Prospective bidirectional associations between depression and chronic kidney diseases.
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ABSTRACT:
SUBMITTER: Zheng X
PROVIDER: S-EPMC9240037 | biostudies-literature |
REPOSITORIES: biostudies-literature
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Project description:OBJECTIVES:Depression frequently co-occurs with multiple chronic diseases in complex, costly, and dangerous patterns of multimorbidity. The field of health psychology may benefit from evaluating the temporal characteristics of depression's associations with common diseases, and from determining whether depression is a central connector in multimorbid disease clusters. The present review addresses these issues by focusing on 4 of the most prevalent diseases: hypertension, ischemic heart disease, arthritis, and diabetes. METHOD:Study 1 assessed how prior chronic disease diagnoses were associated with current depression in a large, cross-sectional, population-based study. It assessed depression's centrality using network analysis accounting for disease prevalence. Study 2 presents a systematic scoping review evaluating the extent to which depression was prospectively associated with the onset of the 4 prevalent chronic diseases. RESULTS:In Study 1 depression had the fourth highest betweenness centrality ranking of 26 network nodes and centrally connected many existing diseases and unhealthy behaviors. In Study 2 depression was associated with subsequent incidence of ischemic heart disease and diabetes across multiple meta-analyses. Insufficient information was available about depression's prospective associations with incident hypertension and arthritis. CONCLUSIONS:Depression is central in patterns of multimorbidity and is associated with incident disease for several of the most common chronic diseases, justifying the focus on screening and treatment of depression in those at risk for developing chronic disease. Future research should investigate the mediating and moderating roles of health behaviors in the association between depression and the staggered emergence over time of clusters of multimorbid chronic diseases. (PsycINFO Database Record (c) 2019 APA, all rights reserved).
| S-EPMC6706317 | biostudies-literature
Project description:AimWomen with diabetes have a higher prevalence of chronic kidney disease (CKD) risk factors compared with men, but whether they are at higher risk for incident CKD remains uncertain.MethodsThis was a prospective, observational cohort study of 1464 patients with diabetes and normal renal function, recruited from primary care clinics at a vertically integrated healthcare system in Seattle, WA, USA. The primary predictor was sex. Incident CKD was defined by an estimated glomerular filtration rate (eGFR) <60 mL/min per 1.73 m(2) by Chronic Kidney Disease-Epidemiology equations or sex-specific microalbuminuria (urine albumin/creatinine ratio ≥25 mg/g for women or ≥17 mg/g for men).ResultsOf the 1464 patients (52.0% women), CKD incidence rates were 154.0 and 144.3 cases per 1000 patient-years for women and men, respectively. In the competing risks regression, women had an increased risk of incident CKD (sub-hazard ratio 1.37, 95% confidence interval (CI) 1.17, 1.60) compared with men after adjustment for demographics, baseline eGFR and duration of diabetes, which persisted after additional adjustment for CKD risk factors, depressive symptoms and diabetes self-care (sub-hazard ratio 1.35, 95% CI 1.15, 1.59). Sex differences in incident CKD were consistent across age groups and appeared to be driven by differences in the development of low eGFR rather than microalbuminuria.ConclusionWomen with diabetes had a higher risk of incident CKD compared with men, which could not be entirely explained by differences in biologic CKD risk factors, depression or diabetes self-care. Additional work is needed determine if these sex differences contribute to worse outcomes in women with diabetes.
| S-EPMC4465880 | biostudies-literature
Project description:BackgroundMetabolic syndrome components-waist circumference, high-density lipoprotein cholesterol (HDL-C), triglycerides, systolic blood pressure and fasting glucose-are cross-sectionally associated with depression and anxiety with differing strength. Few studies examine the relationships over time or whether antidepressants have independent effects.MethodsParticipants were from the Netherlands Study of Depression and Anxiety (NESDA; N = 2,776; 18-65 years; 66% female). At baseline, 2- and 6-year follow-up, participants completed diagnostic interviews, depression and anxiety symptom inventories, antidepressant use assessment, and measurements of the five metabolic syndrome components. Data were analyzed for the consistency of associations between psychopathology indicators and metabolic syndrome components across the three assessment waves, and whether psychopathology or antidepressant use at one assessment predicts metabolic dysregulation at the next and vice versa.ResultsConsistently across waves, psychopathology was associated with generally poorer values of metabolic syndrome components, particularly waist circumference and triglycerides. Stronger associations were observed for psychopathology symptom severity than diagnosis. Antidepressant use was independently associated with higher waist circumference, triglycerides and number of metabolic syndrome abnormalities, and lower HDL-C. Symptom severity and antidepressant use were associated with subsequently increased number of abnormalities, waist circumference, and glucose after 2 but not 4 years. Conversely, there was little evidence that metabolic syndrome components were associated with subsequent psychopathology outcomes.ConclusionsSymptom severity and antidepressant use were independently associated with metabolic dysregulation consistently over time and also had negative consequences for short-term metabolic health. This is of concern given the chronicity of depression and anxiety and prevalence of antidepressant treatment.
| S-EPMC5111740 | biostudies-literature
Project description:Background. Although several studies have examined the association between chronic kidney disease (CKD) and hyperuricemia (HUA), the direction of the association remains unclear. We aimed to investigate whether there was a bidirectional association between them. Methods. The present study was conducted in three analyses. Analysis I included 25,433 participants free of HUA at baseline to evaluate the associations between CKD and estimated glomerular filtration rate (eGFR) with incident HUA. Analysis II had 28,422 participants free of CKD at baseline to analyze the relationships between HUA and serum uric acid (sUA) with new-onset CKD. Cox proportional hazards regression models were applied to evaluate the association involved in Analysis I and II. Analysis III included 31,028 participants with complete data and further dissected the bidirectional association between sUA and eGFR using cross-lag models. Results. New-onset HUA and CKD were observed in the first round of the follow-up study among 1597 and 1212 participants, respectively. A significantly higher risk of HUA was observed in individuals with CKD compared to individuals without CKD (HR = 1.58, 95% CI: 1.28–1.95). The adjusted HRs (95% CIs) of HUA were 3.56 (2.50–5.05) for the participants in the group of eGFR less than 60 mL·min−1·1.73 m−2, 1.61 (1.42–1.83) for those in the group of eGFR between 60 and 90 mL·min−1·1.73 m−2, and 1.74 (1.42–2.14) for those in the group of eGFR more than 120 mL·min−1·1.73 m−2, compared with the group of eGFR between 90 and 120 mL·min−1·1.73 m−2. A higher risk of CKD was also observed in individuals with HUA compared to individuals without HUA (HR = 1.28, 95% CI: 1.12–1.47). Compared with the first quintile of sUA, the adjusted HR (95% CI) of CKD was 1.24 (1.01–1.51) for the participants in the fourth quantile. There was a bidirectional relationship between sUA and eGFR, with the path coefficients (ρ1 = −0.024, p < 0.001) from baseline eGFR to follow-up sUA and the path coefficients (ρ2 = −0.015, p = 0.002) from baseline sUA to follow-up eGFR. Conclusions. The present study indicated that CKD and HUA were closely associated, and there was a bidirectional relationship between sUA and eGFR.
| S-EPMC9914133 | biostudies-literature
Project description:Chronic kidney disease (CKD) is a global health problem with a genetic component. Genome-wide association studies have identified variants associated with specific CKD etiologies, but their genetic overlap has not been well studied. This study examined SNP associations across different CKD etiologies and CKD stages using data from 5,034 CKD patients of the German Chronic Kidney Disease study. In addition to confirming known associations, a systemic lupus erythematosus-associated risk variant at TNXB was also associated with CKD attributed to type 1 diabetes (p = 2.5 × 10-7), a membranous nephropathy-associated variant at HLA-DQA1 was also associated with CKD attributed to systemic lupus erythematosus (p = 5.9 × 10-6), and an IgA risk variant at HLA-DRB1 was associated with both CKD attributed to granulomatosis with polyangiitis (p = 2.0 × 10-4) and to type 1 diabetes (p = 4.6 × 10-11). Associations were independent of additional risk variants in the respective genetic regions. Evaluation of CKD stage showed a significant association of the UMOD risk variant, previously identified in population-based studies for association with kidney function, for advanced (stage ≥G3b) compared to early-stage CKD (≤stage G2). Shared genetic associations across CKD etiologies and stages highlight the role of the immune response in CKD. Association studies with detailed information on CKD etiology can reveal shared genetic risk variants.
| S-EPMC5655008 | biostudies-literature
Project description:BackgroundChronic kidney disease (CKD) is closely associated with cardiovascular disease. We aimed to examine the association of Life's Essential 8 (LE8), the recently updated measurement of cardiovascular health, with the prevalence of CKD among US adults.Methods and resultsThis population-based cross-sectional study used data from the National Health and Nutrition Examination Survey from 2007 to 2018 and included adults aged ≥20 years. Multivariable logistic and restricted cubic spline models were used to assess the associations between LE8 and CKD. Among 24 960 participants, 4437 were determined to have CKD (weighted percentage, 14.11%). After the adjustment of potential confounders, higher LE8 scores were associated with reduced odds of CKD (odds ratio for each 10-point increase, 0.79 [95% CI, 0.76-0.83]), and a nonlinear dose-response relationship was observed. Similar patterns were also identified in the associations of health behavior and health factor scores with CKD. Meanwhile, higher scores for blood glucose (odds ratio, for each 10-point increase, 0.88 [95% CI, 0.87-0.90]) and blood pressure (odds ratio, for each 10-point increase, 0.92 [95% CI, 0.91-0.94]) in the LE8 component are significantly associated with a lower prevalence of CKD. The inversed association of LE8 score and CKD was significantly stronger among middle-aged, male, and coupled participants.ConclusionsLE8 was negatively associated with the prevalence of CKD in a nonlinear fashion. Promoting adherence to optimal cardiovascular health levels may be beneficial to reduce the burden of CKD.
| S-EPMC10863789 | biostudies-literature
Project description:BackgroundAlthough prior observational studies indicate an association between cardiovascular diseases (CVDs) and frozen shoulder (FS), the potential causal relationship between them remains uncertain. This study aims to explore the genetic causal relationship between CVDs and FS using Mendelian randomization (MR).MethodsGenetic variations closely associated with FS were obtained from the FinnGen Consortium. Summary data for CVD, including atrial fibrillation (AF), coronary artery disease (CAD), heart failure (HF), myocardial infarction (MI), stroke, and ischemic stroke (IS), were sourced from several large-scale genome-wide association studies (GWAS). MR analysis was performed using inverse variance weighting (IVW), MR Egger, and weighted median methods. IVW, as the primary MR analysis method, complemented by other sensitivity analyses, was utilized to validate the robustness of the results. Further reverse MR analysis was conducted to explore the presence of reverse causal relationships.ResultsIn the forward MR analysis, genetically determined risk of stroke and IS was positively associated with FS (OR [95% CI] = 1.58 (1.23-2.03), P < 0.01; OR [95% CI] = 1.46 (1.16-1.85), P < 0.01, respectively). There was no strong evidence of an effect of genetically predicted other CVDs on FS risk. Sensitivity analyses confirmed the robustness of the results. In the reverse MR analysis, no causal relationships were observed between FS and various CVDs.ConclusionThe study suggests that stroke increases the risk of developing FS. However, further basic and clinical research is needed to substantiate our findings.
| S-EPMC10837867 | biostudies-literature
Project description:BackgroundPrevious studies have explored the associations between circulating inflammatory cytokines and blinding eye diseases, including glaucoma, cataract and macular degeneration. However, the causality of these associations remains controversial. This study employs a bidirectional Mendelian randomization (MR) study to investigate the causal relationships between 41 circulating inflammatory cytokines and these blinding eye diseases.MethodsSummary data for glaucoma, cataract, macular degeneration and 41 circulating inflammatory cytokines were publicly available. The inverse variance weighted (IVW) method was employed as the main analysis method. Additionally, various sensitivity tests, including MR-Egger regression, weighted median, weight mode, Cochran's Q test, MR pleiotropy Residual Sum and Outlier test, and leave-one-out test, were conducted to evaluate sensitivity and stability of results.ResultsThe IVW analysis identified six circulating inflammatory cytokines causally associated with the risk of blinding eye diseases: Monokine induced by interferon-gamma (MIG) for glaucoma, interleukin-1 receptor antagonist (IL-1ra), IL-6, IL-10, and platelet derived growth factor BB (PDGFbb) for cataract, and MIG and hepatocyte growth factor (HGF) for macular degeneration. However, it is noteworthy that none of these associations remained significant after Bonferroni correction (p < 0.0004). Reverse MR analyses indicated that cataract may lead to a decrease in vascular endothelial growth factor (VEGF) levels (OR: 3.326 × 10-04, 95% CI: 5.198 × 10-07 - 2.129 × 10-01, p = 0.0151).ConclusionThis study highlights the potential roles of specific inflammatory cytokines in the development of glaucoma, cataract and macular degeneration. Moreover, it suggests that VEGF is likely to be involved in cataract development downstream. These findings offer insights for early prevention and novel therapeutic strategies for these blinding eye diseases.
| S-EPMC10848324 | biostudies-literature
Project description:BackgroundMore and more evidence suggests a close association between depression and hepatobiliary diseases, but its causal relationship is not yet clear.MethodUsing genome-wide association studies (GWAS) to summarize data, independent genetic variations associated with depression were selected as instrumental variables. Firstly, we designed a univariate Mendelian randomization (UVMR) analysis with two samples and simultaneously conducted reverse validation to evaluate the potential bidirectional causal relationship between depression and various hepatobiliary diseases. Secondly, we conducted a multivariate Mendelian randomization (MVMR) analysis on diseases closely related to depression, exploring the mediating effects of waist to hip ratio, hypertension, and daytime nap. The mediating effects were obtained through MVMR. For UVMR and MVMR, inverse variance weighted method (IVW) is considered the most important analytical method. Sensitivity analysis was conducted using Cochran'Q, MR Egger, and Leave-one-out methods.ResultsUVMR analysis showed that depression may increase the risk of non-alcoholic fatty liver disease (OR, 1.22; 95% CI, 1.03-1.46; p=0.0248) in liver diseases, while depression does not increase the risk of other liver diseases; In biliary and pancreatic related diseases, depression may increase the risk of cholelithiasis (OR, 1.26; 95% CI, 1.05-1.50; p=0.0120), chronic pancreatitis (OR, 1.61; 95% CI, 1.10-2.35; p=0.0140), and cholecystitis (OR, 1.23; 95% CI, 1.03-1.48; p=0.0250). In addition, through reverse validation, we found that non-alcoholic fatty liver disease, cholelithiasis, chronic pancreatitis, cholecystitis, or the inability to increase the risk of depression (p>0.05). The waist to hip ratio, hypertension, and daytime nap play a certain role in the process of depression leading to non-alcoholic fatty liver disease, with a mediating effect of 35.8%.ConclusionDepression is a susceptibility factor for non-alcoholic fatty liver disease, and the causal effect of genetic susceptibility to depression on non-alcoholic fatty liver disease is mediated by waist-hip ratio, hypertension, and daytime nap.
| S-EPMC11002219 | biostudies-literature
Project description:BackgroundStudies have revealed that patients with chronic kidney disease (CKD) have dietary patterns different from those of the general population. However, no studies have compared the dietary patterns of between patients with early-stages (stages 1-3a) and late-stages (stages 3b-5) of CKD. Our objective was to investigate the associations between dietary patterns in early and late-stage CKD.MethodsWe analyzed 4480 participants with CKD at various stages based on the data recorded between 2007 and 2016 from the database of the American National Health and Nutrition Examination Survey.ResultsIn total, 3683 and 797 participants had early and late-stage CKD, respectively. Through principal components analysis, the dietary intake dimension was reduced from 63 variables to 3 dietary patterns. We adopted logistic regression for analysis. The three dietary patterns are as follows: (1) saturated fatty acids and mono-unsaturated fatty acids (MUFA); (2) vitamins and minerals; and (3) cholesterols and polyunsaturated fatty acids (PUFA). These 3 patterns explained > 50% of dietary nutrient intake. Results indicated that among participants with dietary patterns 2 (vitamins and minerals) and 3 (cholesterols and PUFA), those with low intakes were more likely to have late-stage CKD. The odds ratios for patterns 2 and 3 were 1.74 (95% CI: 1.21-2.50) and 1.66 (95% CI: 1.13-2.43), respectively.ConclusionsThis study revealed that intakes of vitamins and minerals and cholesterols and PUFA were associated with the stages of CKD.
| S-EPMC8939097 | biostudies-literature