Kidney; Male; Oxidative Stress; Rats, Wistar; Uremia; Vitamin E

Renal dysfunction is closely associated with endothelial damage leading to cardiovascular disease. However, the extent to which endothelial damage induced by uremia is modulated by aging is poorly known. Aging can render endothelial cells more susceptible to apoptosis through an oxidative stress-dependent pathway. We examined whether senescence-associated to oxidative stress determines the injury induced by the uremia in endothelial cells. Human umbilical vein endothelial cells (HUVEC) was incubated with human uremic serum and, in the animal model, endothelial cells were obtained from aortas of uremic and no uremic rats. Vitamin C was used to prevent oxidative stress. Senescence, assessed by telomere length and enzyme-betagalactosidase (β-gal), reactive oxygen species (ROS), mitochondrial depolarization (JC-1 probe), caspase 3, and apoptosis were determined by flow cytometry. NF-κB activity was determined by Western blot. Uremic serum increased ROS and NF-κB in young and aging HUVEC. However only in aging cells, uremic serum induced apoptosis (vs young HUVEC, p<0.01). The endothelial damage induced by uremia seems to be related with the increased oxidative stress, since in both HUVEC and in the experimental model of renal disease in rats, vitamin C prevents endothelial apoptosis. However, vitamin C did not decrease the oxidative stress associated to senescence. These results showed that as compared with young cells, senescent cells have high sensitivity to damage associated to the oxidative stress induced by the uremia. Consequently, protecting senescent endothelial cells from increased oxidative stress might be an effective therapeutic approach in the treatment of vascular disorders in chronic kidney diseases.

Topics: Aged; Animals; Apoptosis; Ascorbic Acid; Cells, Cultured; Cellular Senescence; Endothelium, Vascular; Female; Humans; In Vitro Techniques; Male; Middle Aged; Models, Animal; NF-kappa B; Oxidative Stress; Rats, Wistar; Reactive Oxygen Species; Serum; Uremia

Previous studies have shown that the increase of carbamylated LDL (cLDL), a product of nonenzymatic modification of LDL in human serum by urea-derived cyanate, may cause cardiovascular complications in patients with chronic renal insufficiency. This study examined the inhibitory effect of ascorbic acid, alpha-tocopherol and lycopene on LDL carbamylation in an in vitro model system.. After isolation of LDL from plasma using an ultracentrifuge technique, cyanate was added to it and then LDL carbamylation was measured in both the absence and presence of ascorbic acid, alpha-tocopherol and/or lycopene by the colorimetric method at 530 nm.. The findings indicated that these vitamins inhibit LDL carbamylation and the most effective vitamin of the three is lycopene. Moreover, the effect of lycopene on this process increased in the presence of ascorbic acid and alpha-tocopherol.. This study indicated that ascorbic acid, alpha-tocopherol and lycopene with antioxidant activity can probably inhibit LDL carbamylation and therefore may have a role in ameliorating atherosclerotic risk of patients with kidney failure. However in vitro and in vivo investigations are required to confirm the exact effects of these vitamins on patients suffering from uremic disorders.

Topics: Adult; alpha-Tocopherol; Ascorbic Acid; Atherosclerosis; Carotenoids; Citrulline; Cyanates; Electrophoresis, Agar Gel; Humans; Lipoproteins, LDL; Lycopene; Male; Protein Processing, Post-Translational; Uremia; Vitamins; Young Adult

Oxalic acid is thought to be a significant uremic toxin that participates in the pathogenesis of uremic syndrome. AIM OF THE STUDY was to summarise results which we obtained during the study ofoxalic acid in biological fluids (plasma, saliva, urine and dialysate) in patients suffering from chronic kidney diseases (CKD), stage 3-5 and after renal transplantation.. In the retrospective study were investigated 28 healthy subjects, 112 CKD stage 1-4 patients, 39 haemodialysis patients and 27 CAPD patients. Besides 21 patients were investigated after renal transplantation. We used the following therapeutic methods: maximal water diuresis, diet with low (2g/day) and high (15g/day) sodium chloride intake, administration intravenous furosemide (20mg) and renal replacement therapy [CAPD, haemodialysis (HD), haemofiltration (HF) and postdilution haemodiafiltration (HDF)] and renal transplantation. Oxalic acid was determined by spectrophotometric method using oxalate oxidase which is free from vitamin C interference. Vitamin C was determined by spectrophotometric method.. In CKD patients and those after renal transplantation direct relationships between plasma oxalic acid and serum creatinine were found (r = 0.904 and 0.943, respectively, P < 0.001). Despite of high plasma oxalic acid in uremic patients (23.1 +/- 10 micromol/l), there was no significant difference in salivary oxalic acid between control subjects (126.5 +/- 18 micromol/l) and CKD stage 3-4 patients (133.9 +/- 23.7 micromol/I). The urinary excretion of oxalic acid during maximal water diuresis in healthy subjects (n = 15) (from 37.5 +/- 17.4 to 110.2 +/- 49.3 micromol/4 hours) and after intravenous furosemide (CKD stage 3-4, n = 15) (from 34.5 +/- 5.5 to 66.7 +/- 8.1 micromol/3 hours) increased significantly, but was not affected by high intake of NaCI in diet (CKD stage 3-4, n = 12). One tablet of Sorbifer Durules containing 100 mg Fe2+ and 60 mg vitamin C did not lead to further increase of uremic hyperoxalemia in haemodialysis patients. Four-hour HD, H F and HDF led to the significant decrease of plasma oxalic acid, but the most significant decrease was observed during HDF (63.3%).. The results of this study indicate, that renal replacement therapy is not effective for permanent reduction of elevated plasma levels of oxalic acid--important uremic toxin.

Topics: Adult; Ascorbic Acid; Chronic Disease; Creatinine; Diuresis; Female; Humans; Kidney Diseases; Kidney Transplantation; Male; Middle Aged; Oxalic Acid; Renal Dialysis; Sodium Chloride, Dietary; Toxins, Biological; Uremia

Topics: Anemia; Ascorbic Acid; Calcium Oxalate; Dose-Response Relationship, Drug; Drug Administration Routes; Humans; Hyperoxaluria; Iron Compounds; Renal Dialysis; Treatment Outcome; Uremia; Vitamins

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

50 Patients with chronic renal failure undergoing hemodialysis with or without porphyria cutanea tarda (PCT)-like skin changes were investigated. The total porphyrin amount in erythrocytes, plasma and dialysate and the distribution of porphyrin metabolites in plasma and dialysate were measured. In plasma, the group of patients with skin changes (referred as PCU = porphyria cutanea uremica) showed significantly increased uroporphyrin levels as compared to the non-symptomatic group. In addition, significant differences concerning the ratio uro-/coproporphyrin in plasma were shown: non-symptomatic patients with 0.87, as opposed to the PCU group with 3.7. Considerable differences between the level of vitamin ingestion were identified between the groups. Patients with PCU took distinctly less vitamins C, E and B than patients without symptoms.

Topics: Adolescent; Adult; Aged; Aged, 80 and over; Ascorbic Acid; Coproporphyrins; Dose-Response Relationship, Drug; Female; Humans; Kidney Failure, Chronic; Kidney Function Tests; Male; Middle Aged; Porphyria Cutanea Tarda; Reference Values; Renal Dialysis; Risk Factors; Uremia; Uroporphyrins; Vitamin B Complex; Vitamin E; Vitamins

To evaluate the states of inflammation, oxidative stress and carbonyl stress in uremic patients and analyze their relationships.. One hundred and twenty-eight cases were divided into 6 groups: non-dialysis uremia group (n=25), peritoneal dialysis group (n=19), hemophan(Hem) membrane dialysis group (n=25), polyamide (PS) membrane dialysis group (n=25), diabetes with normal renal function group (n= 23) and normal control group (n=11). Spectrophotometry and immune turbidimetry were used to measure the serum SOD, VitC, VitE, MDA and total carbonyl compounds (TCC) levels.. Compared with non-uremia groups, the uremia groups had lower serum SOD, VitE and VitC levels, but higher CRP, MDA and TCC levels (P < 0.01). The peritoneal dialysis group had higher SOD, VitC, VitE levels in comparison with the Hem group, but did not differ from PS group in those levels (P > 0.05). The MDA and TCC levels in the peritoneal dialysis group were lower than those in the two hemodialysis groups, but there were no significant differences in CRP level between the groups. Compared with Hem group, the PS group had higher VitC, VitE levels, higher TCC clearance, and the same SOD, MDA, CRP and pre-dialysis TCC levels. When the variables were analyzed with TCC, the results of multi-variate regression showed that the standardized coefficients were MDA (0.727, P < 0.01), CRP (0.370, P < 0.01), SOD (0.192, P < 0.05), VitC (-0.153, P < 0.01), VitE (0.054, P = 0.30) respectively.. Uremic patients are in inflammatory, oxidative-stress and carbonyl-stress states. Inflammation and oxidative stress are probably the important mechanism of carbonyl stress. It is not yet clear whether dialysis methods can influence uremic inflammatory, oxidative-stress or carbonyl-stress state.

Topics: Adult; Ascorbic Acid; C-Reactive Protein; Female; Glycation End Products, Advanced; Humans; Inflammation; Male; Malondialdehyde; Middle Aged; Nephelometry and Turbidimetry; Oxidative Stress; Protein Carbonylation; Renal Dialysis; Spectrophotometry; Superoxide Dismutase; Uremia; Vitamin E

Human erythrocytes can take up dehydroascorbate on the glucose transporter 1 (GLUT 1) and reduce it to ascorbate. Intraerythrocyte ascorbate was proved to be directly responsible for decreased oxidation of extraerythrocytic ascorbate. In addition to spontaneous and irreversible loss of ascorbate in plasma, the hemodialysis (HD) process itself consumes plasma ascorbate. However, intraerythrocyte ascorbate status in uremic patients during HD has yet to be reported.. Plasma and intraerythrocyte ascorbate, dehydroascorbate, GLUT 1 expression on erythrocyte membranes, and in vitro studies of "erythrocyte ascorbate recycling" were investigated in age- and sex-matched healthy subjects (control group) and HD patients (HD group).. Intraerythrocyte ascorbate concentrations decreased after 1 HD session compared with pre-HD and recovered to pre-HD values 2 days later, whereas plasma ascorbate concentrations did not recover. In vitro studies suggested that erythrocytes of HD patients have a stronger ability to maintain intracellular ascorbate concentrations compared with healthy subjects. This ability could be inhibited by cytochalasin B (GLUT 1 inhibitor). We also found increased GLUT 1 expression (P = 0.002) on erythrocyte membranes in the HD group compared with the control group.. Erythrocytes of uremic patients lost large amounts of ascorbate during HD, but regained it to the pre-HD level 2 days later. Enhanced GLUT 1 expression on erythrocyte membranes for HD patients may contribute to better preservation of intracellular ascorbate compared with healthy subjects.

Topics: Aged; Ascorbic Acid; Blotting, Western; Chromatography, High Pressure Liquid; Cytochalasin B; Dehydroascorbic Acid; Erythrocyte Membrane; Erythrocytes; Female; Glucose Transporter Type 1; Humans; Kidney Diseases; Male; Middle Aged; Renal Dialysis; Time Factors; Uremia

Oxidative stress plays a role in many disease states. These diseases have an increased incidence in uremia, and particularly in hemodialysis (HD) patients. This suggests an increased exposure to oxidative stress. An imbalance between oxidants and antioxidants has been suggested in uremic patients on HD. However, the respective influence of uremia and dialysis procedure has not been evaluated. It is postulated that antioxidant capacity in uremic patients is reduced, yet the mechanism remains unclear. We have determined the levels of lipid peroxidation expressed as thiobarbituric acid-reactive substances. We assessed oxidative protein damage by carbonyl content and activities of antioxidant enzymes including superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx) in predialysis uremic patients and in end-stage renal disease (ESRD) patients before and after hemodialysis. Vitamin E and vitamin C levels, reduced glutathione and sulfhydryl content were also studied. We found enhanced oxidative stress in ESRD patients undergoing HD and in predialysis uremic patients. This was mostly due to defective antioxidant enzyme levels. Preventive modalities, including use of biocompatible membranes, ultrapure dialysate, exogenous supplementation of antioxidant vitamins, extracorporeal removal of reactive oxygen species (ROS) and oxidatively modified substances, would appear highly desirable to reduce complications in the long-term dialysis patients.

Topics: Antioxidants; Ascorbic Acid; Catalase; Erythrocytes; Glutathione Peroxidase; Humans; Kidney Failure, Chronic; Oxidative Stress; Renal Dialysis; Superoxide Dismutase; Thiobarbituric Acid Reactive Substances; Uremia; Vitamin E

A convenient and valid method for the determination of ascorbic acid(AA) and dehydroascorbic acid(DHAA) in plasma and dialysate from patients with uremia by high performance liquid chromatography with electrochemical detection is described. A mixture of 0.8 g/L metaphosphoric acid and 18% (volume fraction) perchloric acid was used as a protein precipitant and the extractant for AA from biosamples. It was also a good stabilizer for AA in samples. The proposed method is satisfied for routine screening of vitamin C in clinical applications with a correlation coefficient of more than 0.99 in the range of 2 mumol/L-40 mumol/L AA. The within-day precision was less than 8.9% and 10.55% for AA and DHAA, respectively. The recoveries of AA in plasma and dialysate were over 95% and 78%, respectively.

Topics: Ascorbic Acid; Chromatography, High Pressure Liquid; Dehydroascorbic Acid; Dialysis Solutions; Electrochemistry; Humans; Renal Dialysis; Uremia

Oxalic acid is one of the well-known uremic toxins that participates in the pathogenesis of uremic syndrome. Secondary hyperoxalemia is a common feature in patients with chronic renal failure, but oxalate removal is not adequately accomplished by renal replacement therapy. In our series of patients, the plasma level of oxalic acid was significantly elevated, while the plasma vitamin C was in the normal range or in the upper margin of the normal range. The peritoneal clearance of oxalic acid was significantly lower in comparison to the peritoneal clearance of urea. Peritoneal clearance and peritoneal transfer of oxalic acid and other examined parameters increased using dialysis solution containing 2.5% glucose in comparison to dialysis solution containing 1.5% glucose. The significant hyperoxalemia of our patients persisted despite the relatively high peritoneal transfer of oxalic acid during continuous ambulatory peritoneal dialysis. The clearance of oxalic acid related to the clearance of urea was 58.1% during hemodialysis, 74.2% during postdilution hemofiltration, and 69.0% during postdilution hemodiafiltration. The sieving coefficient of oxalic acid during postdilution hemofiltration was 74.0% of urea sieving coefficient. The most significant decrease of plasma oxalic acid was observed during postdilution hemodiafiltation (63.3%). These results suggest that currently, renal replacement therapy is not effective enough for a permanent reduction of plasma oxalic acid.

Topics: Adult; Ascorbic Acid; Female; Hemodiafiltration; Humans; Kidney Failure, Chronic; Male; Middle Aged; Oxalic Acid; Peritoneal Dialysis, Continuous Ambulatory; Renal Dialysis; Renal Replacement Therapy; Toxins, Biological; Uremia

Uremic patients undergoing hemodialysis often have increased oxidant stress and accumulation of uremic toxins. Hemodialysis, per se, often can exacerbate oxidant stress and may be inefficient at removing hydrophobic or protein bound toxins. We describe a new hemodialytic method that incorporates liposomes and antioxidants to remove hydrophobic/uremic toxins and minimize free radical mediated damage. In vitro experiments measured advanced oxidation protein products (AOPP), malonaldehyde, reactive carbonyls, and the removal of platelet activating factor (PAF) and bilirubin during extracorporeal circulation with or without liposomes. We observed a significant reduction of oxidation products as well as a significant removal of PAF and bilirubin compared to normal hemodialysis.

Topics: Animals; Antioxidants; Ascorbic Acid; Bilirubin; Blood Proteins; Cattle; Extracorporeal Circulation; Free Radical Scavengers; Humans; Liposomes; Malondialdehyde; Oxidation-Reduction; Oxidative Stress; Phosphatidylcholines; Phospholipids; Platelet Activating Factor; Renal Dialysis; Serum Albumin, Bovine; Toxins, Biological; Uremia; Vitamin E

Vitamin C is currently considered a potent water-soluble antioxidant and it appeared reasonable to study the metabolic changes of vitamin C in uraemia and during haemodialysis.. We measured the levels of ascorbic, dehydroascorbic and diketogulonic acids in sera of uraemic patients before and during haemodialysis, using the 2,4-dinitrophenylhydrazine method.. The results indicate that the levels of ascorbic and dehydroascorbic acids in uraemic sera are low in comparison with controls, but the levels of diketogulonic acid are higher than in healthy persons. The comparison of ratios between levels of these substances in uraemic sera and in normal sera indicate that the oxidation of ascorbic acid to dehydroascorbic in uraemia proceeds much slower than in controls. We propose that uraemic patients are characterized by pronounced deficiency of dehydroascorbic acid. A marked decrease of ascorbic and diketogulonic acid plasma levels, and a pronounced increase of dehydroascorbic acid levels during haemodialysis was observed. Ratios between plasma levels of ascorbic and dehydroascorbic acids following haemodialysis are the same as in healthy persons.. Uraemic patients are characterized by marked deficiency of dehydroascorbic acid and this deficiency can be partially corrected by haemodialysis.

Topics: Adolescent; Adult; Ascorbic Acid; Dehydroascorbic Acid; Female; Humans; Male; Middle Aged; Renal Dialysis; Uremia

Topics: Aged; Ascorbic Acid; Biopsy; Female; Humans; Kidney Glomerulus; Nephritis, Interstitial; Uremia

Recent studies have demonstrated a marked increase in the level of advanced glycation end products (AGEs) in the plasma, skin and amyloid fibrils of hemodialysis (HD) patients. The presence of AGEs in (beta2m) forming amyloid fibrils has been established in a previous immunochemical study relying on a monoclonal anti-AGE antibody. In the present study, Western blot analysis and immunohistochemistry reveal that the epitope recognized by this antibody is N epsilon-(carboxymethyl)lysine (CML) and that CML is one of the AGE structures present in amyloid fibrils. Thus, two AGE structures, CML and pentosidine, are now recognized in dialysis-related amyloidosis. AGE accumulation in uremia is not accounted for by elevated glucose levels. Since CML and pentosidine formation are closely linked to oxidative processes, we tested the hypothesis that a high oxidative stress enhanced AGE formation in HD patients. We focused on ascorbic acid (AA) because AA is easily oxidized under oxidative stress and its oxidized form (oxiAA) is a source of CML and pentosidine. In vitro incubation of beta2m with AA under atmospheric oxygen resulted in: (1) the rapid appearance of characteristic physicochemical properties of AGEs (brown color, fluorescence, polymerization tendency); (2) the transformation of beta2m into AGE-modified beta2m recognized by a specific monoclonal antibody; and (3) the accelerated formation of CML in beta2m and beta2m-peptide, recognized by mass spectrometry. A similar in vitro incubation of human serum albumin disclosed a parallel production of pentosidine measured by high-performance liquid chromatographic assay. In HD patients, the degree of AA oxidation, assessed as the ratio of oxiAA to total ascorbate, was more than twice as high as that of normal subjects (0.87 +/- 0.16 vs. 0.35 +/- 0.11, P < 0.0001), suggesting the presence of an increased oxidative stress. Interestingly, plasma level of oxiAA was correlated with the plasma levels of protein linked (P < 0.01, r2 = 0.25) and free (P < 0.05, r2 = 0.22) pentosidine. Altogether these results demonstrate that AGE, that is, CML and pentosidine, production is accelerated under oxidative stress, even in the absence of glucose. They suggest that, in uremia, CML and pentosidine production is determined both by an increased oxidative stress and the availability of precursors such as oxiAA. Finally, both CML and pentosidine contribute to the AGEs present in dialysis-related amyloid fibrils.

Topics: Amino Acid Sequence; Amyloid; Arginine; Ascorbic Acid; beta 2-Microglobulin; Glycation End Products, Advanced; Humans; Immunohistochemistry; In Vitro Techniques; Kidney Failure, Chronic; Lysine; Molecular Structure; Oxidative Stress; Renal Dialysis; Spectrometry, Fluorescence; Spectrometry, Mass, Fast Atom Bombardment; Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization; Uremia

Depletion of antioxidants and the presence of products of free radical damage in plasma suggest that oxidative stress is increased in uremia. We have developed an application of electron spin resonance spectroscopy, and used this method to show that a stable oxidizing component or components of plasma accumulate in uremia. No oxidizing activity was detectable in plasma from subjects with normal renal function. The oxidant was detected by its capacity to oxidize the spin trap 3,5-dibromo-4-nitrosobenzene sulphonate (DBNBS). The oxidant was dialyzable from plasma, had an upper molecular weight limit of about 3,000 Daltons and was stable over many months. Physiological plasma concentrations of vitamin C, a water soluble congener of vitamin E and reduced glutathione were unable to inhibit the oxidizing capacity of uremic plasma. Thus, uremia is associated with accumulation of an endogenous oxidizing activity at much higher concentrations than in subjects with normal renal function.

Topics: Adult; Antioxidants; Ascorbic Acid; Azides; Benzenesulfonates; Chromans; Creatinine; Electron Spin Resonance Spectroscopy; Endopeptidases; Female; Glutathione; Humans; Hydrolysis; Leukocyte Count; Male; Middle Aged; Neutrophils; Nitroso Compounds; Oxidants; Oxidation-Reduction; Renal Dialysis; Spin Labels; Uremia; Vitamin E

Topics: Acids; Aluminum; Animals; Ascorbic Acid; Citrates; Citric Acid; Diet; Intestinal Absorption; Lactates; Lactic Acid; Rats; Uremia

A new metabolite of ascorbic acid has been isolated by a multi-step chromatographic procedure both from normal human urine and uremic plasma. Nuclear Magnetic Resonance studies, and chemical and enzymic analyses indicated that the compound is a conjugated structure consisting of equimolar ascorbic and beta-D-glucuronic acids. We determined the pKa value of the ascorbic acid moiety of the compound on the basis of variations of ultraviolet absorbances as a function of pH. Results showed that glucuronic acid is coupled to the 2-position of ascorbic acid.

Topics: Ascorbic Acid; Glucuronates; Humans; Hydrogen-Ion Concentration; Magnetic Resonance Spectroscopy; Spectrophotometry, Ultraviolet; Uremia

Plasma levels of ascorbic acid (AA) and dehydroascorbic acid (DHA) were estimated in 27 patients of end stage renal failure (ESRF) on standard conservative therapy (group A) and 9 patients of ESRF on maintenance haemodialysis (MHD; group B). Fourteen healthy subjects matched for age and sex served as control (group C). The dietary intake of vitamin C was significantly decreased in group A than in group B compared to control. Similarly, plasma AA was significantly lowered to 0.801 +/- 0.283 mg per cent in group A compared to 1.421 +/- 0.47 mg per cent in control. While it was just lowered to 1.058 +/- 0.272 mg per cent in group B. Although plasma level of DHA was raised to 0.243 +/- 0.486 mg per cent and 0.166 +/- 0.54 mg per cent in groups A and B respectively, the increase was not statistically significant. In our present study, the DHA/AA ratio was found to be inversely proportional to the plasma AA. Further, this ratio has been claimed to be a better indicator of overall reducing atmosphere (i.e., profile of vitamin C) of the body.

Topics: Ascorbic Acid; Ascorbic Acid Deficiency; Dehydroascorbic Acid; Eating; Female; Humans; Kidney Failure, Chronic; Male; Middle Aged; Renal Dialysis; Uremia

The middle-molecular-weight uremic toxins which accumulate in uremic plasma seem to be associated with various uremic disorders such as uremic neuropathy and defects in the sodium pump. By a multi-step chromatographic method, two fractions of these toxins were isolated and studied because one inhibits microtubule formation in vitro (fraction 2-5), and the other impairs the sodium pump in living erythrocytes (fraction 2-3). An additional chromatographic method allows the separation of these fractions and isolation of two components: fractions 2-3-V and 2-5-III. Analyses by UV and 1H NMR spectrometry identified these compounds as two different ascorbic acid derivatives. 2-3-V is not yet totally identified and 2-5-III corresponds to ascorbic acid 2-sulfate. These two metabolites exert no toxic effects but they have the same chromatographic behavior as uremic toxins.

Topics: Ascorbic Acid; Chromatography, Ion Exchange; Humans; Magnetic Resonance Spectroscopy; Spectrophotometry, Ultraviolet; Toxins, Biological; Uremia

To examine the possible effects of hyperoxalaemia on anaerobic metabolism and erythrocyte pyruvate kinase activity, we induced a rise in plasma oxalate in 11 dialysis patients by the oral administration of ascorbic acid, 500 mg day-1 for 3 weeks. Blood samples were taken from the same antecubital vein before and after the supplementation period, without venous stasis, after an overnight fast. This protocol allowed patients to be used as their own controls. Five healthy subjects underwent an identical protocol to exclude any effect of ascorbate per se. Mean (SEM) plasma oxalate (mumol l-1) rose from 30.3 (3.5) to 48.4 (6.1) in patients and from 1.4 (0.2) to 6.8 (0.9) in healthy subjects. Whole blood ascorbate (mg l-1) rose from 7.0 (0.7) to 26.6 (2.5) in patients and from 9.3 (1.2) to 17.8 (1.8) in healthy subjects (reference range 7.5-20.0 mg l-1). No changes were observed in either group in plasma creatinine, bicarbonate, haemoglobin, or erythrocyte 2,3,diphosphoglycerate (2,3 DPG) after the 3 week supplementation period. Before supplementation lactate generation (area under curve, mmol min l-1) in the 5 min following a 60 s period of standardized ischaemic forearm exercise was significantly (P = 0.026) greater in patients [69.1 (4.7)] than in healthy subjects [46.9 (6.7)]; no significant change in lactate generation occurred in either group after ascorbate-induced hyperoxalaemia. We conclude that changes in plasma oxalate of the order of 20 mumol l-1 have no significant effect on lactate generation or 2,3,DPG levels in uraemic subjects.

Topics: 2,3-Diphosphoglycerate; Adult; Ascorbic Acid; Diphosphoglyceric Acids; Erythrocytes; Forearm; Humans; Ischemia; Lactates; Lactic Acid; Male; Middle Aged; Oxalates; Oxalic Acid; Peritoneal Dialysis, Continuous Ambulatory; Physical Exertion; Renal Dialysis; Uremia

The erythrocytes from 19 chronic hemodialysis patients were examined for Heinz bodies and their sensitivity to oxidant stress. Heinz bodies were found in 63% of patients and an elevated level of oxidized hemoglobin in 36%. When exposed to acetylphenhydrazine oxidant stress, 84% had a normal response and 95% had stable reduced glutathione levels. Ascorbic-acid-induced oxidant stress was tolerated by 84%. The activities of enzymes associated with the hexose monophosphate shunt were examined and found to be intact. This study demonstrates an increased number of Heinz bodies in hemodialysis patients. However, this is not due to an increased sensitivity to oxidant stress. Other mechanisms must be sought to explain the presence of Heinz bodies in these patients.

Topics: Adult; Aged; Ascorbic Acid; Erythrocytes; Female; Heinz Bodies; Hemoglobins; Humans; Male; Microscopy, Phase-Contrast; Middle Aged; Oxidation-Reduction; Pentose Phosphate Pathway; Renal Dialysis; Spectrophotometry; Uremia

Oxalate nephrotoxicosis was determined, by renal biopsy, to be the cause of azotemia in a goat. The origin of the oxalate was determined to be a high concentration of ascorbic acid that had been administered parenterally to the goat. Ascorbic acid has been documented as a cause of oxalate nephrotoxicosis in human beings.

Topics: Animals; Ascorbic Acid; Biopsy; Female; Goat Diseases; Goats; Kidney; Mastitis; Oxalates; Ultrasonography; Uremia

Topics: Adult; Ascorbic Acid; Endothelium, Vascular; Humans; Middle Aged; Oxalates; Oxalic Acid; Peritoneal Dialysis, Continuous Ambulatory; Renal Dialysis; Uremia; von Willebrand Factor

Among uremic toxins in the middle molecular mass range, 1H, 13C-nuclear magnetic resonance, ultraviolet spectrometry, and chromatographic analyses allow identification of the main component of the so-called "2-5-3 fraction" as ascorbic acid 2-sulfate, a conjugated metabolite of ascorbic acid. We previously (Clin Nephrol 1986;25:212-8) showed an inhibitory effect of the 2-5-3 fraction on microtubule formation. Therefore, we tested the action of ascorbic acid 2-sulfate and its synthetized enantiomers on tubulin polymerization. Because these molecules did not exert any inhibitory effect, we hypothesize that the 2-5-3 fraction is a mixture of compounds in which only a very low quantity of the inhibitory factor is present.

Topics: Ascorbic Acid; Chromatography, High Pressure Liquid; Energy Transfer; Humans; Magnetic Resonance Spectroscopy; Microtubules; Molecular Structure; Spectrophotometry, Ultraviolet; Tubulin; Uremia

An enzymatic assay for the determination of oxalate in plasma was developed which is specific, simple, rapid and requires no specialised equipment; interference from vitamin C was removed by incubation of acidified plasma ultrafiltrate with ascorbate oxidase prior to oxalate estimation. Recoveries were 93 +/- 11% and the inter-batch coefficient of variation for 31 determinations at an oxalate level of 24 mumol/l was 10%. The assay is linear up to 300 mumol/l with a detection limit of 2 mumol/l. The reference range, based on results from 25 healthy volunteers, was defined as less than 2-5 mumol/l which is similar to levels established for the in vivo isotope dilution technique. The assay has an added advantage over the latter method, which requires a urine collection, in that it can be applied to plasma from anuric patients. A linear correlation (r = 0.68, p less than 0.001) was found between plasma oxalate and serum creatinine in individuals with varying degrees of renal failure.

Topics: Ascorbic Acid; Creatinine; False Positive Reactions; Humans; Hydrogen-Ion Concentration; Methods; Oxalates; Oxidoreductases; Ultrafiltration; Uremia

Secondary oxalosis in chronic hemodialyzed patients is caused by impaired renal excretion and inadequate removal of oxalic acid during hemodialysis. Ascorbic acid is a precursor of oxalic acid. We report a parathyroidectomized patient with chronic renal failure, on hemodialysis, who received over a period of several months a total dose of 91.0 g ascorbic acid i.v. The plasma oxalic acid level in this patient was 14-fold higher than in healthy persons. Increased oxalic acid synthesis from its precursor ascorbic acid may be responsible for hyperoxalemia, high content of oxalic acid in myocardium, aorta and lung, and calcium oxalate deposition in soft tissues. Application of high doses of ascorbic acid should be avoided in hemodialysed patients with chronic renal failure.

Topics: Adult; Aorta; Ascorbic Acid; Calcinosis; Calcium Oxalate; Cardiomyopathies; Humans; Hyperparathyroidism, Secondary; Lung; Male; Nephritis, Interstitial; Parathyroid Glands; Renal Dialysis; Uremia

Plasma vitamin E levels and the ascorbate cyanide test were assessed in 15 chronic hemodialysis (HD) patients (group A) exposed to persistently elevated chloramine levels in the dialysis water. The vitamin E levels in these patients, who had evidence of oxidant induced hemolytic anemia, were compared to 15 chronic HD patients exposed to low chloramine levels (group B) and 17 controls (group C). Vitamin E levels were found to be significantly lower in group A than in either groups B or C (p less than 0.001). Within group A, levels were lower in those patients who had a positive ascorbate cyanide test (p less than 0.05). Upon removal of chloramines from the dialysis water, vitamin E levels in group A were no longer significantly different from those found in groups B or C.

Topics: Ascorbic Acid; Chloramines; Cyanides; Erythrocytes; Female; Hemoglobin A; Humans; Male; Renal Dialysis; Uremia; Vitamin E; Water

Blood concentration of water-soluble vitamins were measured in patients with mild chronic renal insufficiency, uremic undialyzed and dialyzed patients and control subjects. The whole blood concentration of B1 was significantly lower in dialyzed patients. Plasma levels of B2 were elevated in uremic and dialyzed patients and plasma B6 was significantly increased in dialyzed patients. Serum levels of B12 and folic acid were elevated in uremic and dialyzed patients. The results of this study differ from those reported from Europe and the U.S.A. These geographical differences may arise primarily from differences in staple food, vegetable intake, and traditional methods of food preparation.

Topics: Adult; Aged; Ascorbic Acid; Female; Folic Acid; Humans; Kidney Failure, Chronic; Male; Middle Aged; Pyridoxine; Renal Dialysis; Riboflavin; Thiamine; Uremia; Vitamin B 12; Vitamins

The mean plasma oxalic acid level is increased in renal failure. The mean plasma oxalic acid level was 74.8 +/- 18.5 mumol/l in 15 patients with chronic renal failure and 129.9 +/- 47.7 mumol/l in 31 patients on chronic haemodialysis which are several times higher than the normal range (16.8 +/- 6.0 mumol/l). During haemodialysis oxalic acid showed a behaviour similar to that of creatinine. The increased plasma oxalic acid levels are due to the accumulation of oxalic acid in renal insufficiency and additional metabolic factors increasing endogenous synthesis of oxalic acid. The administration of pyridoxine caused a decrease of the mean plasma oxalic acid level by 46% (32.0 to 56.1%) in 6 out of 8 chronic haemodialysis patients. This occurred most probably by correcting a vitamin B6 deficiency. Investigations of the intraerythrocyte glutamic oxalacetic transaminases showed, that the action of pyridoxine therapy on the endogenous oxalic acid synthesis can be explained by an increase of available pyridoxal-5-phosphate, the active metabolite of vitamin B6. The administration of vitamin B1, however, caused no statistically significant decrease of the plasma oxalic acid levels. Other influences on plasma oxalic acid synthesis result from the diminished excretion of the precursors of oxalic acid glycolic acid and ascorbic acid. The conversion of glycolic acid to glycine is probably increased in uraemia. The administration of 1 g ascorbic acid after each haemodialysis caused a striking increase of the plasma oxalic acid levels up to 240% of the initial value within 2 weeks, as a consequence of an increased metabolism of accumulated ascorbic acid. Increased plasma oxalic acid levels seem to be an important factor for calcium oxalate deposits in uraemia.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Ascorbic Acid; Aspartate Aminotransferases; Combined Modality Therapy; Erythrocytes; Glycolates; Humans; Kidney Failure, Chronic; Kidney Function Tests; Oxalates; Oxalic Acid; Pyridoxine; Renal Dialysis; Thiamine; Uremia

The baseline concentrations of MDA in the RBC membranes and the MDA production in the erythrocytes following stimulation with ascorbate and cyanide are compared in a group of uraemic patients on chronic haemodialysis and in one treated with CAPD. Lower baseline concentrations and smaller production of MDA following in vitro stimulation, point to a better function of the pentose-phosphate shunt in CAPD patients than in haemodialysis.

Topics: Adolescent; Adult; Ascorbic Acid; Child; Cyanides; Erythrocytes; Female; Humans; In Vitro Techniques; Male; Malonates; Malondialdehyde; Middle Aged; Pentose Phosphate Pathway; Peritoneal Dialysis, Continuous Ambulatory; Renal Dialysis; Uremia

Red blood cells (RBC) of uremic or control subjects have been exposed to an oxidative stress by ascorbate and cyanide. The spectrophotometric determination of the sulfhemoglobin production has been used as a reliable method for the measurement of the hexose monophosphate shunt. The sulfhemoglobin production by RBC was significantly higher in uremic than in control subjects. Uremic plasma increased this production in uremic as well as in control RBC while control plasma was ineffective under the same conditions. In vitro the guanidinopropionic acid had the same toxic effect on normal RBC. These results suggest that the abnormal sulfhemoglobin production by uremic RBC might be due to an increased plasma concentration of guanidinopropionic acid in uremia.

Topics: Ascorbic Acid; Cyanides; Erythrocytes; Female; Guanidines; Humans; Kinetics; Male; Propionates; Uremia

A red cell metabolic abnormality, which diminishes the maximum activity of the pentose phosphate shunt, occurs in some uremic patients, even those adequately dialyzed with fluids prepared from distilled or charcoal-filtered water. Within individual patients the severity of this abnormality does not change even after 9 mo of consecutive hemodialyses. However, between patients it does correlate inversely with hematocrit. When erythrocytes from patients with the abnormality are stressed with oxidant compounds, such as ascorbate, erythrocyte glucose consumption and lactate formation are abnormally increased, while lactate/pyruvate ratios abnormally diminish. Concomitantly, red cell glycolytic intermediates, including fructose-1,6-diphosphate, glyceraldehyde-3-phosphate, 3-phosphoglycerate, phosphoenol pyruvate, and pyruvate, markedly accumulate. Surprisingly, no increase of 2-phosphoglycerate occurs, which suggests that inefficient phosphoglyceromutase activity underlies this perturbation of erythrocyte metabolism and its associated hemolytic process.

Topics: Ascorbic Acid; Blood Glucose; Cyanides; Diphosphoglyceric Acids; Erythrocytes; Heinz Bodies; Hematocrit; Humans; Hydrogen-Ion Concentration; Lactates; Methemoglobin; Methylene Blue; NADH, NADPH Oxidoreductases; Phosphoglucomutase; Pyruvates; Renal Dialysis; Sulfhemoglobin; Uremia

The effect of uremia on ethanol metabolism was investigated. Uremia was induced in male Spraque-Dawley rats by removal of approximately 85 per cent of the renal mass. Control animals had a sham operation. The mean activity of alcohol dehydrogenase was markedly increased in the uremic rats to 2.12 +/- 0.13 (S.E.M.) mumoles per milligram of protein per hours as compared with a control value of 1.39 +/- 0.13 mumoles per milligram of protein per hour (p less than 0.001). There were no changes in the activity of the microsomal ethanol oxidizing system, in catalase activity present in the microsomes, or in the rates of ethanol disappearance from the blood. Uremia resulted in decreases in microsomal cytochrome -450, but no changes in cytochrome b5, NADPH-cytochrome c reductase, or in the activities of aniline hydroxylase and aminopyrine demethylase. The increase in alcohol dehydrogenase activity could not be reproduced by incubation of liver from a normal rat with uremic rat plasma, uremic human serum, or urea. Also, the increase in the enzyme activity was not associated with changes in leucocyte ascorbic acid levels. The cause and physiologic significance of the increase in alcohol dehydrogenase activity in uremia remain to be elucidated.

Topics: Alcohol Oxidoreductases; Animals; Ascorbic Acid; Cytochrome Reductases; Ethanol; Liver; Male; Metabolic Clearance Rate; Microsomes, Liver; Oxidation-Reduction; Rats; Uremia

Topics: Anemia, Hemolytic; Ascorbic Acid; Cell Survival; Charcoal; Chloramines; Chromium Radioisotopes; Erythrocytes; Filtration; Hemolysis; Hexosephosphates; Humans; Methemoglobin; Osmosis; Renal Dialysis; Uremia; Water Pollution, Chemical; Water Supply; Water-Electrolyte Balance

Topics: Ascorbic Acid; Blood; Carbon Radioisotopes; Enzyme Activation; Erythrocytes; Flavin-Adenine Dinucleotide; Flavins; Glucosephosphate Dehydrogenase Deficiency; Glutathione Reductase; Hemolysis; Humans; Liver Cirrhosis; Methylene Blue; Riboflavin; Umbilical Cord; Uremia

Topics: Ascorbic Acid; Autoanalysis; Bilirubin; Blood Glucose; Blood Urea Nitrogen; Evaluation Studies as Topic; Glucose Oxidase; Indicators and Reagents; Methods; Peroxidases; Quaternary Ammonium Compounds; Sulfonic Acids; Thiazoles; Uremia

Topics: Ascorbic Acid; Ascorbic Acid Deficiency; Chronic Disease; Diet Therapy; Female; Humans; Male; Renal Dialysis; Uremia

The platelet ascorbic acid concentration was measured in 26 normal subjects and found to be 20 times as high as in plasma. This is in agreement with previous reports in the literature. The platelets of patients with uraemia, leukaemia, and megaloblastic anaemia had a lower than normal platelet ascorbic acid content. In uraemia and megaloblastic anaemia the plasma ascorbic acid concentration was normal suggesting that a platelet defect may be responsible for the low platelet ascorbic acid content. In leukaemia the low platelet ascorbic acid content is probably secondary to a low plasma level.

Topics: Acute Disease; Adolescent; Adult; Anemia, Macrocytic; Ascorbic Acid; Blood Platelet Disorders; Blood Platelets; Female; Humans; Leukemia; Leukemia, Lymphoid; Leukemia, Myeloid; Male; Plasma; Uremia

Topics: Anemia, Hemolytic; Ascorbic Acid; Carbon Radioisotopes; Cell Survival; Chromium Radioisotopes; Erythrocytes; Glucose; Glucosephosphate Dehydrogenase Deficiency; Heinz Bodies; Hemolysis; Hexosephosphates; Humans; Metabolism, Inborn Errors; Primaquine; Renal Dialysis; Sulfonamides; Uremia; Water

Topics: Anemia, Hemolytic; Antimalarials; Ascorbic Acid; Carbon Isotopes; Cell Survival; Chromium Isotopes; Erythrocytes; Glucose; Heinz Bodies; Hexosephosphates; Humans; Renal Dialysis; Sulfhemoglobin; Sulfonamides; Uremia

Topics: Animals; Ascorbic Acid; Blood Urea Nitrogen; Dogs; Drug Antagonism; Female; Kidney; Mannitol; Nitrogen; Protein Binding; Rats; Renal Dialysis; Stereoisomerism; Tetracycline; Tritium; Uremia

Topics: Adolescent; Adult; Ascorbic Acid; Biological Assay; Child; Drowning; Female; Humans; Hypothalamo-Hypophyseal System; Hypothalamus; Luteinizing Hormone; Male; Middle Aged; Neoplasms; Ovary; Pituitary Hormone-Releasing Hormones; Poisoning; Uremia; Vascular Diseases; Wounds and Injuries

Topics: Anemia; Ascorbic Acid; Cobalt; Humans; Injections, Intramuscular; Uremia; Urologic Diseases

Topics: Amyloid; Amyloidosis; Ascorbic Acid; Asthma; Cortisone; Nephrosis; Uremia; Vitamins