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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., (© 2019 Stichting European Society for Clinical Investigation Journal Foundation.)

Background/aims: The heritability of end-stage renal disease (ESRD) among adoptees has not been examined so far. By studying adoptees and their biological and adoptive parents, it is possible to differentiate between the genetic causes and environmental causes of familial aggregation. This nationwide study aimed to disentangle the genetic and shared environmental contribution to the familial transmission of ESRD., Methods: We performed a family study for Swedish-born adoptees (born between 1945 until 1995) and their biological and adoptive parents. The Swedish Multi-Generation Register was linked to the National Patient Registry for the period 1964-2012. ESRD was defined as patients in active uremic care, that is, chronic dialysis or kidney transplantation. OR for ESRD was determined for adoptees with an affected biological parent with ESRD compared with adoptees without a biological parent with ESRD. The OR for ESRD was also calculated in adoptees with an adoptive parent with ESRD compared with adoptees with an adoptive parent without ESRD. Moreover, heritability for ESRD was estimated with Falconer's regression., Results: A total of 111 adoptees, 463 adoptive parents, and 397 biological parents were affected by ESRD. The OR for ESRD was 6.41 in adoptees (95% CI 2.96-13.89) of biological parents diagnosed with ESRD. The OR for ESRD was 2.40 in adoptees (95% CI 0.76-7.60) of adoptive parents diagnosed with ESRD. The heritability of ESRD was 59.5 ± 18.2%., Conclusion: The family history of ESRD in a biological parent is an important risk factor for ESRD. The high heritability indicates that genetic factors play an important role in understanding the etiology of ESRD., (© 2017 S. Karger AG, Basel.)

Objective: Familial risks of glomerulonephritis (acute, chronic and unspecified glomerulonephritis) have not been studied. This study aims to determine the familial risks of glomerulonephritis., Methods: Individuals born from1932 onwards diagnosed with glomerulonephritis (acute [n = 7011], chronic [n = 10,242] and unspecified glomerulonephritis [n = 5762]) were included. The familial risk (Standardized incidence ratio = SIR) was calculated for individuals whose parents/full-siblings were diagnosed with glomerulonephritis compared to those whose parents/full-siblings were not. The procedure was repeated for spouses. Familial concordant risk (same disease in proband and exposed relative) and discordant risk (different disease in proband and exposed relative) of glomerulonephritis were determined., Results: Familial concordant risks (parents/full-sibling history) were: SIR = 3.57 (95% confidence interval, 2.77-4.53) for acute glomerulonephritis, SIR = 3.84 (3.37-4.36) for chronic glomerulonephritis and SIR = 3.75 (2.85-4.83) for unspecified glomerulonephritis. High familial risks were observed if two or more relatives were affected; the SIR was 209.83 (150.51-284.87) in individuals with at least one affected parent as well as one full-sibling. The spouse risk was only moderately increased (SIR = 1.53, 1.33-1.75)., Conclusions: Family history of glomerulonephritis is a strong predictor for glomerulonephritis, and is a potentially useful tool in clinical risk assessment. Our data emphasize the contribution of familial factors to the glomerulonephritis burden in the community. Key Messages The familial risks (full-sibling/parent history) of glomerulonephritis (acute, chronic and unspecified glomerulonephritis) have not been determined previously. The familial risks of glomerulonephritis were increased among individuals with family history of acute, chronic or unspecified glomerulonephritis. The familial risks of glomerulonephritis were slightly increased among spouses indicating a modest non-genetic contribution. Very high familial risks were observed in multiplex families, i.e. with one or more affected first-degree relatives.

Background: The value of family history as a risk factor for kidney failure has not been determined in a nationwide setting., Aim: This nationwide family study aimed to determine familial risks for kidney failure in Sweden., Methods: The Swedish multi-generation register on 0-78-year-old subjects were linked to the Swedish patient register and the Cause of death register for 1987-2010. Individuals diagnosed with acute kidney failure (n = 10063), chronic kidney failure (n = 18668), or unspecified kidney failure (n = 3731) were included. Kidney failure patients with cystic kidney disease, congenital kidney and urinary tract malformations, urolithiasis, and rare inherited kidney syndromes, and hyperoxaluria were excluded. Standardized incidence ratios (SIRs) were calculated for individuals whose parents/siblings were diagnosed with kidney failure compared to those whose parents or siblings were not., Results: The concordant (same disease) familial risks (sibling/parent history) were increased for chronic kidney failure SIR = 2.02 (95% confidence interval, CI 1.90-2.14) but not for acute kidney failure SIR = 1.08 (95% CI 0.94-1.22) and for unspecified kidney failure SIR = 1.25 (95% CI 0.94-1.63). However, the discordant (different disease) familial risk for acute kidney failure SIR = 1.19 (95% CI 1.06-1.32) and unspecified kidney failure SIR = 1.63 (95% CI 1.40-1.90) was significantly increased in individuals with a family history of chronic kidney failure. The familial risk for chronic kidney failure was similar for males SIR = 2.04 (95% CI 1.90-2.20) and females SIR = 1.97 (95% CI 1.78-2.17). Familial risks for chronic kidney failure were highest at age of 10-19 years SIR = 6.33 (95% CI 4.16-9.22)., Conclusions: The present study shows that family history is an important risk factor for chronic kidney failure but to a lower degree for acute kidney failure and unspecified kidney failure.

Background: Chronic kidney disease has been associated with socioeconomic disparities and neighbourhood deprivation. We aimed to determine whether there is an association between neighbourhood deprivation and end stage renal disease (ESRD), and whether this association is independent of individual-level sociodemographic factors and comorbidities., Methods: National Swedish data registers were used. The entire Swedish population aged 20-69 years was followed from January 1, 2001 until December 31, 2010. Data were analysed by multilevel logistic regression, with individual-level sociodemographic factors (age, marital status, family income, education level, country of birth, urban/rural status, and mobility) and comorbidities at the first level and neighbourhood deprivation at the second level., Results: Neighbourhood deprivation was significantly associated with ESRD (age-adjusted odds ratio [OR] 1.45, 95% confidence interval [CI] 1.34-1.56 in men and OR 1.59, 95% CI 1.44-1.75 in women). The ORs for ESRD in men and women living in the most deprived neighbourhoods remained significantly increased when adjusted for age and individual-level sociodemographic factors (OR 1.25, 95% CI 1.15-1.35 in men and OR 1.30, 95% CI 1.17-1.44 in women). In the full model, which took account of sociodemographic factors and comorbidities, the ORs for ESRD remained significantly increased (OR 1.17, 95% CI 1.07-1.27 in men and OR 1.18, 95% CI 1.06-1.31 in women)., Conclusion: Neighbourhood deprivation is independently associated with ESRD in both men and women irrespective of individual-level sociodemographic factors and comorbidities., (Copyright © 2014 European Federation of Internal Medicine. Published by Elsevier B.V. All rights reserved.)