ArticleInternational journal of nephrology2011
Primary hyperoxaluria.
Article in International journal of nephrology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers, 1 of them a synthesis that pooled it.
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
48 citing papers in PubMed, 1 synthesis or guideline pooled it, 119 citations in OpenAlex.
- Clinical features and mutational spectrum of Chinese patients with primary hyperoxaluria type 2.Urolithiasis · 2024Pooled it
- Nedosiran in pediatric patients with PH1 and relatively preserved kidney function, a phase 2 study (PHYOX8).Pediatric nephrology (Berlin, Germany) · 2025Trial
- Plasma oxalate and eGFR are correlated in primary hyperoxaluria patients with maintained kidney function-data from three placebo-controlled studies.Pediatric nephrology (Berlin, Germany) · 2021Trial
- Determinants of enteric hyperoxaluria in the SAMP1/YitFc mouse model of spontaneous ileitis.Gut microbes · 2026Article
- Clinical and molecular spectrum of primary hyperoxaluria type 1 in Tunisia: pediatric presentation and minimum observed prevalence.Pediatric nephrology (Berlin, Germany) · 2026Article
- Primary hyperoxaluria type 1-current practice in the siRNA era: an ERA Genes & Kidney Working Group survey.Clinical kidney journal · 2026Article
- Beyond expensive innovations: affordable and effective strategies for managing tubulopathies in adults.Clinical kidney journal · 2026Review
- Population Pharmacokinetic and Pharmacodynamic Modelling and Simulation for Nedosiran Clinical Development and Dose Guidance in Pediatric Patients with Primary Hyperoxaluria Type 1.Clinical pharmacokinetics · 2025Article
- Hyperoxaluria: Diagnosis and Treatment.The Urologic clinics of North America · 2025Review
- Article
- PHYOX3: Nedosiran Long-Term Safety and Efficacy in Patients With Primary Hyperoxaluria Type 1.Kidney international reports · 2025Article
- Nedosiran population pharmacokinetic and pharmacodynamic modelling and simulation to guide clinical development and dose selection in patients with primary hyperoxaluria type 1.British journal of clinical pharmacology · 2024Article
- Nedosiran Safety and Efficacy in PH1: Interim Analysis of PHYOX3.Kidney international reports · 2024Article
- Restored glyoxylate metabolism after AGXT gene correction and direct reprogramming of primary hyperoxaluria type 1 fibroblasts.iScience · 2024Article
- [Primary hyperoxaluria type 1-a rare hereditary metabolic disorder as cause of livedo racemosa].Dermatologie (Heidelberg, Germany) · 2024Article
- Primary hyperoxaluria: a case series.Journal of medical case reports · 2023Article
- Article
- Oxalate (dys)Metabolism: Person-to-Person Variability, Kidney and Cardiometabolic Toxicity.Genes · 2023Review
- Article
- Oxalate nephropathy in an elderly patient with newly diagnosed celiac disease - a case report.BMC nephrology · 2023Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Primary hyperoxalurias (PH) are inborn errors in the metabolism of glyoxylate and oxalate. PH type 1, the most common form, is an autosomal recessive disorder caused by a deficiency of the liver-specific enzyme alanine, glyoxylate aminotransferase (AGT) resulting in overproduction and excessive urinary excretion of oxalate. Recurrent urolithiasis and nephrocalcinosis are the hallmarks of the disease. As glomerular filtration rate decreases due to progressive renal damage, oxalate accumulates leading to systemic oxalosis. Diagnosis is often delayed and is based on clinical and sonographic findings, urinary oxalate assessment, DNA analysis, and, if necessary, direct AGT activity measurement in liver biopsy tissue. Early initiation of conservative treatment, including high fluid intake, inhibitors of calcium oxalate crystallization, and pyridoxine in responsive cases, can help to maintain renal function in compliant subjects. In end-stage renal disease patients, the best outcomes have been achieved with combined liver-kidney transplantation which corrects the enzyme defect.
Identifiers
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.