Renal tubular acidosis 3

Summary

Renal tubular acidosis 3 (MONDO:0009967) is a disease. A subtype of renal tubular acidosis — broader associated-gene and molecular evidence is on the parent page (see Disease family below).

Clinical features

No curated clinical features (Orphanet) for this disease.

Identifiers

Disease identifiers

Field	Value
Canonical name	renal tubular acidosis 3
Mondo ID	MONDO:0009967
MeSH	C537759
OMIM	267200
UMLS	C1849435
MedGen	336601
GARD	0015228
Is cancer (heuristic)	no

Also known as: bicarbonate-wasting RTA · renal tubular acidosis 3 · renal tubular acidosis III · renal tubular acidosis, distal, type 3 · RTA, bicarbonate-wasting type · RTA, dislocation type

Disease family

This is a subtype of renal tubular acidosis. Genetic, therapeutic, and trial evidence is largely curated at the broader-term level — see the parent page for the associated-gene cohort and molecular evidence.

Classification path: disease › human disease › disease by developmental or physiological process › metabolic disease › disorder of acid-base balance › acidosis disorder › renal tubular acidosis › renal tubular acidosis 3

Related subtypes (4): proximal renal tubular acidosis, renal tubular acidosis, distal, 3, with or without sensorineural hearing loss, neuroaxonal dystrophy renal tubular acidosis, hyperkalemic renal tubular acidosis

Genetics & variants

GWAS landscape

No GWAS associations recorded — common-variant (GWAS) studies don’t cover this disease (typical for Mendelian / rare diseases). See the curated gene cohort and Mendelian overlap below.

Variant details and genetic-evidence tiers

No tiered GWAS variants or ClinVar records for this disease.

Genes & proteins

No associated-gene cohort resolved for this disease. Atlas builds the molecular and therapeutic sections — associated genes, protein families, druggability, pathways, interactions, and drug associations — by aggregating over a disease’s associated genes (resolved via GWAS / GenCC / ClinVar / CIViC), and none resolved here. This is expected for antibody-mediated, autoimmune, or otherwise non-gene-defined conditions; the curated evidence for this disease is its clinical features, GWAS susceptibility, and clinical trials (above).

Function

No pathway enrichment — requires an associated-gene cohort.

Therapeutics

No druggable-target or therapeutic data for this disease’s cohort.

Clinical trials & evidence

Clinical trials

Clinical trials: 0.