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Introduction: Sleep apnea (SA) is an important comorbidity in end-stage renal disease (ESRD) patients. The association between SA and cardiac and neurological disease is known. This study investigates the relationship between SA and cardiovascular and cerebrovascular outcomes in the ESRD population. Methods: In a retrospective cohort study, the United States Renal Data System was queried to identify ESRD patients aged 18–100 years in whom hemodialysis had been initiated between 2005 and 2013. Diagnoses of SA and clinical comorbidities were determined from International Classification of Disease-9 codes. Demographic variables were obtained from Centers for Medicare and Medicaid Services Form-2728. Logistic regression was used to examine the association of SA with myocardial infarction (MI) or with stroke, controlling for demographic and clinical variables. Results: Of 858,131 subjects meeting the inclusion criteria, 587 had central SA, and 22,724 had obstructive SA. The SA cohort was younger, more likely to be male and Caucasian compared to the non-SA cohort. Patients with SA also had more tobacco and alcohol use, hypertension, heart failure, and diabetes. Central SA (aRR = 1.69, 95% CI = 1.28–2.23) and obstructive SA (aRR = 1.15, 95% CI = 1.09–1.21) were associated with an increased risk of stroke but not MI. Conclusion: In the ESRD population, a diagnosis of central SA or obstructive SA increased the risk of stroke, but not MI. Early identification and treatment of SA in the ESRD population may help reduce the risk of stroke in these patients. [ABSTRACT FROM AUTHOR]

Laura I Ortiz-Lopez,1,2 Vivek Choudhary,1,3 Wendy B Bollag1,3– 5 1Department of Physiology, Medical College of Georgia at Augusta University, Augusta, GA, 30912, USA; 2Department of Neuroscience and Regenerative Medicine, Medical College of Georgia at Augusta University, Augusta, GA, 30912, USA; 3Charlie Norwood VA Medical Center, Augusta, GA, 30904, USA; 4Department of Dermatology, Medical College of Georgia at Augusta University, Augusta, GA, 30912, USA; 5Department of Medicine, Medical College of Georgia at Augusta University, Augusta, GA, 30912, USACorrespondence: Wendy B Bollag, Department of Physiology, Medical College of Georgia at Augusta University, 1120 15th Street, Augusta, GA, 30912, USA, Tel +1 706 721-0698, Fax +1 706 721-7299, Email wbollag@augusta.eduAbstract: Psoriasis is a complex disease triggered by genetic, immunologic, and environmental stimuli. Many genes have been linked to psoriasis, like the psoriasis susceptibility genes, some of which are critical in keratinocyte biology and epidermal barrier function. Still, the exact pathogenesis of psoriasis is unknown. In the disease, the balance between the proliferative and differentiative processes of keratinocytes becomes altered. Multiple studies have highlighted the role of dysregulated immune cells in provoking the inflammatory responses seen in psoriasis. In addition to immune cells, accumulating evidence shows that keratinocytes are involved in psoriasis pathogenesis, as discussed in this review. Although certain immune cell-derived factors stimulate keratinocyte hyperproliferation, activated keratinocytes can also produce anti-microbial peptides, cytokines, and chemokines that can promote their proliferation, as well as recruit immune cells to help initiate and reinforce inflammatory feedback loops. Psoriatic keratinocytes also show intrinsic differences from normal keratinocytes even after removal from the in vivo inflammatory environment; thus, psoriatic keratinocytes have been found to exhibit abnormal calcium metabolism and possible epigenetic changes that contribute to psoriasis. The Koebner phenomenon, in which injury promotes the development of psoriatic lesions, also provides evidence for keratinocytes’ contributions to disease pathogenesis. Furthermore, transgenic mouse studies have confirmed the importance of keratinocytes in the etiology of psoriasis. Finally, in addition to immune cells and keratinocytes, data in the literature support roles for other cell types, tissues, and systems in psoriasis development. These other contributors are all potential targets for therapies, suggesting the importance of a holistic approach when treating psoriasis.Keywords: anti-microbial peptides, inflammation, innate immunity, Koebner phenomenon, skin