Familial risks of glomerulonephritis – a nationwide family study in Sweden

Akrawi, Delshad Saleh; Li, Xinjun; Sundquist, Jan; Fjellstedt, Erik; Sundquist, Kristina; Zöller, Bengt

doi:10.3109/07853890.2016.1169316

Cited by 2 publications

(8 citation statements)

References 23 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…10 However, the present adoption study extends on our previous study as we have indicated that genetic factors are important in the familial transmission of glomerulonephritis. Shared familial environmental factors did not contribute significantly to the risk factors.…”

Section: Discussionsupporting

confidence: 75%

“…Existing knowledge regarding the involvement of common variants in the aetiology of glomerulonephritis is scarce although common variants have been associated with other kidney disorders. 10 A high familial relative risk (FRR) of glomerulonephritis was found in this Swedish study: FRR 3.57 for acute glomerulonephritis, FRR 3.84 for chronic glomerulonephritis and FRR 3.75 for unspecified glomerulonephritis. [2][3][4][5][6] Glomerulonephritis may run in families according to previous studies.…”

Section: Introductionmentioning

confidence: 57%

“…[7][8][9] Akrawi et al recently determined the familial risk of glomerulonephritis in a nationwide register-based family study conducted in Sweden. 10 A high familial relative risk (FRR) of glomerulonephritis was found in this Swedish study: FRR 3.57 for acute glomerulonephritis, FRR 3.84 for chronic glomerulonephritis and FRR 3.75 for unspecified glomerulonephritis. 10 Familial clustering might, however, be related to both genetic and shared environmental factors.…”

Section: Introductionmentioning

confidence: 57%

“…10 A high familial relative risk (FRR) of glomerulonephritis was found in this Swedish study: FRR 3.57 for acute glomerulonephritis, FRR 3.84 for chronic glomerulonephritis and FRR 3.75 for unspecified glomerulonephritis. 10 Familial clustering might, however, be related to both genetic and shared environmental factors. For instance, infections may induce glomerulonephritis and may also cluster in families.…”

Section: Introductionmentioning

confidence: 57%

“…These include as variants in the following genes: UMOD, PRKAG2, APOL1 and MYH9. 10 Familial clustering might, however, be related to both genetic and shared environmental factors. [7][8][9] Akrawi et al recently determined the familial risk of glomerulonephritis in a nationwide register-based family study conducted in Sweden.…”

Section: Introductionmentioning

confidence: 99%

See 4 more Smart Citations

Heritability of glomerulonephritis: A Swedish adoption study

Akrawi

Zöller

Fjellstedt

et al. 2019

Eur J Clin Investigation

Self Cite

View full text Add to dashboard Cite

Background: Glomerulonephritis clusters in families. However, infections are common inducers of glomerulonephritis and may also cluster in families. Studies of adoptees and their biological and adoptive parents may disentangle genetic from environmental causes of familial clustering. This is the first adoption study aimed to estimate the genetic contribution to the familial transmission of glomerulonephritis. Materials and methods: We performed a family study for Swedish-born adoptees (born 1945-2000) and their biological and adoptive parents. The Swedish Multi-Generation Register was linked to the Hospital Inpatient Register for the period 1964-2012 and the Hospital Outpatient Register for 2001-2012. Odds ratio (OR) for glomerulonephritis was determined for adoptees with a biological parent with glomerulonephritis compared with adoptees without an affected biological parent.Similarly, the OR for glomerulonephritis was also determined in adoptees with an affected adoptive parent compared with adoptees without an affected adoptive parent.Heritability was estimated to be twice the observed tetrachoric correlation among adoptees and biological parents, under the assumption that only additive genetic factors contribute to the similarity between biological parents and adoptees. Results: The OR for glomerulonephritis was 4.08 in adoptees (95% confidence interval [CI] 1.79-9.27, P-value = 0.001) of biological parents diagnosed with glomerulonephritis. The OR for glomerulonephritis was 1.67 in adoptees (95% CI 0.53-5.26, P-value = 0.380) of adoptive parents diagnosed with glomerulonephritis. The heritability was 48%. Conclusion: Family history of glomerulonephritis in a biological parent is a risk factor for glomerulonephritis. The present study indicates that genetic factors play an important role in the aetiology of glomerulonephritis. K E Y W O R D Sadoption, epidemiology, genetics, glomerulonephritis, kidney diseases 2 of 7 | AKRAWI et Al.

show abstract

Section: Discussionsupporting

confidence: 75%

Section: Introductionmentioning

confidence: 57%

Section: Introductionmentioning

confidence: 57%

Section: Introductionmentioning

confidence: 57%

Section: Introductionmentioning

confidence: 99%

See 3 more Smart Citations

Heritability of glomerulonephritis: A Swedish adoption study

Akrawi

Zöller

Fjellstedt

et al. 2019

Eur J Clin Investigation

Self Cite

View full text Add to dashboard Cite

show abstract

Epidemiology of Familial Aggregation of Venous Thromboembolism

Zöller

et al. 2016

Semin Thromb Hemost

Self Cite

View full text Add to dashboard Cite

Familial aggregation (clustering) of venous thromboembolism (VTE) is the clustering of VTE within a family. Though several genes, such as antithrombin, protein C, protein S, factor V, and prothrombin are associated with the familial clustering of VTE, these loci only partially explain the familial aggregation of VTE. The epidemiology of the familial aggregation of VTE exhibits typical characteristics of complex traits. The family history of VTE in first-degree relatives is associated with a two to three times increased familial relative risk (FRR). The FRR of VTE is higher in younger individuals, increases with a number of affected relatives, decreases as the familial relationship becomes more distant, increases with severity (unprovoked), and exhibits slightly stronger male transmission (Carter effect). High FRR is observed in individuals with two or more affected siblings (FRR > 50). Because familial aggregation represents the sum of shared family environmental and genetic factors, one should not assume that evidence of familial aggregation implies genetic effects. However, studies in twins, extended families, adoptees, and spouses indicate a weak involvement of shared environmental factors to the familial aggregation of VTE. Moreover, familial aggregation of VTE fulfills the Hill's criteria for causation. In conclusion, familial aggregation of VTE signals a clinically relevant inherent predisposition for VTE.

show abstract

Familial risks of glomerulonephritis – a nationwide family study in Sweden

Cited by 2 publications

References 23 publications

Heritability of glomerulonephritis: A Swedish adoption study

Heritability of glomerulonephritis: A Swedish adoption study

Epidemiology of Familial Aggregation of Venous Thromboembolism

Contact Info

Product

Resources

About