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3
Pathophys.
2
Phenotypes
1
Gaps
3
Pathograph
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Classifications

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Discussions and Knowledge Gaps

1
Is persistent hyperoxaluria ever a direct consequence of HAO1/glycolate oxidase deficiency, or was the reported hyperoxaluria due to another unresolved cause?
KNOWLEDGE GAP OPEN gap_hao1_hyperoxaluria_causality
The best human source describes glycolate oxidase deficiency as essentially benign and says the unique patient had hyperoxaluria of unknown etiology. More cases or functional human data are needed before wiring HAO1 deficiency into the calcium oxalate nephrolithiasis pathograph.

Pathophysiology

3
HAO1 Glycolate Oxidase Deficiency
Biallelic HAO1 variants impair hepatic glycolate oxidase activity, reducing oxidation of glycolate to glyoxylate.
hepatocyte CL:0000182
HAO1 hgnc:4809
glyoxylate metabolic process GO:0046487 ↓ DECREASED
glycolate oxidase activity GO:0003973 ↓ DECREASED
peroxisome GO:0005777
Show evidence (2 references)
PMID:24996905 SUPPORT Human Clinical
"Direct DNA sequencing of glycolate oxidase gene (HAO1) revealed a homozygous c.814-1G>C mutation"
Supports biallelic HAO1 variation as the genetic lesion in isolated glycolic aciduria.
PMID:28752386 SUPPORT Human Clinical
"Further analysis of the liver biopsy demonstrated absent GO enzyme activity, confirming GO deficiency in this case."
Directly supports absent glycolate oxidase activity in a human patient.
Isolated Hyperglycolic Aciduria
Glycolate accumulates in urine when HAO1/glycolate oxidase activity is lost. The initially described affected siblings had markedly elevated glycolic acid with normal oxalate, citrate, and glycerate, supporting a primarily biochemical phenotype.
Show evidence (1 reference)
PMID:24996905 SUPPORT Human Clinical
"The proband showed markedly increased urinary glycolic acid excretion with normal excretion of oxalate, citrate and glycerate."
Supports the biochemical phenotype and absence of hyperoxaluria in the index family.
Usually Benign Biochemical Disorder
Published cases frame glycolate oxidase deficiency as rare and essentially benign. Persistent hyperoxaluria has been reported once, but that report explicitly treated the hyperoxaluria as unexplained rather than a proven direct consequence of HAO1 loss.
Show evidence (2 references)
PMID:28752386 SUPPORT Human Clinical
"Deficiency of GO is a very rare disorder with only two previously published cases. It is considered to be an essentially benign inborn error of metabolism."
Supports the benign-biochemical interpretation of HAO1 deficiency.
PMID:28752386 PARTIAL Human Clinical
"The present case is unique in that GO deficiency is associated with persistent hyperoxaluria."
Supports an observed association with persistent hyperoxaluria in one patient, but the same abstract says the patient also had hyperoxaluria of unknown etiology, so the causal edge remains cautious.

Pathograph

Use the checkboxes to hide or show graph categories. Hover nodes for evidence and cross-linked metadata.
Pathograph: causal mechanism network for HAO1-Related Glycolate Oxidase Deficiency Interactive directed graph showing how pathophysiology mechanisms, phenotypes, genetic factors and variants, experimental models, environmental triggers, and treatments relate through causal and linked edges.

Phenotypes

2
Hyperglycolic aciduria Biochemical
Show evidence (1 reference)
PMID:24996905 SUPPORT Human Clinical
"The proband showed markedly increased urinary glycolic acid excretion with normal excretion of oxalate, citrate and glycerate."
Supports hyperglycolic aciduria as the defining biochemical phenotype.
Persistent hyperoxaluria in one reported case Biochemical HP:0003159
Show evidence (1 reference)
PMID:28752386 PARTIAL Human Clinical
"The present case is unique in that GO deficiency is associated with persistent hyperoxaluria."
Supports a single-case association, not a definitive or recurrent disease feature.
{ }

Source YAML

click to show
name: HAO1-Related Glycolate Oxidase Deficiency
creation_date: "2026-07-06T06:09:44Z"
description: >-
  HAO1-related glycolate oxidase deficiency is a very rare autosomal recessive
  inborn error of glyoxylate-precursor metabolism caused by biallelic HAO1
  variants. HAO1 encodes hepatic glycolate oxidase, a hydroxyacid oxidase that
  oxidizes glycolate to glyoxylate. Loss of glycolate oxidase activity causes
  isolated hyperglycolic aciduria and is generally described as essentially
  benign; one reported patient had persistent hyperoxaluria of unknown etiology,
  so hyperoxaluria is modeled as an observed but not yet definitive downstream
  consequence of HAO1 loss.
category: Metabolic Disorder
parents:
- Inborn Error of Metabolism
- Disorder of Glyoxylate and Oxalate Metabolism
synonyms:
- HAO1 deficiency
- Hydroxyacid oxidase 1 deficiency
- Glycolate oxidase deficiency
- Isolated glycolic aciduria
classifications:
  icimd_category:
  - classification_value: glyoxylate_and_oxalate
    notes: >-
      ICIMD category 13.1, disorders of glyoxylate and oxalate metabolism.
      HAO1/glycolate oxidase acts upstream of glyoxylate and oxalate production.
pathophysiology:
- name: HAO1 Glycolate Oxidase Deficiency
  description: >-
    Biallelic HAO1 variants impair hepatic glycolate oxidase activity, reducing
    oxidation of glycolate to glyoxylate.
  role: trigger
  genes:
  - preferred_term: HAO1
    term:
      id: hgnc:4809
      label: HAO1
  molecular_functions:
  - preferred_term: glycolate oxidase activity
    term:
      id: GO:0003973
      label: (S)-2-hydroxy-acid oxidase activity
    modifier: DECREASED
  cellular_components:
  - preferred_term: peroxisome
    term:
      id: GO:0005777
      label: peroxisome
  biological_processes:
  - preferred_term: glyoxylate metabolic process
    term:
      id: GO:0046487
      label: glyoxylate metabolic process
    modifier: DECREASED
  cell_types:
  - preferred_term: hepatocyte
    term:
      id: CL:0000182
      label: hepatocyte
  evidence:
  - reference: PMID:24996905
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Direct DNA sequencing of glycolate oxidase gene (HAO1) revealed a homozygous c.814-1G>C mutation"
    explanation: Supports biallelic HAO1 variation as the genetic lesion in isolated glycolic aciduria.
  - reference: PMID:28752386
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Further analysis of the liver biopsy demonstrated absent GO enzyme activity, confirming GO deficiency in this case."
    explanation: Directly supports absent glycolate oxidase activity in a human patient.
  downstream:
  - target: Isolated Hyperglycolic Aciduria
    causal_link_type: DIRECT
    description: Glycolate oxidase deficiency causes increased urinary glycolate.
    evidence:
    - reference: PMID:24996905
      supports: SUPPORT
      evidence_source: HUMAN_CLINICAL
      snippet: "defective splice variant of glycolate oxidase as the cause of isolated asymptomatic glycolic aciduria."
      explanation: Directly links defective glycolate oxidase to isolated glycolic aciduria.
- name: Isolated Hyperglycolic Aciduria
  description: >-
    Glycolate accumulates in urine when HAO1/glycolate oxidase activity is lost.
    The initially described affected siblings had markedly elevated glycolic
    acid with normal oxalate, citrate, and glycerate, supporting a primarily
    biochemical phenotype.
  role: central_effector
  chemical_entities:
  - preferred_term: glycolate
    term:
      id: CHEBI:29805
      label: glycolate
    modifier: INCREASED
  - preferred_term: glyoxylate
    term:
      id: CHEBI:36655
      label: glyoxylate
    modifier: DECREASED
  evidence:
  - reference: PMID:24996905
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "The proband showed markedly increased urinary glycolic acid excretion with normal excretion of oxalate, citrate and glycerate."
    explanation: Supports the biochemical phenotype and absence of hyperoxaluria in the index family.
  downstream:
  - target: Usually Benign Biochemical Disorder
    causal_link_type: DIRECT
    description: Published human cases describe glycolate oxidase deficiency as essentially benign.
- name: Usually Benign Biochemical Disorder
  description: >-
    Published cases frame glycolate oxidase deficiency as rare and essentially
    benign. Persistent hyperoxaluria has been reported once, but that report
    explicitly treated the hyperoxaluria as unexplained rather than a proven
    direct consequence of HAO1 loss.
  role: consequence
  evidence:
  - reference: PMID:28752386
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "Deficiency of GO is a very rare disorder with only two previously published cases. It is considered to be an essentially benign inborn error of metabolism."
    explanation: Supports the benign-biochemical interpretation of HAO1 deficiency.
  - reference: PMID:28752386
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: "The present case is unique in that GO deficiency is associated with persistent hyperoxaluria."
    explanation: >-
      Supports an observed association with persistent hyperoxaluria in one
      patient, but the same abstract says the patient also had hyperoxaluria of
      unknown etiology, so the causal edge remains cautious.
phenotypes:
- category: Biochemical
  name: Hyperglycolic aciduria
  description: Markedly increased urinary glycolic acid/glycolate excretion.
  evidence:
  - reference: PMID:24996905
    supports: SUPPORT
    evidence_source: HUMAN_CLINICAL
    snippet: "The proband showed markedly increased urinary glycolic acid excretion with normal excretion of oxalate, citrate and glycerate."
    explanation: Supports hyperglycolic aciduria as the defining biochemical phenotype.
- category: Biochemical
  name: Persistent hyperoxaluria in one reported case
  description: >-
    Persistent hyperoxaluria was reported in one HAO1-deficient patient, but the
    etiology was not established and should not be generalized across the
    disorder.
  phenotype_term:
    preferred_term: Hyperoxaluria
    term:
      id: HP:0003159
      label: Hyperoxaluria
  evidence:
  - reference: PMID:28752386
    supports: PARTIAL
    evidence_source: HUMAN_CLINICAL
    snippet: "The present case is unique in that GO deficiency is associated with persistent hyperoxaluria."
    explanation: Supports a single-case association, not a definitive or recurrent disease feature.
discussions:
- discussion_id: gap_hao1_hyperoxaluria_causality
  prompt: >-
    Is persistent hyperoxaluria ever a direct consequence of HAO1/glycolate
    oxidase deficiency, or was the reported hyperoxaluria due to another
    unresolved cause?
  kind: KNOWLEDGE_GAP
  status: OPEN
  attaches_to:
  - pathophysiology#Usually Benign Biochemical Disorder
  rationale: >-
    The best human source describes glycolate oxidase deficiency as essentially
    benign and says the unique patient had hyperoxaluria of unknown etiology.
    More cases or functional human data are needed before wiring HAO1 deficiency
    into the calcium oxalate nephrolithiasis pathograph.
notes: >-
  Package seed 13.1.03.01; OMIM:605023. No exact MONDO disease term was found
  in the local MONDO adapter for HAO1-related glycolate oxidase deficiency, so
  the entry is named from the gene/enzyme defect and evidence-backed phenotype.