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| Primary immunodeficiency or monogenic inflammatory bowel disease v9.18 | CFH |
Ida Ertmanska changed review comment from: PMID: 36211394 Gouda et al., 2022 Egyptian cohort of 40 patients with LN, lupus nephritis (23) or PIGN, post-infectious glomerulonephritis (17), tested for genetic variants in CFH and CD46 genes. VUS CFH:p.F614S variant was found in 28 (70%) of patients: 17 (74%) of LN patients, and 11 (65%) of PIGN patients. 3 Pathogenic CFH mutations were detected in a heterozygous state in LN patients: c.514C>T (p.Q172*), c.2103G>A (p.W701*), and c.3288G>A (p.W1096*). PMID: 35084692 Shears et al., 2022 Forty patients, median age 19 (range 3–62) years, were identified with terminal complement deficiencies. 2 White European patients had CFH variants and meningococcal infections and septicemia; 1 patient had non-meningococcal sepsis. Both were homozygous for CFH c.2T>C, p.Met1? variant (related?). PMID: 32064578 Brodszki et al., 2020 "Complement deficiencies account for ~5% of PIDs." <30 patients reported with CFH variants according to the lit review. PMID: 31440263 Sissy et al., 2019 13 patients reported with 7 different homozygous CFH variants and Factor H deficiency (primarily resulting in severe or multiple infections—mainly meningococcal infections—or severe autoimmune diseases). However, in this cohort, all 13 patients with CFH variants presented with kidney disease and no recurrent infections. PMID: 14978182 Dragon-Durey et al., 2004 Reported are 16 FH-deficient patients. Among six patients with homozygous deficiency, four presented with membranoproliferative glomerulonephritis, and two with atypical hemolytic uremic syndrome (HUS). The ten other patients had heterozygous FH deficiency and developed atypical HUS. No mention of recurring infections in these patients - authors pose that previously reported susceptibility to meningococcal disease is secondary to acquired C3 or C5-C9 deficiencies. Functional: PMID: 12091909 Pickering et al., 2002 - mouse Cfh knockout caused membranoproliferative glomerulonephritis, seen at 8 months old. CFH is associated with AD,AR Complement factor H deficiency, OMIM:609814 and AD, AR {Hemolytic uremic syndrome, atypical, susceptibility to, 1}, OMIM:235400, among others (OMIM accessed 22nd Jun 2026). The association between CFH and semidominant atypical hemolytic-uremic syndrome is Definitive in ClinGen (Complement-Mediated Kidney Diseases GCEP, July 2023); CFH-related AR C3 glomerulonephritis is also Definitive (Complement-Mediated Kidney Diseases GCEP, Feb 2024).; to: PMID: 36211394 Gouda et al., 2022 Egyptian cohort of 40 patients with LN, lupus nephritis (23) or PIGN, post-infectious glomerulonephritis (17), tested for genetic variants in CFH and CD46 genes. VUS CFH:p.F614S variant was found in 28 (70%) of patients: 17 (74%) of LN patients, and 11 (65%) of PIGN patients. 3 Pathogenic CFH mutations were detected in a heterozygous state in LN patients: c.514C>T (p.Q172*), c.2103G>A (p.W701*), and c.3288G>A (p.W1096*). PMID: 35084692 Shears et al., 2022 Forty patients, median age 19 (range 3–62) years, were identified with terminal complement deficiencies. 2 White European patients had CFH variants and meningococcal infections and septicemia; 1 of these patients also had non-meningococcal sepsis. Both were homozygous for CFH c.2T>C, p.Met1? variant (related?). PMID: 32064578 Brodszki et al., 2020 "Complement deficiencies account for ~5% of PIDs." <30 patients reported with CFH variants according to the lit review. PMID: 31440263 Sissy et al., 2019 13 patients reported with 7 different homozygous CFH variants and Factor H deficiency (primarily resulting in severe or multiple infections—mainly meningococcal infections—or severe autoimmune diseases). However, in this cohort, all 13 patients with CFH variants presented with kidney disease and no recurrent infections. PMID: 14978182 Dragon-Durey et al., 2004 Reported are 16 FH-deficient patients. Among six patients with homozygous deficiency, four presented with membranoproliferative glomerulonephritis, and two with atypical hemolytic uremic syndrome (HUS). The ten other patients had heterozygous FH deficiency and developed atypical HUS. No mention of recurring infections in these patients - authors pose that previously reported susceptibility to meningococcal disease is secondary to acquired C3 or C5-C9 deficiencies. Functional: PMID: 12091909 Pickering et al., 2002 - mouse Cfh knockout caused membranoproliferative glomerulonephritis, seen at 8 months old. CFH is associated with AD,AR Complement factor H deficiency, OMIM:609814 and AD, AR {Hemolytic uremic syndrome, atypical, susceptibility to, 1}, OMIM:235400, among others (OMIM accessed 22nd Jun 2026). The association between CFH and semidominant atypical hemolytic-uremic syndrome is Definitive in ClinGen (Complement-Mediated Kidney Diseases GCEP, July 2023); CFH-related AR C3 glomerulonephritis is also Definitive (Complement-Mediated Kidney Diseases GCEP, Feb 2024). |
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| Primary immunodeficiency or monogenic inflammatory bowel disease v9.9 | CFH |
Ida Ertmanska changed review comment from: PMID: 36211394 Gouda et al., 2022 Egyptian cohort of 40 patients with LN, lupus nephritis (23) or PIGN, post-infectious glomerulonephritis (17), tested for genetic variants in CFH and CD46 genes. VUS CFH:p.F614S variant was found in 28 (70%) of patients: 17 (74%) of LN patients, and 11 (65%) of PIGN patients. 3 Pathogenic CFH mutations were detected in a heterozygous state in LN patients: c.514C>T (p.Q172*), c.2103G>A (p.W701*), and c.3288G>A (p.W1096*). PMID: 35084692 Shears et al., 2022 Forty patients, median age 19 (range 3–62) years, were identified with terminal complement deficiencies. 2 White European patients had CFH variants and meningococcal infections and septicemia; 1 patient had non-meningococcal sepsis. Both were homozygous for CFH c.2T>C, p.Met1? variant (related?). PMID: 32064578 Brodszki et al., 2020 "Complement deficiencies account for ~5% of PIDs." <30 patients reported with CFH variants according to the lit review. PMID: 31440263 Sissy et al., 2019 13 patients reported with 7 different homozygous CFH variants and Factor H deficiency (primarily resulting in severe or multiple infections—mainly meningococcal infections—or severe autoimmune diseases). However, in this cohort, all 13 patients with CFH variants presented with kidney disease and no recurrent infections. PMID: 14978182 Dragon-Durey et al., 2004 Reported are 16 FH-deficient patients. Among six patients with homozygous deficiency, four presented with membranoproliferative glomerulonephritis, and two with atypical hemolytic uremic syndrome (HUS). The ten other patients had heterozygous FH deficiency and developed atypical HUS. CFH is associated with AD,AR Complement factor H deficiency, OMIM:609814 and AD, AR {Hemolytic uremic syndrome, atypical, susceptibility to, 1}, OMIM:235400, among others (OMIM accessed 22nd Jun 2026). The association between CFH and semidominant atypical hemolytic-uremic syndrome is Definitive in ClinGen (Complement-Mediated Kidney Diseases GCEP, July 2023); CFH-related AR C3 glomerulonephritis is also Definitive (Complement-Mediated Kidney Diseases GCEP, Feb 2024).; to: PMID: 36211394 Gouda et al., 2022 Egyptian cohort of 40 patients with LN, lupus nephritis (23) or PIGN, post-infectious glomerulonephritis (17), tested for genetic variants in CFH and CD46 genes. VUS CFH:p.F614S variant was found in 28 (70%) of patients: 17 (74%) of LN patients, and 11 (65%) of PIGN patients. 3 Pathogenic CFH mutations were detected in a heterozygous state in LN patients: c.514C>T (p.Q172*), c.2103G>A (p.W701*), and c.3288G>A (p.W1096*). PMID: 35084692 Shears et al., 2022 Forty patients, median age 19 (range 3–62) years, were identified with terminal complement deficiencies. 2 White European patients had CFH variants and meningococcal infections and septicemia; 1 patient had non-meningococcal sepsis. Both were homozygous for CFH c.2T>C, p.Met1? variant (related?). PMID: 32064578 Brodszki et al., 2020 "Complement deficiencies account for ~5% of PIDs." <30 patients reported with CFH variants according to the lit review. PMID: 31440263 Sissy et al., 2019 13 patients reported with 7 different homozygous CFH variants and Factor H deficiency (primarily resulting in severe or multiple infections—mainly meningococcal infections—or severe autoimmune diseases). However, in this cohort, all 13 patients with CFH variants presented with kidney disease and no recurrent infections. PMID: 14978182 Dragon-Durey et al., 2004 Reported are 16 FH-deficient patients. Among six patients with homozygous deficiency, four presented with membranoproliferative glomerulonephritis, and two with atypical hemolytic uremic syndrome (HUS). The ten other patients had heterozygous FH deficiency and developed atypical HUS. No mention of recurring infections in these patients - authors pose that previously reported susceptibility to meningococcal disease is secondary to acquired C3 or C5-C9 deficiencies. Functional: PMID: 12091909 Pickering et al., 2002 - mouse Cfh knockout caused membranoproliferative glomerulonephritis, seen at 8 months old. CFH is associated with AD,AR Complement factor H deficiency, OMIM:609814 and AD, AR {Hemolytic uremic syndrome, atypical, susceptibility to, 1}, OMIM:235400, among others (OMIM accessed 22nd Jun 2026). The association between CFH and semidominant atypical hemolytic-uremic syndrome is Definitive in ClinGen (Complement-Mediated Kidney Diseases GCEP, July 2023); CFH-related AR C3 glomerulonephritis is also Definitive (Complement-Mediated Kidney Diseases GCEP, Feb 2024). |
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| Primary immunodeficiency or monogenic inflammatory bowel disease v2.536 | SLC9A3 | Arina Puzriakova reviewed gene: SLC9A3: Rating: AMBER; Mode of pathogenicity: ; Publications: ; Phenotypes: ; Mode of inheritance: | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v2.535 | SLC9A3 |
Arina Puzriakova Added phenotypes Diarrhea 8, secretory sodium, congenital, OMIM:616868 for gene: SLC9A3 Publications for gene: SLC9A3 were updated from 26358773; 33346580 to 26358773; 31276831; 30633106; 33346580 |
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| Primary immunodeficiency or monogenic inflammatory bowel disease v2.400 | SLC9A3 | Ivone Leong Classified gene: SLC9A3 as Amber List (moderate evidence) | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v2.400 | SLC9A3 | Ivone Leong Gene: slc9a3 has been classified as Amber List (Moderate Evidence). | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v2.399 | SLC9A3 | Ivone Leong Phenotypes for gene: SLC9A3 were changed from Very Early Onset Inflammatory Bowel Disease; Congenital sodium diarrhoea to Very Early Onset Inflammatory Bowel Disease; Diarrhea 8, secretory sodium, congenital, OMIM:616868 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v2.396 | SLC9A3 | Ivone Leong Publications for gene: SLC9A3 were set to PMID: 26358773 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v2.392 | SLC9A3 |
Kelsey Jones gene: SLC9A3 was added gene: SLC9A3 was added to Primary immunodeficiency. Sources: Expert Review Mode of inheritance for gene: SLC9A3 was set to BIALLELIC, autosomal or pseudoautosomal Publications for gene: SLC9A3 were set to PMID: 26358773 Phenotypes for gene: SLC9A3 were set to Very Early Onset Inflammatory Bowel Disease; Congenital sodium diarrhoea Penetrance for gene: SLC9A3 were set to Incomplete Review for gene: SLC9A3 was set to AMBER Added comment: Described as a monogenic cause of VEOIBD (recognised criteria for the R15 panel). 2 patients from unrelated families in a series of 9 cases with SLC9A3-related congenital sodium diarrhoea developed intestinal inflammation/IBD (PMID: 26358773). GWAS have indicated a strong association between SLC9A3 and IBD, and there are supportive mouse models (reviewed in PMID: 26358773).Included on a monogenic IBD gene panel proposed by The Paediatric IBD Porto Group of ESPGHAN (PMID: 33346580). Sources: Expert Review |
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| Primary immunodeficiency or monogenic inflammatory bowel disease v1.94 | UNC93B1 | Louise Daugherty commented on gene: UNC93B1: Gene rating submitted by Kimberly Gilmour and Austen Worth on behalf of London North GLH for the GMS Immunology specialist test group. As discussed with the GMS Immunology Specialist Test Group during webex call 28th March 2019 and confirmed in follow up email 6th September the Specialist Test Group all agreed there is enough evidence to rate this gene Green. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v1.94 | C9 | Louise Daugherty commented on gene: C9: Gene rating submitted by Kimberly Gilmour and Austen Worth on behalf of London North GLH for the GMS Immunology specialist test group. As discussed with the GMS Immunology Specialist Test Group during webex call 28th March 2019 and confirmed in follow up email 6th September the Specialist Test Group all agreed there is enough evidence to rate this gene Green. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v1.94 | UNC93B1 | Louise Daugherty commented on gene: UNC93B1: Gene rating submitted by Tracy Briggs, David Gokhale and Abigal Rousseau on behalf of North West GLH for the GMS Immunology specialist test group. As discussed with the GMS Immunology Specialist Test Group during webex call 28th March 2019 and confirmed in follow up email on 20th June the Specialist Test Group all agreed there is enough evidence to rate this gene Green. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v1.94 | C9 | Louise Daugherty commented on gene: C9: Gene rating submitted by Tracy Briggs, David Gokhale and Abigal Rousseau on behalf of North West GLH for the GMS Immunology specialist test group. As discussed with the GMS Immunology Specialist Test Group during webex call 28th March 2019 and confirmed in follow up email on 20th June the Specialist Test Group all agreed there is enough evidence to rate this gene Green. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v1.94 | UNC93B1 | Kimberly Gilmour reviewed gene: UNC93B1: Rating: GREEN; Mode of pathogenicity: ; Publications: ; Phenotypes: ; Mode of inheritance: | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v1.94 | C9 | Kimberly Gilmour reviewed gene: C9: Rating: GREEN; Mode of pathogenicity: ; Publications: ; Phenotypes: ; Mode of inheritance: | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v1.94 | UNC93B1 | Tracy Briggs reviewed gene: UNC93B1: Rating: GREEN; Mode of pathogenicity: ; Publications: ; Phenotypes: ; Mode of inheritance: | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v1.94 | C9 | Tracy Briggs reviewed gene: C9: Rating: GREEN; Mode of pathogenicity: ; Publications: ; Phenotypes: ; Mode of inheritance: | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v1.60 | UNC93B1 | Louise Daugherty Source NHS GMS was added to UNC93B1. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v1.60 | C9 | Louise Daugherty Source NHS GMS was added to C9. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v1.59 | UNC93B1 | Louise Daugherty Source North West GLH was added to UNC93B1. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v1.59 | C9 | Louise Daugherty Source North West GLH was added to C9. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v1.58 | UNC93B1 | Louise Daugherty Source London North GLH was added to UNC93B1. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease v1.58 | C9 | Louise Daugherty Source London North GLH was added to C9. | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | UNC93B1 | Louise Daugherty marked gene: UNC93B1 as ready | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | UNC93B1 | Louise Daugherty edited their review of gene: UNC93B1 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | C9 | Louise Daugherty commented on gene: C9 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | UNC93B1 | Sophie Hambleton reviewed gene: UNC93B1 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | UNC93B1 | Eleanor Williams classified UNC93B1 as Green List (high evidence) | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | UNC93B1 | Eleanor Williams commented on gene: UNC93B1 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | C9 | Louise Daugherty marked gene: C9 as ready | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | C9 | Louise Daugherty classified C9 as Green List (high evidence) | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | C9 | Louise Daugherty edited their review of gene: C9 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | C9 | Sophie Hambleton reviewed gene: C9 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | C9 | Louise Daugherty commented on C9 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | UNC93B1 | Louise Daugherty classified UNC93B1 as Amber List (moderate evidence) | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | UNC93B1 | Louise Daugherty commented on UNC93B1 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | UNC93B1 | Louise Daugherty commented on UNC93B1 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | C9 | Louise Daugherty commented on C9 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | UNC93B1 | Louise Daugherty commented on UNC93B1 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | C9 | Louise Daugherty commented on C9 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | UNC93B1 | Louise Daugherty reviewed UNC93B1 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | C9 | Louise Daugherty reviewed C9 | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | C9 | Louise Daugherty Added gene to panel | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
| Primary immunodeficiency or monogenic inflammatory bowel disease | C9 | Louise Daugherty Added gene to panel | |||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||