hemolytic disease of the newborn with Kell alloimmunization

Summary

hemolytic disease of the newborn with Kell alloimmunization (MONDO:0017164) is a disease. A subtype of hemolytic anemia — broader associated-gene and molecular evidence is on the parent page (see Disease family below).

At a glance

• Prevalence: >1 / 1000 (United Kingdom) [Orphanet-validated]

Clinical features

Epidemiology

Prevalence records

1 prevalence record(s), Orphanet:

Type	Class	Value	Geography	Validation
Annual incidence	>1 / 1000	116	United Kingdom	Validated

Identifiers

Disease identifiers

Field	Value
Canonical name	hemolytic disease of the newborn with Kell alloimmunization
Mondo ID	MONDO:0017164
Orphanet	275944
UMLS	C0472751
MedGen	632769
GARD	0021038
Is cancer (heuristic)	no

Also known as: anti-K HDN · maternal anti-Kell alloimmunization

Disease family

This is a subtype of hemolytic anemia. 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 body system or component › hematologic disorder › anemia › normocytic anemia › hemolytic anemia › hemolytic disease of the newborn with Kell alloimmunization

Related subtypes (10): familial hemolytic anemia, Heinz body anemia, lethal hemolytic anemia-genital anomalies syndrome, hereditary elliptocytosis, Shiga toxin-associated hemolytic uremic syndrome, hereditary stomatocytosis, autoimmune hemolytic anemia, 6-phosphogluconate dehydrogenase deficiency, non-autoimmune hemolytic anemia, paroxysmal nocturnal hemoglobinuria

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.