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Page 1
The primary hyperoxalurias.
Leumann E, Hoppe B. Leumann E, et al. J Am Soc Nephrol. 2001 Sep;12(9):1986-1993. doi: 10.1681/ASN.V1291986. J Am Soc Nephrol. 2001. PMID: 11518794 Review. No abstract available.
Hydroxyproline Metabolism and Oxalate Synthesis in Primary Hyperoxaluria.
Fargue S, Milliner DS, Knight J, Olson JB, Lowther WT, Holmes RP. Fargue S, et al. J Am Soc Nephrol. 2018 Jun;29(6):1615-1623. doi: 10.1681/ASN.2017040390. Epub 2018 Mar 27. J Am Soc Nephrol. 2018. PMID: 29588429 Free PMC article.
Background Endogenous oxalate synthesis contributes to calcium oxalate stone disease and is markedly increased in the inherited primary hyperoxaluria (PH) disorders. The incomplete knowledge regarding oxalate synthesis complicates discovery of new treatments. ...
Background Endogenous oxalate synthesis contributes to calcium oxalate stone disease and is markedly increased in the inherited primary …
Glycolate metabolism by Hep G2 cells.
Holmes RP, Sexton WJ, Applewhite JC, Kennedy M, Assimos DG. Holmes RP, et al. J Am Soc Nephrol. 1999 Nov;10 Suppl 14:S345-7. J Am Soc Nephrol. 1999. PMID: 10541260
The pathways of oxalate synthesis in humans are not well defined despite their clinical significance in primary hyperoxaluria and idiopathic calcium oxalate nephrolithiasis. Furthermore, the functional roles, if any, of this synthesis have not been elucidated. ...
The pathways of oxalate synthesis in humans are not well defined despite their clinical significance in primary hyperoxaluria …
Endogenous Oxalate Production in Primary Hyperoxaluria Type 1 Patients.
Garrelfs SF, van Harskamp D, Peters-Sengers H, van den Akker CHP, Wanders RJA, Wijburg FA, van Goudoever JB, Groothoff JW, Schierbeek H, Oosterveld MJS. Garrelfs SF, et al. J Am Soc Nephrol. 2021 Dec 1;32(12):3175-3186. doi: 10.1681/ASN.2021060729. Epub 2021 Dec 1. J Am Soc Nephrol. 2021. PMID: 34686543 Free PMC article.
BACKGROUND: Primary hyperoxaluria type 1 (PH1) is an inborn error of glyoxylate metabolism, characterized by increased endogenous oxalate production. ...
BACKGROUND: Primary hyperoxaluria type 1 (PH1) is an inborn error of glyoxylate metabolism, characterized by increased endogen …
Characterization of CHK-336, A First-in-Class, Liver-Targeted, Small-Molecule Lactate Dehydrogenase Inhibitor for Hyperoxaluria Treatment.
Cox JH, Boily MO, Caron A, Sheng T, Wu J, Ding J, Gaudreault S, Chong O, Surendradoss J, Gomez R, Lester J, Dumais V, Li X, Gumpena R, Hall MD, Waterson AG, Stott G, Flint AJ, Moore WJ, Lowther WT, Knight J, Percival MD, Tong V, Oballa R, Powell DA, King AJ. Cox JH, et al. J Am Soc Nephrol. 2025 Apr 7;36(8):1535-1547. doi: 10.1681/ASN.0000000690. J Am Soc Nephrol. 2025. PMID: 40193200 Free PMC article.
KEY POINTS: Primary hyperoxalurias are genetic diseases defined by elevated hepatic oxalate production and higher incidence of kidney stones. ...BACKGROUND: Primary hyperoxalurias (PH) 1-3 are genetic diseases defined by elevated hepatic oxalate produc …
KEY POINTS: Primary hyperoxalurias are genetic diseases defined by elevated hepatic oxalate production and higher incidence of …
Phenotype-Genotype Correlations and Estimated Carrier Frequencies of Primary Hyperoxaluria.
Hopp K, Cogal AG, Bergstralh EJ, Seide BM, Olson JB, Meek AM, Lieske JC, Milliner DS, Harris PC; Rare Kidney Stone Consortium. Hopp K, et al. J Am Soc Nephrol. 2015 Oct;26(10):2559-70. doi: 10.1681/ASN.2014070698. Epub 2015 Feb 2. J Am Soc Nephrol. 2015. PMID: 25644115 Free PMC article.
Primary hyperoxaluria (PH) is a rare autosomal recessive disease characterized by oxalate accumulation in the kidneys and other organs. ...
Primary hyperoxaluria (PH) is a rare autosomal recessive disease characterized by oxalate accumulation in the kidneys and othe …
An Investigational RNAi Therapeutic Targeting Glycolate Oxidase Reduces Oxalate Production in Models of Primary Hyperoxaluria.
Liebow A, Li X, Racie T, Hettinger J, Bettencourt BR, Najafian N, Haslett P, Fitzgerald K, Holmes RP, Erbe D, Querbes W, Knight J. Liebow A, et al. J Am Soc Nephrol. 2017 Feb;28(2):494-503. doi: 10.1681/ASN.2016030338. Epub 2016 Jul 18. J Am Soc Nephrol. 2017. PMID: 27432743 Free PMC article.
Primary hyperoxaluria type 1 (PH1), an inherited rare disease of glyoxylate metabolism, arises from mutations in the enzyme alanine-glyoxylate aminotransferase. ...Notably, ALN-GO1 reduced urinary oxalate concentration up to 50% after a single dose in the genetic mo …
Primary hyperoxaluria type 1 (PH1), an inherited rare disease of glyoxylate metabolism, arises from mutations in the enzyme al …
Oxalobacter formigenes-Derived Bioactive Factors Stimulate Oxalate Transport by Intestinal Epithelial Cells.
Arvans D, Jung YC, Antonopoulos D, Koval J, Granja I, Bashir M, Karrar E, Roy-Chowdhury J, Musch M, Asplin J, Chang E, Hassan H. Arvans D, et al. J Am Soc Nephrol. 2017 Mar;28(3):876-887. doi: 10.1681/ASN.2016020132. Epub 2016 Oct 13. J Am Soc Nephrol. 2017. PMID: 27738124 Free PMC article.
Hyperoxaluria is a major risk factor for kidney stones and has no specific therapy, although Oxalobacter formigenes colonization is associated with reduced stone risk. ...Knockdown of the oxalate transporter SLC26A6 also significantly restricted the induction of oxalate tr …
Hyperoxaluria is a major risk factor for kidney stones and has no specific therapy, although Oxalobacter formigenes colonization is a …
Recent developments in our understanding of primary hyperoxaluria type 2.
Cregeen DP, Rumsby G. Cregeen DP, et al. J Am Soc Nephrol. 1999 Nov;10 Suppl 14:S348-50. J Am Soc Nephrol. 1999. PMID: 10541261
The data presented provide a biochemical explanation for the previously observed differences in the tissue distribution of HPR and glyoxylate reductase activities in human subjects and support the claim that diagnoses of primary hyperoxaluria type 2 should be made b …
The data presented provide a biochemical explanation for the previously observed differences in the tissue distribution of HPR and glyoxylat …
Hyperoxaluria Requires TNF Receptors to Initiate Crystal Adhesion and Kidney Stone Disease.
Mulay SR, Eberhard JN, Desai J, Marschner JA, Kumar SV, Weidenbusch M, Grigorescu M, Lech M, Eltrich N, Müller L, Hans W, Hrabě de Angelis M, Vielhauer V, Hoppe B, Asplin J, Burzlaff N, Herrmann M, Evan A, Anders HJ. Mulay SR, et al. J Am Soc Nephrol. 2017 Mar;28(3):761-768. doi: 10.1681/ASN.2016040486. Epub 2016 Sep 9. J Am Soc Nephrol. 2017. PMID: 27612997 Free PMC article.
When fed an oxalate-rich diet, wild-type mice developed progressive CKD, whereas Tnfr1-, Tnfr2-, and Tnfr1/2-deficient mice did not. Despite identical levels of hyperoxaluria, Tnfr1-, Tnfr2-, and Tnfr1/2-deficient mice also lacked the intrarenal CaOx deposition and tubular …
When fed an oxalate-rich diet, wild-type mice developed progressive CKD, whereas Tnfr1-, Tnfr2-, and Tnfr1/2-deficient mice did not. Despite …
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