ascorbic-acid and Proteinuria

Sickle cell disease (SCD), one of the commonest severe monogenic disorders, is caused by the inheritance of two abnormal haemoglobin (beta-globin) genes. SCD can cause severe pain, significant end-organ damage, pulmonary complications, and premature death. Kidney disease is a frequent and potentially severe complication in people with SCD. Chronic kidney disease (CKD) is defined as abnormalities of kidney structure or function present for more than three months. Sickle cell nephropathy refers to the spectrum of kidney complications in SCD. Glomerular damage is a cause of microalbuminuria and can develop at an early age in children with SCD, with increased prevalence in adulthood. In people with sickle cell nephropathy, outcomes are poor as a result of the progression to proteinuria and chronic kidney insufficiency. Up to 12% of people who develop sickle cell nephropathy will develop end-stage renal disease. This is an update of a review first published in 2017.. To assess the effectiveness of any intervention for preventing or reducing kidney complications or chronic kidney disease in people with sickle cell disease. Possible interventions include red blood cell transfusions, hydroxyurea, and angiotensin-converting enzyme inhibitors (ACEIs), either alone or in combination.. We searched for relevant trials in the Cochrane Cystic Fibrosis and Genetic Disorders Group Trials Register, CENTRAL, MEDLINE, Embase, seven other databases, and two other trials registers.. Randomised controlled trials (RCTs) comparing interventions to prevent or reduce kidney complications or CKD in people with SCD. We applied no restrictions related to outcomes examined, language, or publication status.. Two review authors independently assessed trial eligibility, extracted data, assessed the risk of bias, and assessed the certainty of the evidence (GRADE).. We are unsure if hydroxyurea improves glomerular filtration rate or reduces hyperfiltration in children aged nine to 18 months, but it may improve their ability to concentrate urine and may make little or no difference to the incidence of acute chest syndrome, painful crises, and hospitalisations. We are unsure if ACEI compared to placebo has any effect on preventing or reducing kidney complications in adults with normal blood pressure and microalbuminuria. We are unsure if ACEI compared to vitamin C has any effect on preventing or reducing kidney complications in children with normal blood pressure and microalbuminuria. No RCTs assessed red blood cell transfusions or any combined interventions to prevent or reduce kidney complications. Due to lack of evidence, we cannot comment on the management of children aged over 18 months or adults with any known genotype of SCD. We have identified a lack of adequately designed and powered studies, although we found four ongoing trials since the last version of this review. Only one ongoing trial addresses renal function as a primary outcome in the short term, but such interventions have long-term effects. Trials of hydroxyurea, ACEIs or red blood cell transfusion in older children and adults are urgently needed to determine any effect on prevention or reduction of kidney complications in people with SCD.

Topics: Acute Chest Syndrome; Adolescent; Adult; Anemia, Sickle Cell; Angiotensin-Converting Enzyme Inhibitors; Antisickling Agents; Ascorbic Acid; Captopril; Child; Creatinine; Humans; Hydroxyurea; Kidney Failure, Chronic; Lisinopril; Proteinuria

Topics: Amyloidosis; Ascorbic Acid; Biopsy; Humans; Hypoproteinemia; Kidney; Kidney Diseases; Liver Extracts; Microscopy, Electron; Polyuria; Proteinuria

Eighteen children with steroid-sensitive nephrotic syndrome (SSNS) were studied. The control group comprised 20 healthy children. The following indirect parameters of reactive oxygen species activity were determined in nephrotic patients during four stages of the disease (full relapse before prednisone administration, disappearance of proteinuria, prednisone cessation, unmaintained remission): plasma malondialdehyde (MDA) levels, copper/zinc superoxide dismutase (CuZn SOD) activity and glutathione peroxidase (GPX) activity in erythrocytes, reduced glutathione (GSH) and vitamin C levels in whole blood, and vitamin E level in serum. Increased MDA levels, reduced vitamin C levels, and enhanced CuZn SOD activity were found in relapse. GSH concentration was high during all four stages. Vitamin E level was also increased, parallel to the pattern of serum lipids. GPX activity remained low during the proteinuria stage and in remission. We conclude that the majority of abnormal findings can be attributed to the hyperlipidemia of NS. Low GPX activity may be a factor limiting the antioxidant capacity in NS. The present study is inconclusive regarding the role of free radicals in the proteinuria of NS.

Topics: Adolescent; Anti-Inflammatory Agents; Antioxidants; Ascorbic Acid; Child; Child, Preschool; Cholesterol, HDL; Cholesterol, LDL; Glutathione; Glutathione Peroxidase; Humans; Nephrotic Syndrome; Prednisone; Proteinuria; Reactive Oxygen Species; Superoxide Dismutase; Triglycerides

Vitamin C may reduce inflammation and is inversely associated with mortality in the general population. We investigated the association of plasma vitamin C with all-cause mortality in renal transplant recipients (RTR); and whether this association would be mediated by inflammatory biomarkers. Vitamin C, high sensitive C-reactive protein (hs-CRP), soluble intercellular cell adhesion molecule 1 (sICAM-1), and soluble vascular cell adhesion molecule 1 (sVCAM-1) were measured in a cohort of 598 RTR. Cox regression analyses were used to analyze the association between vitamin C depletion (≤28 µmol/L; 22% of RTR) and mortality. Mediation analyses were performed according to Preacher and Hayes's procedure. At a median follow-up of 7.0 (6.2-7.5) years, 131 (21%) patients died. Vitamin C depletion was univariately associated with almost two-fold higher risk of mortality (Hazard ratio (HR) 1.95; 95% confidence interval (95%CI) 1.35-2.81,

Topics: Adult; Ascorbic Acid; Ascorbic Acid Deficiency; Biomarkers; Body Composition; Body Mass Index; C-Reactive Protein; Creatinine; Dietary Supplements; Endpoint Determination; Female; Follow-Up Studies; Humans; Inflammation; Intercellular Adhesion Molecule-1; Kidney; Kidney Diseases; Kidney Transplantation; Male; Middle Aged; Mortality; Proportional Hazards Models; Prospective Studies; Proteinuria; Vascular Cell Adhesion Molecule-1

The present study investigated the possible involvement of nitric oxide/soluble guanylyl cyclase (NO/sGC) pathway in ascorbic acid (AA)-mediated protection against acute kidney injury (AKI) in rats. The rats were subjected to bilateral renal ischemia by occluding renal pedicles for 40 min followed by reperfusion for 24 h. The AKI was assessed in terms of measuring creatinine clearance (CrCl), blood urea nitrogen (BUN), plasma uric acid, potassium level, fractional excretion of sodium (FeNa), and microproteinuria. The NO level and oxidative stress in renal tissues were assessed by measuring myeloperoxidase activity, thiobarbituric acid reactive substances, superoxide anion generation, and reduced glutathione level. AA (50 and 100 mg/kg, p.o.) was administered for 3 days before subjecting rats to AKI. In separate groups, the nitric oxide synthase inhibitor, L-NAME (20 mg/kg, i.p.) and sGC inhibitor, methylene blue (50 mg/kg, i.p.) was administered prior to AA treatment in rats. The significant decrease in CrCl and increase in BUN, plasma uric acid, potassium, FeNa, microproteinuria, and oxidative stress in renal tissues demonstrated ischemia-reperfusion-induced AKI in rats. The AA treatment ameliorated ischemia-reperfusion-induced AKI along with the increase in renal NO level. The pretreatment with L-NAME and methylene blue abolished protective effect of AA. It is concluded that AA protects against ischemia-reperfusion-induced AKI. Moreover, the NO/sGC pathway finds its definite involvement in AA-mediated reno-protective effect.

Topics: Acute Kidney Injury; Animals; Antioxidants; Ascorbic Acid; Blood Urea Nitrogen; Creatinine; Drug Evaluation, Preclinical; Guanylate Cyclase; Kidney; Male; Nitric Oxide; Oxidative Stress; Proteinuria; Rats, Wistar; Receptors, Cytoplasmic and Nuclear; Signal Transduction; Soluble Guanylyl Cyclase; Uric Acid

In fawn-hooded hypertensive (FHH) rats, a model of hypertension, impaired preglomerular resistance, hyperfiltration, and progressive renal injury, we recently observed that supporting perinatal nitric oxide (NO) availability with the NO donor molsidomine persistently reduced blood pressure (BP) and ameliorated renal injury in male and female offspring. However, beneficial effects of perinatal molsidomine treatment were more pronounced in female than in male FHH rats.. To evaluate whether such protective effects could also be achieved with micronutrients, and whether the gender-dependent differences could be confirmed, we tested perinatal exposure to the micronutrients L-arginine, taurine, vitamin C, and vitamin E (ATCE) in FHH rats. Perinatal micronutrients increased urinary NO metabolite, sodium and potassium excretion only at 4 weeks of age, i.e., at the end of treatment.. From 12 weeks onwards, control males had a significantly higher systolic BP (SBP) than females (P < 0.01); however after perinatal micronutrients, this difference was no longer present, indicating a pronounced antihypertensive effect of perinatal micronutrients in males (interaction P < 0.001). Development of proteinuria was attenuated by perinatal micronutrients in males and females. However, only females showed reduced glomerular filtration rate, filtration fraction, and glomerulosclerosis (GS) after perinatal micronutrients.. In sum, perinatal micronutrients that enhance NO availability ameliorated development of hypertension and proteinuria in FHH rats. Antihypertensive effects were more pronounced in male FHH offspring, whereas renal protective effects were more pronounced in female FHH offspring. Mechanisms underlying gender-specific consequences of perinatal micronutrients require further study.

Topics: Animals; Arginine; Ascorbic Acid; Blood Pressure; Dietary Supplements; Female; Hypertension; Kidney Diseases; Male; Micronutrients; Molsidomine; Nitric Acid; Nitric Oxide Donors; Potassium; Proteinuria; Rats; Rats, Inbred Strains; Sex Factors; Sodium; Taurine; Vitamin E

Exercise-induced proteinuria is a common consequence of physical activity, although its mechanism is not clear. Oxidant stress has been proposed as one of different factors involved in postexercise proteinuria in rats. In this study we investigated whether reactive oxygen radicals generated during exercise play a role in exercise-induced proteinuria in sedentary and trained men.. The validity of oxidant stress following stepwise maximal exercise on proteinuria was investigated in sedentary and trained subjects before and after antioxidant vitamin treatment (A, C, and E) for 2 months. While protein carbonyl content in serum and thiobarbituric acid reactive substances (TBARS) in erythrocytes and urine were used as oxidant stress markers, total protein, albumin, beta(2)-microglobulin in urine were assayed for proteinuria in five consecutive specimens after exercise. Urines were collected before exercise, then 30 min, 2, 8 and 24 h postexercise.. Increased urinary protein levels and mixed type proteinuria were determined after 30 min of exercise in sedentary and trained subjects. Proteinuria was normalized at 2 and 8 h specimens. However, glomerular type proteinuria was identified at 24 h specimen in both groups. Oxidant stress markers were significantly elevated in sedentary and trained subjects. Antioxidant treatment prevented the increase in oxidant stress markers, urinary protein levels and the occurrence of glomerular type proteinuria after exhaustive exercise at 24 h in both groups.. These findings suggest that the exercise-induced oxidant stress may contribute to exercise-induced proteinuria in sedentary and trained men.

Topics: Adult; Antioxidants; Ascorbic Acid; Exercise; Humans; Life Style; Male; Oxidative Stress; Proteinuria; Reactive Oxygen Species; Rest; Time Factors; Vitamin A; Vitamin E

The goal of this study was to test the hypothesis that increases in oxidative stress in Dahl S rats on a high-salt diet help to stimulate renal nuclear factor-kappaB (NF-kappaB), renal proinflammatory cytokines, and chemokines, thus contributing to hypertension, renal damage, and dysfunction. We specifically studied whether antioxidant treatment of Dahl S rats on high Na intake would decrease renal inflammation and thus attenuate the hypertensive and adverse renal responses. Sixty-four 7- to 8-wk-old Dahl S or R/Rapp strain rats were maintained for 5 wk on high Na (8%) or high Na + vitamins C (1 g/l in drinking water) and E (5,000 IU/kg in food). Arterial and venous catheters were implanted at day 21. By day 35 in the high-Na S rats, antioxidant treatment significantly increased the renal reduced-to-oxidized glutathione ratio and decreased renal cortical H(2)O(2) and O(2)(*-) release and renal NF-kappaB. Antioxidant treatment with vitamins C and E in high-Na S rats also decreased renal monocytes/macrophages in the glomeruli, cortex, and medulla, decreased tumor necrosis factor-alpha by 39%, and decreased monocyte chemoattractant protein-1 by 38%. Vitamin-treated, high-Na S rats also experienced decreases in arterial pressure, urinary protein excretion, renal tubulointerstitial damage, and glomerular necrosis and increases in glomerular filtration rate and renal plasma flow. In conclusion, antioxidant treatment of high-Na Dahl S rats decreased renal inflammatory cytokines and chemokines, renal immune cells, NF-kappaB, and arterial pressure and improved renal function and damage.

Topics: Animals; Anti-Inflammatory Agents; Antihypertensive Agents; Antioxidants; Ascorbic Acid; Blood Pressure; Chemokine CCL2; Disease Models, Animal; Glomerular Filtration Rate; Glutathione; Heart Rate; Hydrogen Peroxide; Hypertension; Inflammation; Interleukin-6; Kidney; Macrophages; Monocytes; NF-kappa B; Oxidative Stress; Proteinuria; Rats; Rats, Inbred Dahl; Renal Circulation; Sodium Chloride, Dietary; Superoxides; Time Factors; Tumor Necrosis Factor-alpha; Vitamin E

The goal of this study was to test the hypothesis that oxidative stress in Dahl salt-sensitive (SS) rats on a high-sodium intake contributes to the progression of renal damage, the decreases in renal hemodynamics, and the development of hypertension. We specifically studied whether antioxidant therapy, using vitamins C and E, could help prevent renal damage and glomerular filtration rate (GFR) and renal plasma flow reductions and attenuate the increases in arterial pressure. Thirty-three 7- to 8-week old Dahl SS/Rapp strain rats were placed on either a high-sodium (8%) or a low-sodium (0.3%) diet with or without vitamin E (111 IU/d) in the food and 98 mg/d vitamin C in the drinking water for 5 weeks. Rats were equipped with indwelling arterial and venous catheters at day 21. By day 35 in the rats with high-sodium diet, vitamin C and E treatment significantly decreased renal cortical and medullary O2*- release, mean arterial pressure, urinary protein excretion, glomerular necrosis, and renal tubulointerstitial damage. At this time, GFR significantly decreased in the high-sodium diet group (1.6+/-0.2 mL/min) when compared with either the high-sodium plus vitamins C and E (2.9+/-0.2 mL/min) or the low-sodium diet group (2.9+/-0.3 mL/min). In SS rats on high-sodium diet, renal plasma flow decreased 40%, and this reduced flow was restored by vitamin treatment. In Dahl salt-sensitive hypertension, increased oxidative stress plays an important role in the renal damage, decreases in renal hemodynamics, and increases in arterial pressure that occur. Antioxidant treatment with vitamins C and E improves renal dysfunction, lessens renal injury, and decreases arterial pressure in Dahl salt-sensitive hypertension.

Topics: Animals; Antioxidants; Ascorbic Acid; Blood Pressure; Heart Rate; Hemodynamics; Hypertension; Kidney; Kidney Cortex; Kidney Diseases; Kidney Medulla; Male; Proteinuria; Rats; Rats, Inbred Dahl; Renal Circulation; Sodium Chloride; Superoxides; Vitamin E

By breeding and feeding salt to spontaneously hypertensive rats (SHR) continuously over a long period (until 60 wk old), rats with systolic blood pressures (SBP) of over 270 mmHg were prepared. It was studied whether or not supplying large amounts of vitamin C (200 mg/rat/d) over this period might bring any beneficial effect to blood pressure. Moreover, physico-chemical studies were performed to measure the components and enzymes in the blood and urine at 53 and 60 wk-old, and biochemical studies on vitamin C were also carried out in this experiment. Male (14 rats: 7 wk-old, 100-105 g) and female (15 rats: 7 wk-old, 95-100 g) SHR were divided into three groups and bred continuously for 53 wk. The A group rats were given salt (2.5 g/100 g of diet), the B group rats were given salt and vitamin C (500 mg/100 mL of drinking water), and the C group rats were controls. The results showed almost the same tendencies between male and female rats. The body weights of the SHR in groups A and B were slightly lower than group C. The amount of food intake in groups A and B was almost the same as group C. The amount of water intake was, in the order from highest to lowest, group A, B and C. The SBP of group A rats exhibited the highest value among the three groups. The SBP of group B rats given vitamin C simultaneously with the salt resulted in a low blood pressure level close to that of the controls (group C). Furthermore, the DBP (diastolic blood pressure) also reflected the antihypertensive effect of vitamin C as well. The heartbeat of the rats was highest in group A, and was comparable to the value in the rats receiving vitamin C simultaneously with salt. For the tests on occult blood and protein in the urine, group A rats showed strong positive reactions, whereas the group B and C rats had decreased results for both tests. The organ weights of the liver, stomach, spleen, adrenal gland and kidneys per 100 g rat body weight were not different among the three groups. The values for the bilirubin content, and the enzyme activities of ALT and AST in the blood showed to be the highest in the male rats of group A. The values from the group B rats decreased near to the normal value like the control group. Vitamin C was found to decrease the blood pressure in SHR, and also to work effectively to protect liver and kidney functions even under the condition of very high blood pressure, as high as 250 mmHg.

Topics: Alanine Transaminase; Animals; Ascorbic Acid; Aspartate Aminotransferases; Body Weight; Drinking; Eating; Female; Hematuria; Hypertension; Male; Organ Size; Proteinuria; Rats; Rats, Inbred SHR; Sodium Chloride, Dietary

Glomerular endothelial dysfunction is believed to be responsible for the proteinuria and nephronal damage, namely tubulointerstitial fibrosis and glomerulosclerosis, observed in severe nephrosis such as focal segmental glomerulosclerosis. A dysfunctioning glomerular endothelium is likely to be induced by oxidative stress and oxidized LDL as well as altered immunocirculatory balance with a defective anti-inflammatory pathway. A defective release of vasodilator inconjunction with enhanced production of angiotensin II induces hemodynamic maladjustment by preferential constriction at the efferent arteriole. Such a hemodynamic maladjustment exerts two significant hemodynamic impacts. Close to the efferent constriction, it induces intraglomerular hypertension and glomerulosclerosis. Far from the efferent constriction, it reduces peritubular capillary flow, which eventually leads to tubulointerstitial fibrosis. Treatment with a vasodilator improves the hemodynamic maladjustment but does not completely suppress proteinuria. A successful suppression of proteinuria is accomplished by using Ganoderma lucidum and vitamins C and E. The beneficial effect of Ganoderma lucidum appears to be multifactorial, including the modulation of immunocirculatory balance, antilipid, vasodilator, antiplatelet and improved hemorheology. Together with vitamins C and E, this helps to neutralize oxidative stress and suppress the toxic effect to the glomerular endothelial function.

Topics: Adrenal Cortex Hormones; Angiotensin II; Ascorbic Acid; Calcium Channel Blockers; Dipyridamole; Drug Evaluation; Drug Resistance; Drug Therapy, Combination; Enalapril; Endothelial Cells; Glutathione; Humans; Kidney Function Tests; Kidney Glomerulus; Malondialdehyde; Nephrosis; Oxidative Stress; Phytotherapy; Plants, Medicinal; Platelet Aggregation Inhibitors; Proteinuria; Reishi; Renal Circulation; Treatment Outcome; Vasodilator Agents; Vitamin E

Aution Max AX-4280, an automated urine test-strip analyser, was evaluated in three centres. Method comparison, imprecision, carry-over, linearity, detection limit and drift studies were performed for glucose, protein, blood and leukocytes using Uriflet S 9UB strips. These strips enable measurement of pH, glucose, protein, blood, leukocytes, ketones, bilirubin, urobilinogen and nitrite. Specific gravity is determined by the refractive index method. Within-run and between-day imprecision, assessed using pooled urines and quality control materials, were good. No drift over 24 h or sample carry-over was observed. Method comparison with quantitative methods for glucose, protein and specific gravity yielded good correlations. Ascorbate negatively interfered with haemoglobin, glucose and nitrite measurements. Acetylsalicylic acid lowered pH, the effect being greatest when protein was absent. During the assessment period no malfunction or breakdown was reported. The Aution Max is easy to use and needs minimal maintenance.

Topics: Ascorbic Acid; Aspirin; Chemistry, Clinical; Glucose; Hematuria; Humans; Hydrogen-Ion Concentration; Leukocytes; Multicenter Studies as Topic; Proteinuria; Reproducibility of Results; Specimen Handling; Time Factors; Urinalysis

Vascular endothelial damage has been implicated in the pathophysiology of preeclampsia. Lipid peroxidation may be involved in the process and essential nutrients that can scavenge free radicals, such as vitamin E and C, operate in concert. Antioxidant vitamins E and C were estimated in 30 preeclamptic and 30 normotensive pregnant women. Significantly lowered levels of vitamins E and C were observed in preeclamptic women as compared to controls (P<0.001 and P<0.05 respectively). In patients with preeclampsia antioxidant nutrients may be utilized to a greater extent to counteract free radical-mediated cell disturbances, resulting in a reduction in serum antioxidant levels.

Topics: Adolescent; Adult; Antioxidants; Ascorbic Acid; Birth Weight; Blood Pressure; Delivery, Obstetric; Female; Gestational Age; Humans; Pre-Eclampsia; Pregnancy; Proteinuria; Vitamin E

The protective effect of vitamin E and C on sodium chromate (Cr) and thallium (Tl) induced nephrotoxicity was tested in 10- and 55-day-old rats. The concentrations of Cr and Tl were determined in renal cortex and medulla by atomic absorption spectrometry. Urinary volume and protein excretion as well as blood urea nitrogen (BUN) concentration were determined as parameters of nephrotoxicity. Cr and Tl induced nephrotoxicity was significantly more expressed in adult than in young rats. In Cr and Tl nephrotoxicity the protective effect of vitamin E was evident in both age groups. Vitamin E decreased Tl concentration in renal tissue. Therefore its protective effect is not to be attributed to its known antioxidant effect but to lower Tl concentration in renal tissue. Vitamin C was protective in Cr and Tl induced nephrotoxicity in adult rats without influence on metal concentrations in renal tissue. The dose necessary for protection against toxic Cr action in adult rats was not tolerated by young rats. The combined administration of both vitamins abolished the protective effect against Cr nephrotoxicity of the administration of each vitamin alone in adult rats. When vitamin E and C were administered in Tl treated adult and young rats the protective effect was the same as after the administration of each vitamin alone. Possible mechanisms are discussed.

Topics: Animals; Ascorbic Acid; Blood Urea Nitrogen; Chromates; Female; Kidney; Kidney Diseases; Male; Proteinuria; Rats; Rats, Wistar; Sodium Compounds; Spectrophotometry, Atomic; Thallium; Urination; Vitamin E

The nephrotoxicity of 4-amino-3-S-glutathionylphenol (PAP-GSH), a known metabolite of 4-amino-phenol (PAP), was determined in male Fischer 344 rats. Administration of a single dose of 40 or 60 mumol kg-1 caused a marked elevation in blood urea nitrogen and an increase in the urinary excretion of glucose, protein and gamma-glutamyltransferase (GGT). These changes were associated with histological alterations in the proximal tubule, where at the lower dose the lesion was restricted to the S3 region of the proximal tubule in the medullary rays, while at the higher dose the lesion extended to affect the S3 region in both the medullary rays and the outer stripe of the outer medulla. Studies with [35S]-PAP-GSH at 40 mumol kg-1 showed selective retention of radioactivity in the kidney, relative to other organs 24 h after dosing and that some radioactivity was covalently bound to renal proteins. Pretreatment of animals with probenecid, an inhibitor of renal organic anion transport, or aminooxyacetic acid, an inhibitor of cysteine conjugate beta-lyase, had little or no effect on the toxicity. In contrast, pretreatment of animals with acivicin, an inhibitor of gamma-glutamyltransferase, or co-administration of PAP-GSH with ascorbic acid almost completely protected against the nephrotoxicity. This protection was associated with a decreased concentration of radioactivity from [35S]-PAP-GSH in the kidneys and a decrease in the amount covalently bound to renal protein. Thus, the nephrotoxicity of PAP-GSH may be mediated by oxidation and further processing of the glutathione conjugate via gamma-glutamyltransferase.

Topics: Aminooxyacetic Acid; Animals; Ascorbic Acid; Blood Urea Nitrogen; gamma-Glutamyltransferase; Glutathione; Glycosuria; Ion Transport; Isoxazoles; Kidney; Lyases; Male; Oxidation-Reduction; Phenols; Probenecid; Proteinuria; Rats; Rats, Inbred F344; Sulfur Radioisotopes

Whether a reduction in urinary protein excretion in rats coadministered puromycin aminonucleoside and antioxidants was associated with a reduction in alterations to glomerular epithelial cell (podocyte) ultrastructure was examined. Daily urinary protein excretion was measured in rats that received a single i.v. injection of saline or puromycin aminonucleoside with or without coadministration of antioxidants. The coadministration of alpha-tocopherol/ascorbic acid, dimethyl thiourea, or superoxide dismutase to puromycin aminonucleoside-treated rats reduced proteinuria by approximately 90, 40, and 60%, respectively, over the 18-day period studied. For a second group of rats, daily urinary protein excretion was measured and kidneys were processed for light microscopy and transmission and scanning electron microscopy 4, 5, and 10 days after injection. Transmission electron microscopic morphometric analysis of glomeruli from puromycin aminonucleoside-treated rats coadministered antioxidants revealed significantly reduced foot process effacement on Days, 4, 5, and 10 compared with rats that received puromycin aminonucleoside alone. Thus, at Day 10, puromycin aminonucleoside-treated rats coadministered alpha-tocopherol/ascorbic acid, dimethyl thiourea, or superoxide dismutase contained 90, 74, and 88% (P < 0.01 in all cases) more glomerular epithelial cell filtration slits per unit length of glomerular basement membrane than rats treated with puromycin aminonucleoside alone. In contrast, by scanning electron microscopy, the antioxidants were found to provide no protection against the changes occurring in glomerular epithelial cell bodies and major processes. These results provide further evidence of a role for reactive oxygen species in puromycin aminonucleoside nephrosis and indicate that the antioxidants provide protection against the changes occurring in glomerular epithelial cell foot processes.

Topics: Animals; Antioxidants; Ascorbic Acid; Body Weight; Diuresis; Female; Kidney Glomerulus; Microscopy, Electron; Proteinuria; Puromycin Aminonucleoside; Rats; Rats, Sprague-Dawley; Superoxide Dismutase; Thiourea; Vitamin E

The influence of ascorbic acid (AA, 5 g/kg body weight) on chromate (Cr, 10 mg/kg) induced proteinuria, which is a sensitive parameter of its nephrotoxicity, was investigated in adult female Wistar rats. The concentrations of Cr and ascorbic acid (AA) were determined in renal tissue. Cr nephrotoxicity is related to its intracellular reduction from Cr(VI) to Cr(III). Proteinuria was completely prevented by enhancement of extracellular reduction of Cr(VI) to Cr(III) followed by rapid renal excretion when Cr and AA were given concomitantly. With an interval up to 1 h between Cr and AA, proteinuria was decreased probably by the radical scavenging function of AA. At an interval of 3 h AA enhanced Cr toxicity by increased intracellular Cr reduction. If the interval was increased to 5 h or if Cr was given 24 h after AA, no influence of AA could be detected. Our results confirm that AA is a very effective reductant of Cr which can influence Cr nephrotoxicity in very high concentrations. It depends on the interval between Cr and AA administration whether or not there is a beneficial effect of AA in Cr nephrotoxicity.

Topics: Animals; Ascorbic Acid; Chromates; Female; Kidney; Kidney Diseases; Proteinuria; Rats; Rats, Wistar

Nephrotoxicity of daunorubicin in rats and effect of tocopherol and ascorbic acid on lesions induced in kidneys by daunorubicin were examined. Daunorubicin induced nephrotic syndrome with proteinuria and hypoproteinemia. Histological changes in the glomeruli appeared as a dilatation of capillary loops and enlargement of the urinary space. The glomerular basement membrane showed minimal thickening. In tubuli protein casts were noticed. No beneficial influence of tocopherol and ascorbic acid on daunorubicin related nephrotoxicity was observed.

Topics: Animals; Ascorbic Acid; Daunorubicin; Hypoproteinemia; Kidney; Kidney Glomerulus; Male; Nephrotic Syndrome; Proteinuria; Rats; Rats, Wistar; Vitamin E

Reflectometric measurement of urine test-strips, using the Urotron RL9, was employed to quantify urinary glucose and protein. Although the test-strips (Combur-9-Test) are designed for qualitative use, the reflectance intensities determined by the Urotron RL9 are applicable to quantitative analysis. Reflectance quantitation and conventional colorimetric methods were closely correlated for glucose (r = 0.953) and protein (r = 0.906). Intra-assay coefficients of variation of reflectance value were less than 5%. The negative influence of ascorbic acid on glucose determination was defined quantitatively. A significant positive interference from hemoglobin on protein determination was also demonstrated, but effectively eliminated after compensating for urine color.

Topics: Ascorbic Acid; Bilirubin; Calibration; Colorimetry; Glycosuria; Hemoglobins; Humans; Photometry; Proteinuria; Reproducibility of Results

Topics: Adolescent; Adult; Aged; Amyloidosis; Arthritis, Juvenile; Arthritis, Rheumatoid; Ascorbic Acid; Child; Child, Preschool; Dimethyl Sulfoxide; Drug Evaluation; Glomerular Filtration Rate; Humans; Kidney; Middle Aged; Proteinuria; Scleroderma, Systemic; Sjogren's Syndrome; Ultrasonics

An attempt was made, by means of test strips for leucocytes, eruthrocytes, protein, ketone bodies, nitrate and ascorbic acid to distinguish urine samples with abnormal sediments. The urinary sediment was, at the same time, quantified with the Kova system. It was demonstrated that the teststrip system can separate out nearly all samples containing significant amounts of sediment. In addition, lysed erythrocytes and leucocytes are detected. It is, therefore, suggested to restrict microscopic examination to those samples which have been positive to at least one test strip. It is important that genital cleansing is undertaken before micturition.

Topics: Ascorbic Acid; Chemical Precipitation; Hematuria; Humans; Indicators and Reagents; Ketone Bodies; Leukocytes; Nitrites; Proteinuria; Reagent Strips; Urine

Topics: Acid-Base Equilibrium; Albuminuria; Ascorbic Acid; Bence Jones Protein; Bile Pigments; Bilirubin; Color; Drug Antagonism; Hematuria; Hemoglobinuria; Humans; Indicators and Reagents; Ketone Bodies; Paper; Peroxidases; Phenolphthaleins; Phenols; Povidone; Proteinuria