Identification of people with autosomal dominant polycystic kidney disease using routine data: a cross sectional study

BACKGROUND: Autosomal dominant polycystic kidney disease (ADPKD) causes progressive renal damage and is a leading cause of end-stage renal failure. With emerging therapies it is important to devise a method for early detection. We aimed to identify factors from routine clinical data which can be used to distinguish people with a high likelihood of having ADPKD in a primary health care setting. METHOD: A cross-sectional study was undertaken using data from the Quality Intervention in Chronic Kidney Disease trial extracted from 127 primary care practices in England. The health records of 255 people with ADPKD were compared to the general population. Logistic regression was used to identify clinical features which distinguish ADPKD. These clinical features were used to stratify individual risk using a risk score tool. RESULTS: Renal impairment, proteinuria, haematuria, a diastolic blood pressure over 90 mmHg and multiple antihypertensive medications were more common in ADPKD than the general population and were used to build a regression model (area under the receiver operating characteristic curve; 0.79). Age, gender, haemoglobin and urinary tract infections were not associated with ADPKD. A risk score (range -3 to +10) of ≥0 gave a sensitivity of 70.2% and specificity 74.9% of for detection. CONCLUSIONS: Stratification of ADPKD likelihood from routine data may be possible. This approach could be a valuable component of future screening programs although further longitudinal analyses are needed

Effects of empathy and conflict resolution strategies on psychophysiological arousal and satisfaction in romantic relationships

The present research builds upon the extant literature as it assesses psychophysiological factors in relation to empathy, conflict resolution, and romantic relationship satisfaction. In this study, we examined physiological reactivity of individuals in the context of emotionally laden interactions with their romantic partners. Participants (N = 31) completed self-report measures and attended in-person data collection sessions with their romantic partners. Participants were guided through discussions of problems and strengths of their relationships in vivo with their partners while we measured participants’ skin conductance level (SCL) and interbeat interval (IBI) of the heart. We hypothesized that participants’ level of empathy towards their partners would be reflected by physiological arousal (as measured by SCL and IBI) and relationship satisfaction, such that higher levels of empathy would be linked to changes in physiological arousal and higher relationship satisfaction. Further, we hypothesized that differences would be found in physiological arousal (as measured by SCL and IBI) based on the type of conflict resolution strategy used by participants. Finally, we hypothesized that differences would be found in empathy towards partner and relationship satisfaction based on the type of conflict resolution strategies used by participants. Results partially supported hypotheses and were discussed in light of existing knowledge based on empirical and theoretical source

The contribution of environmental exposure to the etiology of autism spectrum disorder

Autism spectrum disorder (ASD) is a neurodevelopmental condition of heterogeneous etiology. While it is widely recognized that genetic and environmental factors and their interactions contribute to autism phenotypes, their precise causal mechanisms remain poorly understood. This article reviews our current understanding of environmental risk factors of ASD and their presumed adverse physiological mechanisms. It comprehensively maps the significance of parental age, teratogenic compounds, perinatal risks, medication, smoking and alcohol use, nutrition, vaccination, toxic exposures, as well as the role of extreme psychosocial factors. Further, we consider the role of potential protective factors such as folate and fatty acid intake. Evidence indicates an increased offspring vulnerability to ASD through advanced maternal and paternal age, valproate intake, toxic chemical exposure, maternal diabetes, enhanced steroidogenic activity, immune activation, and possibly altered zinc-copper cycles and treatment with selective serotonin reuptake inhibitors. Epidemiological studies demonstrate no evidence for vaccination posing an autism risk. It is concluded that future research needs to consider categorical autism, broader autism phenotypes, as well as autistic traits, and examine more homogenous autism variants by subgroup stratification. Our understanding of autism etiology could be advanced by research aimed at disentangling the causal and non-causal environmental effects, both founding and moderating, and gene-environment interplay using twin studies, longitudinal and experimental designs. The specificity of many environmental risks for ASD remains unknown and control of multiple confounders has been limited. Further understanding of the critical windows of neurodevelopmental vulnerability and investigating the fit of multiple hit and cumulative risk models are likely promising approaches in enhancing the understanding of role of environmental factors in the etiology of ASD.peerReviewe