ReviewClinical kidney journal2022
Primary hyperoxaluria type 1: pathophysiology and genetics.
Review in Clinical kidney journal, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
27 citing papers in PubMed, 43 citations in OpenAlex.
- Determinants of enteric hyperoxaluria in the SAMP1/YitFc mouse model of spontaneous ileitis.Gut microbes · 2026Article
- Targeting the Highly Deleterious G161C and Y260C SNP Variants of the AGXT Protein Involved in Glyoxylate Metabolism Using Tauroursodeoxycholic Acid: A Computational Study.International journal of molecular sciences · 2026Article
- Novel AAV843 Vector-Mediated Gene Replacement Therapy Rescues Primary Hyperoxaluria Type I in Mice.Cells · 2026Article
- Primary Hyperoxaluria With Cardiac Involvement: A Case Series.Arquivos brasileiros de cardiologia · 2026Article
- Steroid hormones and nephrolithiasis: regulation of urine components metabolism and inflammation.Biology of sex differences · 2026Review
- Surgical Management of Pediatric Primary Hyperoxaluria Type 1: An Eight-Patient Case Series in the Pre-siRNA Era.Pediatric transplantation · 2025Article
- Application of Induced Pluripotent Stem Cells (iPSCs) in Hereditary and Viral Diseases of the Liver: Modeling and Treatment.International journal of molecular sciences · 2025Review
- Cell and tissue reprogramming: Unlocking a new era in medical drug discovery.Pharmacological reviews · 2025Review
- Spontaneous ileitis and postsurgical murine models of enteric hyperoxaluria.American journal of physiology. Gastrointestinal and liver physiology · 2025Article
- Effect of the allelic background on the phenotype of primary hyperoxaluria type I.Current opinion in nephrology and hypertension · 2025Review
- Genetics of kidney stones and the role of genetic testing in prevention: a guide for urologists.Frontiers in medicine · 2025Review
- Technologies for Targeted RNA Degradation and Induced RNA Decay.Chemical reviews · 2024Review
- Synthesis andInternational journal of molecular sciences · 2024Article
- A narrative review of monogenic disorders causing nephrolithiasis and chronic kidney disease.Nephrology (Carlton, Vic.) · 2024Review
- Nucleic acid drugs: recent progress and future perspectives.Signal transduction and targeted therapy · 2024Review
- Diagnosis and management of primary hyperoxalurias: best practices.Pediatric nephrology (Berlin, Germany) · 2024Review
- Opportunities in Primary and Enteric Hyperoxaluria at the Cross-Roads Between the Clinic and Laboratory.Kidney international reports · 2024Article
- Article
- Abnormal Porphyrin Metabolism in Autism Spectrum Disorder and Therapeutic Implications.Molecular neurobiology · 2024Review
- Urinary Oxalate Excretion During Pregnancy in Primary Hyperoxaluria Type 1: A Report of 4 Cases.Kidney medicine · 2024Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 2 countries.
Funding
Abstract
Primary hyperoxaluria type 1 (PH1) is a rare genetic form of calcium oxalate kidney stone disease. It is caused by a deficiency in the liver-specific enzyme, alanine:glyoxylate aminotransferase (AGT), a pyridoxal-5'-phosphate (PLP)-dependent enzyme involved in the metabolism of glyoxylate. The excessive endogenous synthesis of oxalate that ensues leads to hyperoxaluria, and the crystallization of the poorly soluble calcium salt of oxalate is responsible for a severe kidney stone disease, which can progress to end-stage renal disease, systemic deposition of oxalate and death. Knowledge about metabolic precursors of glyoxylate and oxalate, molecular pathology of AGT and analytical methods for diagnosis and clinical assessment have allowed a better understanding of the mechanisms underlying PH1 and opened the door to new therapeutic strategies.
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What OpenQuestion holds
Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.