Associated Papers
Global genetic prevalence estimates of primary hyperoxaluria are greater than previously reported.
Mandrile G et al.
Clinical Kidney Journal, 2025
40873808 (PubMed )
Supplement: sfaf194_Supplemental_File.docx
HOGA1 variants in Chinese patients with primary hyperoxaluria type 3: genetic features and genotype-phenotype relationships.
Ge Y et al.
World Journal of Urology, 2023
HOGA1 gene pathogenic variants in primary hyperoxaluria type III: Spectrum of pathogenic sequence variants, and phenotypic association.
Abid A et al.
Human Mutation, 2022
Comprehensive analysis of recessive carrier status using exome and genome sequencing data in 1543 Southern Chinese.
Chau JFT et al.
Npj Genomic Medicine, 2022
35314707 (PubMed )
Supplement: 41525_2022_287_MOESM3_ESM.xlsx › SNV
Renal function can be impaired in children with primary hyperoxaluria type 3.
Allard L et al.
Pediatric Nephrology (berlin, Germany), 2015
4-Hydroxy-2-oxoglutarate aldolase inactivity in primary hyperoxaluria type 3 and glyoxylate reductase inhibition.
Riedel TJ et al.
Biochimica Et Biophysica Acta, 2012
The enzyme 4-hydroxy-2-oxoglutarate aldolase is deficient in primary hyperoxaluria type 3.
Williams EL et al.
Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association, 2012
The enzyme 4-hydroxy-2-oxoglutarate aldolase is deficient in primary hyperoxaluria type III.
Hoppe B
Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association, 2012
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