Air pollution and kidney disease: Review of current evidence

Along with amazing technological advances, the industrial revolution of the mid-19th century introduced new sources of pollution. By the mid-20th century, the effects of these changes were beginning to be felt around the world. Among these changes, health problems due to environmental air pollution are increasingly recognized. At the beginning, respiratory and cardiovascular diseases were emphasized. However, accumulated data indicate that every organ system in the body may be involved, and the kidney is no exception. Although research on air pollution and kidney damage is recent, there is now scientific evidence that air pollution harms the kidney. In this holistic review, we have summarized the epidemiology, disease states and mechanisms of air pollution and kidney damage

Henri Temianka Correspondence; (spivakovsky)

https://digitalcommons.chapman.edu/temianka_correspondence/2868/thumbnail.jp

A new approach in the diagnosis of upper airway resistance syndrome (UARS): PAP method.

Upper airway resistance syndrome (UARS) is characterized by repeated number of arousals at night, and excessive daytime sleepiness or somnolence (EDS). It is often missed in classical polysomnographic diagnostic approaches and misdiagnosed as simple snoring or idiopathic hypersomnia, thereby is often left untreated. We propose that positive airway pressure (PAP), which has shown to be effective against UARS, can be used as a diagnostic tool as well. The study designed to test whether patients with high titration pressures can be diagnosed for UARS, and whether this pressure can be used as the treatment pressure in UARS

A Different Clinical Type of OSAS: REM-Related OSAS

Objective: Rapid eye movement (REM) is an entity in which the collapsibility of upper respiratory tract increases. Different opinions have been proposed with regard to the definition of REM-related obstructive sleep apnea syndrome (OSAS). Some authors consider REM-related OSAS as the first presentation, and others consider it as a different clinical type of OSAS. We aimed to compare the clinical and polysomnographic findings of REM-related and non-REM-related OSAS patients to test whether REM-related OSAS is a different clinical type OSAS or the manifestation of early stage or the onset of OSAS. Methods: The study had a retrospective design. Patients with an initial diagnosis of sleep-related breathing disorders were later diagnosed to have OSAS based on an apnea–hypopnea index (AHI) of ≥5 and were divided into the following two groups: patients with AHINREM of 2 whose REM recordings were obtained for at least 30 min were defined as having “REM-related OSAS,” and those who did not meet this description were defined as having “non-REM-related OSAS.” Results: A total of 329 patients with a mean age of 51±10 years were included in the study. Thirty-five (10.6%) patients with OSAS were REM-related and 294 (89.4%) were non-REM-related. Age, body mass index, smoking status, and concomitant diseases were comparable between groups (p>0.05). In REM-related patients, AHI was lower, REM duration was longer, and mean oxygen saturations were comparatively higher (p<0.05). Conclusion: Similarities between groups in age, body mass index, and concomitant disease suggest that REM-related OSAS is a different clinical type of OSAS, rather than the early phase of OSAS

A new prognostic-predictor marker of cardiovascular disease for obstructive sleep apnea: Pentraxin 3

Obstructive sleep apnea syndrome (OSAS) is characterized by intermittent complete or partial upper airway obstruction during sleep causing hypoxia, sleep disruption, daytime sleepiness, mental and physical effects is the second most common respiratory condition; affecting 0.3- 4% of the middle- aged population (1). OSAS is strongly associated with cardiovascular morbidity and mortality, including an increased risk of endothelial dysfunction and atherosclerosis (2). The increased prevalence of hypertension and atherogenesis among OSAS patients has been attributed to sympathetic activation and endothelial dysfunction, likely resulting from initiation and propagation of inflammatory responses within the microvasculature (3). There is increasing evidence that OSAS associated with inflammatory cytokines and markers such as C-reactive protein (CRP), interleukin-6, fibrinogen, tumor necrosis factor alpha which are closely-involved in atherosclerosis, plaque formation and rupture (4). OSAS, a potent activator of inflammation, inreases CRP which has been used as an inflammatory biomarker for prediction of cardiovascular events;CRP is named as classical short pentraxins and is a acute phase protein produced from the liver in response to inflammatory mediators (5). Pentraxin 3 (PTX3), a new defined member of the pentraxin family, is produced from the major cell types involved in atherosclerotic lesions, including vascular endothelial-smooth muscle cells, macrophages, and neutrophils in response to inflammatory stimuli, however CRP is produced only from liver (6,7). Furthermore, CRP represents a systemic response to local inflammation, whereas PTX3 is rapidly produced directly from damaged tissues and directly reflects only the inflammatory state of the vasculature. The last but not the least PTX3 levels have been reported to be significantly elevated in acute myocardial infarction (7). In the light of these knowledge, PTX3 is able to reflect ACS condition better than CRP, it is highly possible that PTX3 is a superior biomarker to predict future cardiovascular events. Therefore, we speculate that OSAS, directly or indirectly, induces a persisting systemic and vascular inflammation and may cause PTX3 secretion. Since high PTX3 level is a sign of vascular inflammation which is the trigger point for many diseases that may occur secondary to OSAS, might also be a good marker of cardiovascular disease in OSAS. Screening of PTX3 level in OSAS patients may be a useful marker for evaluating the prognosis of OSAS. To address this hypothesis, further prospective studies are warranted to evaluate the role of PTX3 in patients with OSAS