{{Rsnum
|rsid=2015352
|Gene=CLCNKB
|Chromosome=1
|position=16044572
|Orientation=plus
|ReferenceAllele=G
|MissenseAllele=T
|GMAF=0.4036
|Assembly=GRCh38
|GenomeBuild=38.1
|dbSNPBuild=141
|geno1=(G;G)
|geno2=(G;T)
|geno3=(T;T)
|Gene_s=CLCNKB
}}{{ population diversity
| geno1=(G;G)
| geno2=(G;T)
| geno3=(T;T)
| CEU | 0.0 | 0.0 | 0.0
| HCB | 0.0 | 2.2 | 97.8
| JPT | 0.0 | 0.0 | 100.0
| YRI | 0.0 | 0.0 | 0.0
| ASW | 0.0 | 0.0 | 0.0
| CHB | 0.0 | 2.2 | 97.8
| CHD | 0.0 | 0.0 | 0.0
| GIH | 0.0 | 0.0 | 0.0
| LWK | 0.0 | 0.0 | 0.0
| MEX | 0.0 | 0.0 | 0.0
| MKK | 0.0 | 0.0 | 0.0
| TSI | 0.0 | 0.0 | 0.0
| HapMapRevision=28
}}

{{Venter SNP
|rsid=2015352
|allele=T
|frequency=
|uid=1103675030547
|type=homozygous_SNP
|hugo=CLCNKB
|ensembl gene=ENSG00000184908
|ensembl transcript=ENST00000375679
|sift=AFFECT FUNCTION
|disease=Defects in CLCNKB are a cause of Bartter syndrome type 3 (BS type 3) (MIM:607364); also known as classic Bartter syndrome. It is an autosomal recessive form of often severe intravascular volume depletion due to renal salt-wasting associated with low blood pressure, hypokalemic alkalosis, hypercalciuria, and normal serum magnesium levels.
}}

{{GET Evidence
|gene=CLCNKB
|aa_change=Arg27Leu
|aa_change_short=R27L
|impact=not reviewed
|qualified_impact=Insufficiently evaluated not reviewed
|inheritance=unknown
|quality_scores=Array
|dbsnp_id=rs2015352
|overall_frequency_n=5621
|overall_frequency_d=10754
|overall_frequency=0.522689
|n_genomes=38
|n_genomes_annotated=0
|n_haplomes=57
|n_articles=0
|n_articles_annotated=0
|qualityscore_in_silico=1
|qualitycomment_in_silico=Y
|gene_in_genetests=Y
|genetests_testable=Y
|nblosum100=6
|autoscore=1
|webscore=N
}}
{{on chip | 23andMe v3}}