Search

Understanding the genetics of kidney function decline, or trait change in general, is hampered by scarce longitudinal data for GWAS (longGWAS) and uncertainty about how to analyze such data. We use longitudinal UK Biobank data for creatinine-based estimated glomerular filtration rate from 348,275 individuals to search for genetic variants associated with eGFR-decline. This search was performed both among 595 variants previously associated with eGFR in cross-sectional GWAS and genome-wide. We use seven statistical approaches to analyze the UK Biobank data and simulated data, finding that a linear mixed model is a powerful approach with unbiased effect estimates which is viable for longGWAS. The linear mixed model identifies 13 independent genetic variants associated with eGFR-decline, including 6 novel variants, and links them to age-dependent eGFR-genetics. We demonstrate that age-dependent and age-independent eGFR-genetics exhibit a differential pattern regarding clinical progression traits and kidney-specific gene expression regulation. Overall, our results provide insights into kidney aging and linear mixed model-based longGWAS generally. The authors use longitudinal data from the UK Biobank to search for genetic variants associated with kidney function decline. Using a linear mixed model, they identify 13 independent variants, incl. 6 novel, and link them to genetics of kidney aging. [ABSTRACT FROM AUTHOR]

Mitochondrial DNA copy number (mtDNA-CN) is a biomarker for mitochondrial dysfunction associated with several diseases. Previous genome-wide association studies (GWAS) have been performed to unravel underlying mechanisms of mtDNA-CN regulation. However, the identified gene regions explain only a small fraction of mtDNA-CN variability. Most of this data has been estimated from microarrays based on various pipelines. In the present study we aimed to (1) identify genetic loci for qPCR-measured mtDNA-CN from three studies (16,130 participants) using GWAS, (2) identify potential systematic differences between our qPCR derived mtDNA-CN measurements compared to the published microarray intensity-based estimates, and (3) disentangle the nuclear from mitochondrial regulation of the mtDNA-CN phenotype. We identified two genome-wide significant autosomal loci associated with qPCR-measured mtDNA-CN: at HBS1L (rs4895440, p = 3.39 × 10–13) and GSDMA (rs56030650, p = 4.85 × 10–08) genes. Moreover, 113/115 of the previously published SNPs identified by microarray-based analyses were significantly equivalent with our findings. In our study, the mitochondrial genome itself contributed only marginally to mtDNA-CN regulation as we only detected a single rare mitochondrial variant associated with mtDNA-CN. Furthermore, we incorporated mitochondrial haplogroups into our analyses to explore their potential impact on mtDNA-CN. However, our findings indicate that they do not exert any significant influence on our results. [ABSTRACT FROM AUTHOR]

Children play an important role in hepatitis A virus (HAV) transmission but, due to frequent asymptomatic or mild courses, these infections are underrecognized in routine surveillance. Here, we analyzed hepatitis A (HA) seroprevalence, vaccination status and demographic determinants and estimated previous HAV infections in a cross-sectional population-based study of children and adolescents with residence in Germany 2014–2017, performing weighted univariable and multivariable logistic regression. Of 3567 participants aged 3–17 years, serological results were available for 3013 (84.5%), vaccination records for 3214 (90.1%) and both for 2721 (76.3%). Of 2721 with complete results, 467 (17.2%) were seropositive, thereof 412 (15.1%) with and 55 (2.0%) without previous HA vaccination, indicating previous HAV infection. Seropositivity was associated with age, residence in Eastern states, high socioeconomic status and migration background with personal migration experience. Participants with migration background and personal migration experience also had the highest odds ratios for previous HAV infection. Germany remains a country with very low HA endemicity. The current vaccination recommendations focusing on individuals with a high risk for HAV exposure (e.g. travelers to endemic countries) or severe disease appear appropriate. Migration and travel patterns as well as the endemicity in other countries influence the domestic situation, warranting further monitoring. [ABSTRACT FROM AUTHOR]

Tachycardiomyopathy is characterised by reversible left ventricular dysfunction, provoked by rapid ventricular rate. While the knowledge of mitochondria advanced in most cardiomyopathies, mitochondrial functions await elucidation in tachycardiomyopathy. Pacemakers were implanted in 61 rabbits. Tachypacing was performed with 330 bpm for 10 days (n = 11, early left ventricular dysfunction) or with up to 380 bpm over 30 days (n = 24, tachycardiomyopathy, TCM). In n = 26, pacemakers remained inactive (SHAM). Left ventricular tissue was subjected to respirometry, metabolomics and acetylomics. Results were assessed for translational relevance using a human-based model: induced pluripotent stem cell derived cardiomyocytes underwent field stimulation for 7 days (TACH–iPSC–CM). TCM animals showed systolic dysfunction compared to SHAM (fractional shortening 37.8 ± 1.0% vs. 21.9 ± 1.2%, SHAM vs. TCM, p < 0.0001). Histology revealed cardiomyocyte hypertrophy (cross-sectional area 393.2 ± 14.5 µm2 vs. 538.9 ± 23.8 µm2, p < 0.001) without fibrosis. Mitochondria were shifted to the intercalated discs and enlarged. Mitochondrial membrane potential remained stable in TCM. The metabolite profiles of ELVD and TCM were characterised by profound depletion of tricarboxylic acid cycle intermediates. Redox balance was shifted towards a more oxidised state (ratio of reduced to oxidised nicotinamide adenine dinucleotide 10.5 ± 2.1 vs. 4.0 ± 0.8, p < 0.01). The mitochondrial acetylome remained largely unchanged. Neither TCM nor TACH–iPSC–CM showed relevantly increased levels of reactive oxygen species. Oxidative phosphorylation capacity of TCM decreased modestly in skinned fibres (168.9 ± 11.2 vs. 124.6 ± 11.45 pmol·O2·s−1·mg−1 tissue, p < 0.05), but it did not in isolated mitochondria. The pattern of mitochondrial dysfunctions detected in two models of tachycardiomyopathy diverges from previously published characteristic signs of other heart failure aetiologies. [ABSTRACT FROM AUTHOR]

Surveillance of notified Campylobacter enteritis in Germany revealed a recurrent annual increase of cases with disease onset several days after the Christmas and New Year holidays ("winter peak"). We suspected that handling and consumption of chicken meat during fondue and raclette grill meals on the holidays were associated with winter peak Campylobacter infections. The hypothesis was investigated in a case–control study with a case-case design where notified Campylobacter enteritis cases served as case-patients as well as control-patients, depending on their date of disease onset (case-patients: 25/12/2018 to 08/01/2019; control-patients: any other date between 30/11/2018 and 28/02/2019). The study was conducted as an online survey from 21/01/2019 to 18/03/2019. Adjusted odds ratios (aOR) were determined in single-variable logistic regression analyses adjusted for age group and sex. We analysed 182 data sets from case-patients and 260 from control-patients and found associations of Campylobacter infections after the holidays with meat fondue (aOR 2.2; 95% confidence interval (CI) 1.2–3.8) and raclette grill meals with meat (aOR 1.5; 95% CI 1.0–2.4) consumed on the holidays. The associations were stronger when chicken meat was served at these meals (fondue with chicken meat: aOR 2.7; 95% CI 1.4–5.5; raclette grill meal with chicken meat: aOR 2.3; 95% CI 1.3–4.1). The results confirmed our initial hypothesis. To prevent Campylobacter winter peak cases in the future, consumers should be made more aware of the risks of a Campylobacter infection when handling raw meat, in particular chicken, during fondue or raclette grill meals on the holidays. [ABSTRACT FROM AUTHOR]

Borna disease virus-1 (BoDV-1) was recently discovered as cause of severe and often fatal encephalitis in humans. BoDV-1 is known to cause neurological disease in horses and sheep mainly in South and Central Germany. The virus is maintained in bicolored white-toothed shrews (Crocidura leucodon). The incidence of infection and risk factors in humans are completely unresolved. Veterinarians may be disproportionally BoDV-1-exposed through contact to animals not recognized to be BoDV-1 infected. We conducted three serosurveys predominantly in endemic areas of South Germany for the presence of BoDV-1-reactive antibodies. Anonymized residual samples from two serosurveys of veterinarians (n = 736) with interview data on exposures and one serosurvey among blood donors (n = 373) were screened with an indirect immunofluorescence antibody test, followed by a newly developed immunoblot as confirmatory assay. One serum from a 55–59-year-old veterinarian who worked in an animal practice and as a meat inspector but none from blood donors tested positive by the screening and confirmatory assays. We show that seropositive individuals are rare even in areas with highest zoonotic risk and in a group with potentially elevated exposure risk. In light of the low seroprevalence demonstrated here, the high case-fatality rate in clinically observed human BoDV-1 infections is even more impressive. [ABSTRACT FROM AUTHOR]

Purpose: Alveolar echinococcosis is a rare disease caused by the parasite Echinococcus multilocularis. The newly established national database should enable us to determine high-risk areas and evaluate the endemic levels.Methods: The national database was implemented using SQL Workbench. We used EpiInfo™ software to display the prevalence of disease. Moran’s I geodata analysis according to cluster and high risk areas was performed with GeoDa™. SAS Version 9.2 was used for the statistical analysis of the cases (n = 523).Results: The analysis showed a concentration of cases in Baden-Württemberg and Bavaria. Moran’s I showed a heterogeneous case distribution throughout Germany (I = 0.208815, Z = 32.6175, p < 0.001). In the period from 1992 to 2016, the prevalence was 0.64/100,000 inhabitants in the whole of Germany, 2.18/100,000 inhabitants in Baden-Württemberg and 1.48/100,000 inhabitants in Bavaria. The analysis also revealed a difference between men and women, with a prevalence of 0.58/100,000 and 0.69/100,000, respectively. The analysis of spatial autocorrelation and possible risk areas showed that the southeast regions of Baden-Württemberg (I = 0.188514, Z = 11.3197, p < 0.001) and the southwest part of Bavaria (I = 0.176953, Z = 13.5144, p < 0.001) constitute the high risk areas.Conclusions: The prevalence of disease is noticeably high in the Swabian Jura, the Bavarian Alps and the Alpine foothills. Raising awareness and educating doctors in high risk areas may prevent new cases and assist in earlier diagnosis. [ABSTRACT FROM AUTHOR]

An amendment to this paper has been published and can be accessed via a link at the top of the paper. [ABSTRACT FROM AUTHOR]

Myocardial infarction, a leading cause of death in the Western world, usually occurs when the fibrous cap overlying an atherosclerotic plaque in a coronary artery ruptures. The resulting exposure of blood to the atherosclerotic material then triggers thrombus formation, which occludes the artery. The importance of genetic predisposition to coronary artery disease and myocardial infarction is best documented by the predictive value of a positive family history. Next-generation sequencing in families with several affected individuals has revolutionized mutation identification. Here we report the segregation of two private, heterozygous mutations in two functionally related genes, GUCY1A3 (p.Leu163Phefs*24) and CCT7 (p.Ser525Leu), in an extended myocardial infarction family. GUCY1A3 encodes the α1 subunit of soluble guanylyl cyclase (α1-sGC), and CCT7 encodes CCTη, a member of the tailless complex polypeptide 1 ring complex, which, among other functions, stabilizes soluble guanylyl cyclase. After stimulation with nitric oxide, soluble guanylyl cyclase generates cGMP, which induces vasodilation and inhibits platelet activation. We demonstrate in vitro that mutations in both GUCY1A3 and CCT7 severely reduce α1-sGC as well as β1-sGC protein content, and impair soluble guanylyl cyclase activity. Moreover, platelets from digenic mutation carriers contained less soluble guanylyl cyclase protein and consequently displayed reduced nitric-oxide-induced cGMP formation. Mice deficient in α1-sGC protein displayed accelerated thrombus formation in the microcirculation after local trauma. Starting with a severely affected family, we have identified a link between impaired soluble-guanylyl-cyclase-dependent nitric oxide signalling and myocardial infarction risk, possibly through accelerated thrombus formation. Reversing this defect may provide a new therapeutic target for reducing the risk of myocardial infarction. [ABSTRACT FROM AUTHOR]

Fibroblast growth factor 21 (FGF21) is a novel master regulator of metabolic profile. The biological actions of FGF21 are elicited upon its klotho beta (KLB)-facilitated binding to FGF receptor 1 (FGFR1), FGFR2 and FGFR3. We hypothesised that common polymorphisms in the FGF21 signalling pathway may be associated with metabolic risk. At the screening stage, we examined associations between 63 common single-nucleotide polymorphisms (SNPs) in five genes of this pathway (FGF21, KLB, FGFR1, FGFR2, FGFR3) and four metabolic phenotypes (LDL cholesterol - LDL-C, HDL-cholesterol - HDL-C, triglycerides and body mass index) in 629 individuals from Silesian Hypertension Study (SHS). Replication analyses were performed in 5478 unrelated individuals of the Swiss CoLaus cohort (imputed genotypes) and in 3030 directly genotyped individuals of the German Myocardial Infarction Family Study (GerMIFS). Of 54 SNPs that met quality control criteria after genotyping in SHS, 4 (rs4733946 and rs7012413 in FGFR1; rs2071616 in FGFR2 and rs7670903 in KLB) showed suggestive association with LDL-C (P=0.0006, P=0.0013, P=0.0055, P=0.011, respectively) and 1 (rs2608819 in KLB) was associated with body mass index (P=0.011); all with false discovery rate q<0.5. Of these, only one FGFR2 polymorphism (rs2071616) showed replicated association with LDL-C in both CoLaus (P=0.009) and men from GerMIFS (P=0.017). The direction of allelic effect of rs2071616 upon LDL-C was consistent in all examined populations. These data show that common genetic variations in FGFR2 may be associated with LDL-C in subjects of white European ancestry. [ABSTRACT FROM AUTHOR]

Through genome-wide association studies, we have recently identified seven novel loci that confer a substantial increase in risk for coronary artery disease (CAD). Elucidating the mechanisms by which these loci affect CAD risk could have important clinical utility. Here, we investigated whether these loci act through mechanisms involving traditional cardiovascular risk factors. We genotyped 2,037 adult individuals from 520 nuclear families characterised for body mass index, waist-hip ratio, 24-h ambulatory blood pressure, total cholesterol, high-density lipoprotein cholesterol and glucose for the lead single nucleotide polymorphisms (SNPs) in the seven CAD-associated loci. SNP rs599839, representing the locus in the vicinity of the PSRC1 and CELSR2 genes on chromosome 1p13.3, showed a strong association with total cholesterol. The CAD-associated risk allele A of rs599839 (allele frequency 0.78) was associated with a 0.17-mmol/l (95% CI 0.10 to 0.24 mmol/l) higher serum cholesterol level per allele copy ( P = 3.84 × 10−6). The association of the A allele with higher total cholesterol was confirmed in an independent cohort ( n = 847) of healthy adults ( P = 1.0 × 10−4) and related to an effect on low-density lipoprotein (LDL) cholesterol ( P = 8.56 × 10−5). An association of rs599839 with LDL cholesterol was also shown in 1,090 cases with myocardial infarction ( P = 0.0026). None of the other variants showed a strong association with the measured cardiovascular risk factors, suggesting that these loci act through other mechanisms. However, the novel CAD-associated locus in the vicinity of the PSRC1 and CELSR2 genes on chromosome 1 probably enhances CAD risk through an effect on plasma LDL cholesterol. The findings support further investigation of the role of these genes in cholesterol metabolism and coronary risk. [ABSTRACT FROM AUTHOR]

Recent data provided strong evidence for the association of single nucleotide polymorphisms (SNPs) in the lymphotoxin-α (LTA) and galectin-2 (LGALS2) genes with myocardial infarction (MI) in a Japanese population. For populations of other genetic background, the relevance of these polymorphisms in the pathogenesis of MI remains controversial. We aimed to define the role of LTA and LGALS2 SNPs in two German MI populations with markedly different ascertainment strategies. Two different MI populations were studied. In the first population, MI patients were ascertained by a strong family history of MI ( n = 1214). Controls were unrelated disease-free participants of the study ( n = 1080). The second population included patients suffering from sporadic (nonfamilial) MI from the German KORA register ( n = 607). The control group consisted of participants of the WHO MONICA survey in Germany ( n = 1492). TaqMan assays were used to determine the genotypes of 4 SNPs in the LTA genomic region and 1 SNP in the LGALS2 gene. Single SNPs in both genomic regions as well as haplotypes in the LTA genomic region were tested for association in various models of inheritance. No association with MI could be found for any of the examined SNPs in the LTA genomic region and LGALS2 gene, or for haplotypes spanning the LTA genomic region. In two MI populations of European descent with markedly different ascertainment strategies, we were not able to identify a significant association of SNPs in the LTA genomic region or the LGALS2 gene with MI. These variants are unlikely to play a significant role in populations of European origin. [ABSTRACT FROM AUTHOR]

In Volvox carteri, regA acts as a master gene to suppress all germ cell functions in somatic cells. Its product, RegA, has features of a transcriptional repressor. Here we report cDNA sequences representing 15 nuclear genes with properties expected of RegA targets: they are expressed strongly in germ cells and in regA−, but not regA+, somatic cells. Two of them encode polypeptides with no recognizable features, but ten (like three previously sequenced ones) encode chloroplast proteins of known function, and the remaining three encode putative chloroplast proteins of unknown function. This suggests that RegA blocks reproductive development in somatic cells by preventing chloroplast biogenesis, thereby making it impossible for the cells to grow enough to reproduce. [ABSTRACT FROM AUTHOR]

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To assess the sensitivity and specificity of HIV antibody detection in saliva we tested matched serum and saliva samples from HIV-infected and uninfected individuals. Saliva specimens were collected by two different devices of the Salivette system and stored at different temperatures. Samples were tested for HIV antibodies by two commercially available enzyme-linked immunosorbent assays (ELISAs; Wellcome, Biotest). HIV antibodies were detected in 98.5% (Wellcome) and 97.8% (Biotest) of the saliva samples (standard Salivettes) from 135 seropositive individuals. Using the Salivettes flavoured with citric acid the sensitivity was only 22.9%. No reactions in ELISA were found in saliva from HIV-seronegative individuals. Salivary HIV-specific IgA was detected in 90% of seropositive individuals. All positive saliva samples stored at room temperature were still reactive after 20 days; of those stored at 37°C, 23 out of 24 were positive when retested on day 5. Sensitivity of HIV antibody detection in saliva samples dried onto filter paper was 100% when a minimum of 100 μl of saliva was used. HIV antibody testing in saliva is an efficient tool for large scale epidemiological studies when standard Salivettes are used for sample collection. Saliva samples can be stored in Salivettes or dried onto filter paper for several days at room temperature and under tropical conditions (37°C). [ABSTRACT FROM AUTHOR]

We present a three-stage analysis of genome-wide SNP data in 1,222 German individuals with myocardial infarction and 1,298 controls, in silico replication in three additional genome-wide datasets of coronary artery disease (CAD) and subsequent replication in ∼25,000 subjects. We identified one new CAD risk locus on 3q22.3 in MRAS (P = 7.44 × 10−13; OR = 1.15, 95% CI = 1.11–1.19), and suggestive association with a locus on 12q24.31 near HNF1A-C12orf43 (P = 4.81 × 10−7; OR = 1.08, 95% CI = 1.05–1.11). [ABSTRACT FROM AUTHOR]

Assesses whether defined antigens for in vitro testing may improve diagnostic strategies for Mycobacterium tuberculosis. Importance of immunological diagnosis of active tuberculosis (TB) in childhood; In vitro stimulation of peripheral blood mononuclear cells (PBMC) with the secreted antigens ESAT-6 and MPT63.

Hepatitis A is a vaccine-preventable disease with a global distribution. It predominantly occurs in regions with inadequate living conditions, but also affects populations in industrialised countries. Children are frequently involved in the transmission of hepatitis A virus (HAV) and thus play a central role in the epidemiology of hepatitis A. Here, we investigated HAV infections, immunisations, and associated demographic determinants in a nationwide, population-based, cross-sectional survey conducted in Germany from 2003-2006. Out of 17,640 children and adolescents, complete data sets (HAV serology, demographic information and vaccination card) were available for 12,249 (69%), all aged 3-17 years. We found protective antibody levels (>=20 IU/L) in 1,755 (14%) individuals, 1,395 (11%) were vaccinated against hepatitis A, 360 (3%) individuals were HAV seropositive without prior hepatitis A vaccination, thus indicating a previous HAV infection. Antibody prevalence (attributable to vaccination or infection) increased significantly with age. Multivariate logistic regression revealed that predominantly children and adolescents with migration background-even if they were born in Germany-are affected by HAV infections. Our results provide a rationale to emphasise existing vaccination recommendations and, moreover, to consider additional groups with a higher risk of infection for targeted vaccination, especially children with a migration background. [ABSTRACT FROM AUTHOR]

Lyme borreliosis (LB) is the most commonly reported tick-borne disease in Germany. In 9/16 states, notification of erythema migrans (EM), acute neuroborreliosis (NB) and Lyme arthritis (LA) is mandatory. We describe incidence measures, time trends, geographical distribution and frequencies of manifestations to better understand LB epidemiology and target prevention measures. We used cases notified in the 9 states and confirmed by local health offices, 2013-2017, to calculate incidences by time, place and person. Altogether, we observed 56,446 cases. Disease onset peaked yearly in July. Incidence ranged from 26/100,000 (2015) to 41/100,000 (2013) with mean annual incidences 2013-2017 on district level between 0.5/100,000 and 138/100,000. Median age was 54 years with peaks in boys (5-9 years, mean incidence 36/100,000) and women (50-69 years, mean incidence 57/100,000). 95% experienced EM only, 2.7% NB and 2.1% LA. 54% were female, but more men had NB (56%) and LA (53%, p < 0.001). Hospitalisation was recorded for 10% of LA and 71% of NB cases. LB remains an important public health concern in Germany with marked regional variation. To facilitate early diagnosis and treatment, health authorities should raise awareness among physicians and promote prevention strategies among the general population: tick-bite-protection, prompt tick removal and medical consultation. [ABSTRACT FROM AUTHOR]

Background: Arterial hypertension (aHT) is a common comorbidity in patients with type 2 diabetes (T2D). The aim of the present analysis was to determine which predictors are associated with the progression of aHT in participants with T2D.We analyzed data from the sleep-disordered breathing (SDB) sub-study of the DIACORE study, a prospective cohort study of participants with T2D. Blood pressure values were determined at baseline and after a mean follow-up of 2.7 years in a standardized manner with three repeated measurements at rest. Arterial hypertension was defined as blood pressure ≥140/80 mm Hg. Progression of aHT was defined as systolic blood pressure ≥140 mm Hg at follow-up with a concomitant increase of at least 10 mm Hg.Of 1122 participants (41% female, age 66 ± 9 years, body mass index 30.7 ± 5.3 kg/m2), 925 had pre-existing aHT at baseline. At follow-up, 280 had aHT with additional progression. Multivariate regression analysis revealed that systolic blood pressure at baseline (odds ratio [95% confidence interval]: 0.984 [0.976;0.993]; p < 0.001) and age (OR [95%CI]: 1.024 [1.002;1.047]; p = 0.015) were associated with progression of aHT, independently of known modulators. Neither SDB nor its treatment were associated with progression of aHT.In participants with T2D, lower systolic blood pressure at baseline and age but not SDB were associated with progression of aHT.Methods: Arterial hypertension (aHT) is a common comorbidity in patients with type 2 diabetes (T2D). The aim of the present analysis was to determine which predictors are associated with the progression of aHT in participants with T2D.We analyzed data from the sleep-disordered breathing (SDB) sub-study of the DIACORE study, a prospective cohort study of participants with T2D. Blood pressure values were determined at baseline and after a mean follow-up of 2.7 years in a standardized manner with three repeated measurements at rest. Arterial hypertension was defined as blood pressure ≥140/80 mm Hg. Progression of aHT was defined as systolic blood pressure ≥140 mm Hg at follow-up with a concomitant increase of at least 10 mm Hg.Of 1122 participants (41% female, age 66 ± 9 years, body mass index 30.7 ± 5.3 kg/m2), 925 had pre-existing aHT at baseline. At follow-up, 280 had aHT with additional progression. Multivariate regression analysis revealed that systolic blood pressure at baseline (odds ratio [95% confidence interval]: 0.984 [0.976;0.993]; p < 0.001) and age (OR [95%CI]: 1.024 [1.002;1.047]; p = 0.015) were associated with progression of aHT, independently of known modulators. Neither SDB nor its treatment were associated with progression of aHT.In participants with T2D, lower systolic blood pressure at baseline and age but not SDB were associated with progression of aHT.Results: Arterial hypertension (aHT) is a common comorbidity in patients with type 2 diabetes (T2D). The aim of the present analysis was to determine which predictors are associated with the progression of aHT in participants with T2D.We analyzed data from the sleep-disordered breathing (SDB) sub-study of the DIACORE study, a prospective cohort study of participants with T2D. Blood pressure values were determined at baseline and after a mean follow-up of 2.7 years in a standardized manner with three repeated measurements at rest. Arterial hypertension was defined as blood pressure ≥140/80 mm Hg. Progression of aHT was defined as systolic blood pressure ≥140 mm Hg at follow-up with a concomitant increase of at least 10 mm Hg.Of 1122 participants (41% female, age 66 ± 9 years, body mass index 30.7 ± 5.3 kg/m2), 925 had pre-existing aHT at baseline. At follow-up, 280 had aHT with additional progression. Multivariate regression analysis revealed that systolic blood pressure at baseline (odds ratio [95% confidence interval]: 0.984 [0.976;0.993]; p < 0.001) and age (OR [95%CI]: 1.024 [1.002;1.047]; p = 0.015) were associated with progression of aHT, independently of known modulators. Neither SDB nor its treatment were associated with progression of aHT.In participants with T2D, lower systolic blood pressure at baseline and age but not SDB were associated with progression of aHT.Conclusion: Arterial hypertension (aHT) is a common comorbidity in patients with type 2 diabetes (T2D). The aim of the present analysis was to determine which predictors are associated with the progression of aHT in participants with T2D.We analyzed data from the sleep-disordered breathing (SDB) sub-study of the DIACORE study, a prospective cohort study of participants with T2D. Blood pressure values were determined at baseline and after a mean follow-up of 2.7 years in a standardized manner with three repeated measurements at rest. Arterial hypertension was defined as blood pressure ≥140/80 mm Hg. Progression of aHT was defined as systolic blood pressure ≥140 mm Hg at follow-up with a concomitant increase of at least 10 mm Hg.Of 1122 participants (41% female, age 66 ± 9 years, body mass index 30.7 ± 5.3 kg/m2), 925 had pre-existing aHT at baseline. At follow-up, 280 had aHT with additional progression. Multivariate regression analysis revealed that systolic blood pressure at baseline (odds ratio [95% confidence interval]: 0.984 [0.976;0.993]; p < 0.001) and age (OR [95%CI]: 1.024 [1.002;1.047]; p = 0.015) were associated with progression of aHT, independently of known modulators. Neither SDB nor its treatment were associated with progression of aHT.In participants with T2D, lower systolic blood pressure at baseline and age but not SDB were associated with progression of aHT. [ABSTRACT FROM AUTHOR]