pyridoxine has been researched along with Oxaluria, Primary in 33 studies
4,5-bis(hydroxymethyl)-2-methylpyridin-3-ol: structure in first source
vitamin B6 : Any member of the group of pyridines that exhibit biological activity against vitamin B6 deficiency. Vitamin B6 deficiency is associated with microcytic anemia, electroencephalographic abnormalities, dermatitis with cheilosis (scaling on the lips and cracks at the corners of the mouth) and glossitis (swollen tongue), depression and confusion, and weakened immune function. Vitamin B6 consists of the vitamers pyridoxine, pyridoxal, and pyridoxamine and their respective 5'-phosphate esters (and includes their corresponding ionized and salt forms).
Excerpt | Relevance | Reference |
---|---|---|
"Plasma pyridoxine metabolites in plasma and 4-pyridoxic acid excretions in urine were measured in normal subjects, in 7 patients with type-1 hyperoxaluria and in 8 patients with mild metabolic hyperoxaluria, while receiving various doses of pyridoxine." | 7.68 | Metabolism of pyridoxine in mild metabolic hyperoxaluria and primary hyperoxaluria (type 1). ( Edwards, P; Rose, GA, 1991) |
"Plasma pyridoxine metabolites in plasma and 4-pyridoxic acid excretions in urine were measured in normal subjects, in 7 patients with type-1 hyperoxaluria and in 8 patients with mild metabolic hyperoxaluria, while receiving various doses of pyridoxine." | 3.68 | Metabolism of pyridoxine in mild metabolic hyperoxaluria and primary hyperoxaluria (type 1). ( Edwards, P; Rose, GA, 1991) |
"Pyridoxine (vitamin B6), given to patients with primary hyperoxaluria of type I, generally leads to a decrease in urinary excretion of oxalate owing to stimulation of conversion of glyoxylate to glycine instead of oxalate." | 3.67 | [Pyridoxine can normalize oxaluria in idiopathic renal lithiasis]. ( Burckhardt, P; Jacquet, AF; Jaeger, P; Portmann, L, 1986) |
"Accurate diagnosis of primary hyperoxaluria (PH) has important therapeutic consequences." | 3.01 | Genetic assessment in primary hyperoxaluria: why it matters. ( Acquaviva, C; Bacchetta, J; Beck, B; Deesker, L; Garrelfs, S; Groothoff, J; Gupta, A; Mandrile, G; Rumsby, G, 2023) |
"Type 1 primary hyperoxaluria is a genetic disorder caused by deficiency of the liver-specific peroxisomal enzyme alanine-glyoxylate aminotransferase." | 2.49 | Nocturnal home hemodialysis for a patient with type 1 hyperoxaluria. ( Fillaus, JA; Plumb, TJ; Swee, ML, 2013) |
"Primary hyperoxaluria type I is a metabolic disorder caused by the deficiency of the peroxisomal alanine:glyoxylate aminotransferase." | 2.38 | Primary hyperoxaluria type I. ( Brodehl, J; Latta, K, 1990) |
"Primary hyperoxaluria type 1 (PH1) is an inborn error of glyoxylate metabolism, characterized by increased endogenous oxalate production." | 1.62 | Endogenous Oxalate Production in Primary Hyperoxaluria Type 1 Patients. ( Garrelfs, SF; Groothoff, JW; Oosterveld, MJS; Peters-Sengers, H; Schierbeek, H; van den Akker, CHP; van Goudoever, JB; van Harskamp, D; Wanders, RJA; Wijburg, FA, 2021) |
"Primary hyperoxaluria is a rare genetic disorder characterized by oxalate overproduction, leading to kidney failure due to nephrocalcinosis, and is eventually responsible for systemic oxalosis." | 1.48 | Type 1 primary hyperoxaluria: A case report and focus on bone impairment of systemic oxalosis. ( Boivin, G; Caillard, S; Javier, RM; Pijnenburg, L; Rizzo, S, 2018) |
"Primary hyperoxalurias are rare inborn errors of metabolism resulting in increased endogenous production of oxalate that leads to excessive urinary oxalate excretion." | 1.46 | Clinical spectrum of primary hyperoxaluria type 1: Experience of a tertiary center. ( Abdelaziz, H; Abdelrahman, SM; Badr, AM; Bazaraa, HM; Eweeda, KM; Fayez, A; Ghanim, K; Helmy, R; Kotb, MA; Nabhan, MM; Soliman, NA; Tolba, OA, 2017) |
"The hereditary kidney stone disease primary hyperoxaluria type 1 (PH1) is caused by a functional deficiency of the liver-specific, peroxisomal, pyridoxal-phosphate-dependent enzyme, alanine:glyoxylate aminotransferase (AGT)." | 1.43 | Effects of alanine:glyoxylate aminotransferase variants and pyridoxine sensitivity on oxalate metabolism in a cell-based cytotoxicity assay. ( Danpure, CJ; Fargue, S; Holmes, RP; Knight, J; Rumsby, G, 2016) |
"Primary hyperoxalurias are rare recessive inherited inborn errors of glyoxylate metabolism." | 1.37 | [Primary hyperoxaluria]. ( Bacchetta, J; Bertholet-Thomas, A; Cochat, P; Fargue, S; Harambat, J; Sabot, JF, 2011) |
"Pyridoxine (VB6) response in type I primary hyperoxaluria (PHI) is variable, with nearly equal numbers of patients showing partial to complete reductions in oxaluria, and resistance." | 1.33 | Pyridoxine effect in type I primary hyperoxaluria is associated with the most common mutant allele. ( Milliner, DS; Monico, CG; Olson, JB; Rossetti, S, 2005) |
"The detection of type I primary hyperoxaluria is based on the finding of exceedingly high oxalate excretion which is associated with increased glycolate excretion." | 1.28 | Glycolate determination detects type I primary hyperoxaluria in dialysis patients. ( Bianco, O; Finocchiaro, P; Linari, F; Marangella, M; Petrarulo, M; Vitale, C, 1991) |
"Primary hyperoxaluria type I (PH I) is characterized by an excessive endogenous production and excretion of oxalic and glycolic acid." | 1.28 | Vitamin B6 resistant primary hyperoxaluria type I. Report of 5 cases. ( Donckerwolcke, RA; Streefland, M, 1989) |
Timeframe | Studies, this research(%) | All Research% |
---|---|---|
pre-1990 | 5 (15.15) | 18.7374 |
1990's | 6 (18.18) | 18.2507 |
2000's | 5 (15.15) | 29.6817 |
2010's | 13 (39.39) | 24.3611 |
2020's | 4 (12.12) | 2.80 |
Authors | Studies |
---|---|
Garrelfs, SF | 1 |
van Harskamp, D | 1 |
Peters-Sengers, H | 1 |
van den Akker, CHP | 1 |
Wanders, RJA | 1 |
Wijburg, FA | 1 |
van Goudoever, JB | 1 |
Groothoff, JW | 1 |
Schierbeek, H | 1 |
Oosterveld, MJS | 1 |
Mandrile, G | 1 |
Beck, B | 1 |
Acquaviva, C | 1 |
Rumsby, G | 3 |
Deesker, L | 1 |
Garrelfs, S | 1 |
Gupta, A | 1 |
Bacchetta, J | 2 |
Groothoff, J | 1 |
Medina, PG | 1 |
Román, LE | 1 |
Lorenz, EC | 2 |
Lieske, JC | 2 |
Seide, BM | 2 |
Olson, JB | 3 |
Mehta, R | 1 |
Milliner, DS | 5 |
Pijnenburg, L | 1 |
Caillard, S | 1 |
Boivin, G | 1 |
Rizzo, S | 1 |
Javier, RM | 1 |
Dindo, M | 1 |
Conter, C | 1 |
Oppici, E | 2 |
Ceccarelli, V | 1 |
Marinucci, L | 1 |
Cellini, B | 2 |
Sas, DJ | 1 |
Harris, PC | 1 |
Fargue, S | 5 |
Danpure, CJ | 4 |
Plumb, TJ | 1 |
Swee, ML | 1 |
Fillaus, JA | 1 |
Meek, AM | 1 |
Bergstralh, EJ | 1 |
Miyata, N | 1 |
Steffen, J | 1 |
Johnson, ME | 1 |
Koehler, CM | 1 |
Reid, ES | 1 |
Mills, PB | 1 |
Clayton, PT | 1 |
Knight, J | 1 |
Holmes, RP | 1 |
Assimos, DG | 1 |
Soliman, NA | 1 |
Nabhan, MM | 1 |
Abdelrahman, SM | 1 |
Abdelaziz, H | 1 |
Helmy, R | 1 |
Ghanim, K | 1 |
Bazaraa, HM | 1 |
Badr, AM | 1 |
Tolba, OA | 1 |
Kotb, MA | 1 |
Eweeda, KM | 1 |
Fayez, A | 1 |
Hoppe, B | 1 |
Beck, BB | 1 |
Punjabi, OS | 1 |
Riaz, K | 1 |
Mets, MB | 1 |
Cochat, P | 1 |
Bertholet-Thomas, A | 1 |
Sabot, JF | 1 |
Harambat, J | 1 |
Asplin, JR | 1 |
Monico, CG | 1 |
Rossetti, S | 1 |
Marangella, M | 4 |
Castelló Girona, F | 1 |
Riudor Taravilla, E | 1 |
Enríquez Civicos, G | 1 |
Güell Torné, C | 1 |
Fornaguera Soler, F | 1 |
Kist-van Holthe, JE | 1 |
Onkenhout, W | 1 |
van der Heijden, AJ | 1 |
Petrarulo, M | 3 |
Vitale, C | 3 |
Bagnis, C | 1 |
Berutti, S | 1 |
Ramello, A | 1 |
Amoroso, A | 1 |
Cosseddu, D | 1 |
Linari, F | 2 |
Edwards, P | 1 |
Rose, GA | 1 |
Bianco, O | 1 |
Finocchiaro, P | 1 |
Latta, K | 1 |
Brodehl, J | 1 |
Streefland, M | 1 |
Donckerwolcke, RA | 1 |
Yano, S | 1 |
Yoshino, M | 1 |
Nishiyori, A | 1 |
Nakao, M | 1 |
Matsumoto, T | 1 |
Ito, Y | 1 |
Yamashita, F | 1 |
Shimada, A | 1 |
Inokuchi, T | 1 |
Watts, RW | 1 |
Morgan, SH | 1 |
Purkiss, P | 1 |
Mansell, MA | 1 |
Baker, LR | 1 |
Brown, CB | 1 |
Amato, M | 1 |
Donzelli, S | 1 |
Lombardi, M | 1 |
Salvadori, M | 1 |
Carini, M | 1 |
Selli, C | 1 |
Caudarella, R | 1 |
Jaeger, P | 1 |
Portmann, L | 1 |
Jacquet, AF | 1 |
Burckhardt, P | 1 |
Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
---|---|---|---|---|---|---|---|
Outcomes of Metabolic Resuscitation Using Ascorbic Acid, Thiamine, and Glucocorticoids in the Early Treatment of Sepsis.[NCT03422159] | Phase 2 | 140 participants (Actual) | Interventional | 2018-02-05 | Completed | ||
Efficacy of Betaine for Reduction of Urine Oxalate in Patients With Type 1 Primary Hyperoxaluria[NCT00283387] | Phase 2 | 15 participants (Actual) | Interventional | 2007-02-28 | Completed | ||
[information is prepared from clinicaltrials.gov, extracted Sep-2024] |
Defined as the day 4 post-randomization SOFA score minus the initial SOFA score. The Sequential Organ Failure Assessment (SOFA) Score is a mortality prediction score that is based on the degree of dysfunction of six organ systems. The score is calculated on admission and every 24 hours until discharge using the worst parameters measured during the prior 24 hours SOFA score ranges from 0 (no organ dysfunction) to 24 (highest possible score / organ dysfunction). (NCT03422159)
Timeframe: 4 days post-randomization
Intervention | score on a scale (Mean) |
---|---|
Treatment Arm | 2.9 |
Placebo Arm | 1.93 |
Time from admitting to discharge of hospital stay. (NCT03422159)
Timeframe: From admission to the hospital until final discharge, up to 28 days.
Intervention | Days (Mean) |
---|---|
Treatment Arm | 11.5 |
Placebo Arm | 11 |
In-hospital mortality rate. (NCT03422159)
Timeframe: Survival until hospital discharge, up to 28 days.
Intervention | Participants (Count of Participants) |
---|---|
Treatment Arm | 11 |
Placebo Arm | 13 |
Time from admitting to ICU to discharge. (NCT03422159)
Timeframe: From admission to the ICU until final discharge from the ICU, up to an average of 7 days.
Intervention | days (Mean) |
---|---|
Treatment Arm | 4.76 |
Placebo Arm | 4.66 |
ICU mortality rate (NCT03422159)
Timeframe: From admission to hospital until final discharge from the ICU, up to 28 days.
Intervention | Participants (Count of Participants) |
---|---|
Treatment Arm | 6 |
Placebo Arm | 10 |
PCT at 96 hours minus initial PCT, divided by the initial PCT multiplied by 100. (NCT03422159)
Timeframe: 4 days post-randomization
Intervention | Percent (Mean) |
---|---|
Treatment Arm | 63 |
Placebo Arm | 58 |
Defined as the time from starting the active treatment/placebo to discontinuation of all pressors. (NCT03422159)
Timeframe: From start of vasopressor medication to final discontinuation of vasopressor medication, up to 7 days.
Intervention | hours (Mean) |
---|---|
HAT Treatment | 27 |
Comparator | 53 |
Number of days alive and off of the ventilator at day 28. (NCT03422159)
Timeframe: 28 Days post-randomization
Intervention | Days (Mean) |
---|---|
Treatment Arm | 22 |
Placebo Arm | 22.4 |
"The patients were randomly assigned oral betaine or placebo for 2 months, followed by a 2 month washout. Each patient then received the alternate study medication for 2 months.~Urinary Oxalate Excretion was measured by oxalate oxidase. Two 24 hour urine collections were obtained at baseline, and during the eighth week of each study period." (NCT00283387)
Timeframe: baseline, 2 months, 6 months
Intervention | umol/mg (Mean) |
---|---|
Betaine | 1.43 |
Placebo | 1.04 |
9 reviews available for pyridoxine and Oxaluria, Primary
Article | Year |
---|---|
Genetic assessment in primary hyperoxaluria: why it matters.
Topics: Genetic Testing; Genotype; Humans; Hyperoxaluria, Primary; Mutation; Pyridoxine; Transaminases | 2023 |
Molecular basis of primary hyperoxaluria: clues to innovative treatments.
Topics: Alcohol Oxidoreductases; Calcium Oxalate; Gastrointestinal Microbiome; Genetic Therapy; Glyoxylates; | 2019 |
Recent advances in the identification and management of inherited hyperoxalurias.
Topics: Alcohol Oxidoreductases; Fluid Therapy; Genetic Testing; Humans; Hyperoxaluria, Primary; Kidney Calc | 2019 |
Nocturnal home hemodialysis for a patient with type 1 hyperoxaluria.
Topics: Adult; Amino Acid Substitution; Arginine; Circadian Rhythm; Combined Modality Therapy; DNA Mutationa | 2013 |
The primary hyperoxalurias.
Topics: Alcohol Oxidoreductases; Humans; Hyperoxaluria, Primary; Kidney Failure, Chronic; Kidney Transplanta | 2009 |
Hyperoxaluric calcium nephrolithiasis.
Topics: Adolescent; Calcium Oxalate; Calcium, Dietary; Child; Dietary Proteins; Drinking; Humans; Hyperoxalu | 2002 |
Transplantation strategies in type 1 primary hyperoxaluria: the issue of pyridoxine responsiveness.
Topics: Humans; Hyperoxaluria, Primary; Kidney Failure, Chronic; Kidney Transplantation; Pyridoxine | 1999 |
The primary hyperoxalurias.
Topics: Humans; Hyperoxaluria, Primary; Kidney Transplantation; Liver Transplantation; Oxalates; Pyridoxine; | 2001 |
Primary hyperoxaluria type I.
Topics: Age Factors; Alanine Transaminase; Child; Combined Modality Therapy; Female; Genes, Recessive; Human | 1990 |
24 other studies available for pyridoxine and Oxaluria, Primary
Article | Year |
---|---|
Endogenous Oxalate Production in Primary Hyperoxaluria Type 1 Patients.
Topics: Glycine; Glycolates; Glyoxylates; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Oxalates; Pyridoxin | 2021 |
Importance of Assessing Compliance with Conservative Treatment of Primary Hyperoxaluria Type 1: A Case Report of a Patient with I244T/c.969-3C>G Mutation.
Topics: Adolescent; Calcium Oxalate; Conservative Treatment; Female; Fluid Therapy; Follow-Up Studies; Guide | 2020 |
Recovery From Dialysis in Patients With Primary Hyperoxaluria Type 1 Treated With Pyridoxine: A Report of 3 Cases.
Topics: Adult; Female; Homozygote; Humans; Hyperoxaluria, Primary; Kidney Failure, Chronic; Middle Aged; Oxa | 2021 |
Type 1 primary hyperoxaluria: A case report and focus on bone impairment of systemic oxalosis.
Topics: Adult; Biopsy; Bone Density; Calcium Oxalate; Humans; Hyperoxaluria, Primary; Ilium; Kidney Failure, | 2018 |
Multiple mechanisms of action of pyridoxine in primary hyperoxaluria type 1.
Topics: Animals; CHO Cells; Cricetinae; Cricetulus; Humans; Hyperoxaluria, Primary; Pyridoxine | 2013 |
Sustained pyridoxine response in primary hyperoxaluria type 1 recipients of kidney alone transplant.
Topics: Adult; Child; Female; Glomerular Filtration Rate; Humans; Hyperoxaluria, Primary; Kidney Transplanta | 2014 |
Pharmacologic rescue of an enzyme-trafficking defect in primary hyperoxaluria 1.
Topics: Animals; Anti-Infective Agents, Local; CHO Cells; Cricetinae; Cricetulus; Dequalinium; Drug Evaluati | 2014 |
Pyridoxamine and pyridoxal are more effective than pyridoxine in rescuing folding-defective variants of human alanine:glyoxylate aminotransferase causing primary hyperoxaluria type I.
Topics: Animals; CHO Cells; Cricetinae; Cricetulus; Humans; Hyperoxaluria, Primary; Mutation; Protein Foldin | 2015 |
Effects of alanine:glyoxylate aminotransferase variants and pyridoxine sensitivity on oxalate metabolism in a cell-based cytotoxicity assay.
Topics: Animals; Cell Survival; CHO Cells; Cricetulus; Glycolates; Humans; Hyperoxaluria, Primary; Mutation; | 2016 |
Re: Pyridoxamine and Pyridoxal are More Effective than Pyridoxine in Rescuing Folding-Defective Variants of Human Alanine:Glyoxylate Aminotransferase Causing Primary Hyperoxaluria Type I.
Topics: Alanine; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Pyridoxal; Pyridoxamine; Pyridoxine | 2016 |
Clinical spectrum of primary hyperoxaluria type 1: Experience of a tertiary center.
Topics: Adult; Child; Child, Preschool; Cohort Studies; Consanguinity; Egypt; Female; Humans; Hyperoxaluria, | 2017 |
Crystalline retinopathy in primary hyperoxaluria.
Topics: Electroretinography; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Infant; Liver Transplantation; M | 2011 |
[Primary hyperoxaluria].
Topics: Alanine Transaminase; Disease Progression; Genotype; Humans; Hyperoxaluria; Hyperoxaluria, Primary; | 2011 |
Pyridoxine effect in type I primary hyperoxaluria is associated with the most common mutant allele.
Topics: Adolescent; Adult; Alleles; Child; Child, Preschool; Dose-Response Relationship, Drug; Female; Genot | 2005 |
[Results of treatment with oral citrate and pyridoxine in patients with primary hyperoxaluria type 1].
Topics: Citrates; Female; Humans; Hyperoxaluria, Primary; Infant, Newborn; Kidney; Male; Pyridoxine; Radiogr | 1999 |
Pyridoxine-responsive nephrocalcinosis and glycolic aciduria in two siblings without hyperoxaluria and with normal alanine: glyoxalate aminotransferase activity.
Topics: Calcinosis; Child; Female; Glycolates; Humans; Hyperoxaluria, Primary; Kidney Diseases; Male; Pyrido | 2000 |
Oxalate balance studies in patients on hemodialysis for type I primary hyperoxaluria.
Topics: Adult; Calcium Oxalate; Humans; Hyperoxaluria, Primary; Kidney; Male; Oxalates; Pyridoxine; Renal Di | 1992 |
Metabolism of pyridoxine in mild metabolic hyperoxaluria and primary hyperoxaluria (type 1).
Topics: Chromatography, High Pressure Liquid; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Pyridoxic Acid; | 1991 |
Glycolate determination detects type I primary hyperoxaluria in dialysis patients.
Topics: Adolescent; Adult; Chromatography, High Pressure Liquid; Glycolates; Humans; Hyperoxaluria, Primary; | 1991 |
Vitamin B6 resistant primary hyperoxaluria type I. Report of 5 cases.
Topics: Child; Child, Preschool; Drug Resistance; Female; Follow-Up Studies; Humans; Hyperoxaluria; Hyperoxa | 1989 |
Hyperoxaluria type I: therapeutic effects of pyridoxine hydrochloride and inheritance patterns of the disease in a family.
Topics: Child; Child, Preschool; Female; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Male; Pedigree; Pyri | 1988 |
Timing of renal transplantation in the management of pyridoxine-resistant type I primary hyperoxaluria.
Topics: Adolescent; Adult; Drug Resistance; Female; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Kidney Fa | 1988 |
Primary hyperoxaluria: effect of treatment with vitamin B6 and shock waves.
Topics: Adult; HLA Antigens; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Kidney Calculi; Lithotripsy; Mal | 1987 |
[Pyridoxine can normalize oxaluria in idiopathic renal lithiasis].
Topics: Adult; Drug Evaluation; Female; Humans; Hyperoxaluria; Hyperoxaluria, Primary; Jejunoileal Bypass; K | 1986 |