ArticleScientific reports2022
Chronic liver disease and hepatic calcium-oxalate deposition in patients with primary hyperoxaluria type I.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 10 citations in OpenAlex.
- Targeting Oxalate Production by Combining Enzyme Inhibition and Proteolysis Activation: A Novel Therapeutic Approach for Primary Hyperoxaluria Type 1.Journal of medicinal chemistry · 2026Article
- Surgical Management of Pediatric Primary Hyperoxaluria Type 1: An Eight-Patient Case Series in the Pre-siRNA Era.Pediatric transplantation · 2025Article
- LNP-mediated in vivo base editing corrects Agxt to cure primary hyperoxaluria type 1.Clinical and translational medicine · 2025Article
- Metabolic dysfunction associated steatotic liver and kidney stones: what is going on?Current opinion in nephrology and hypertension · 2025Review
- Inhibition of hepatic oxalate overproduction ameliorates metabolic dysfunction-associated steatohepatitis.Nature metabolism · 2024Article
- Multicenter Long-Term Real World Data on Treatment With Lumasiran in Patients With Primary Hyperoxaluria Type 1.Kidney international reports · 2024Article
- Kidney Stone Prevention.Advances in nutrition (Bethesda, Md.) · 2023Review
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Authors and funding
8 authors at 7 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Patients with primary hyperoxaluria type I (PH I) are prone to develop early kidney failure. Systemic deposition of calcium-oxalate (CaOx) crystals starts, when renal function declines and plasma oxalate increases. All tissue, but especially bone, heart and eyes are affected. However, liver involvement, as CaOx deposition or chronic hepatitis/fibrosis has never been reported. We examined liver specimen from 19 PH I patients (aged 1.5 to 52 years at sample collection), obtained by diagnostic biopsy (1), at autopsy (1), or transplantation (17). With polarization microscopy, birefringent CaOx crystals located in small arteries, but not within hepatocytes were found in 3/19 patients. Cirrhosis was seen in one, fibrosis in 10/19 patients, with porto-portal and nodular fibrosis (n = 1), with limitation to the portal field in 8 and/or to central areas in 5 patients. Unspecific hepatitis features were observed in 7 patients. Fiber proliferations were detectable in 10 cases and in one sample transformed Ito-cells (myofibroblasts) were found. Iron deposition, but also megakaryocytes as sign of extramedullary erythropoiesis were found in 9, or 3 patients, respectively. Overall, liver involvement in patients with PH I was more pronounced, as previously described. However, CaOx deposition was negligible in liver, although the oxalate concentration there must be highest.
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