Pulmonary artery hypertension (PAH) is a complex syndrome defined by an elevated mean pulmonary artery pressure on right heart catheterization (RHC) [
27,
28]. Over the last 15 years, it has been increasingly recognized that chronic kidney disease (CKD), especially end-stage renal disease (ESRD), is a risk factor for multifactorial pulmonary hypertension [
28‐
30]. The mechanism is poorly understood but is likely a combination of chronic volume overload with pulmonary vascular remodeling, diastolic dysfunction, elevated cardiac output due to an arterio-venous fistula (AVF) or chronic anemia, and chronic inflammation (11). Furthermore, the presence of PAH in ESRD has been associated with worse clinical outcomes for patients [
31]. Many researchers have studied PAH in ESRD on hemodialysis, but few studies (only 11) have investigated the same with PD as stated in a recent metanalysis [
32]. The sPAP used to diagnose PAH varied among studies; but ranged from > 30 mmHg to > 45 mmHg [
32]. Compared with hemodialysis (HD), the prevalence of PAH was much less in ESRD patients receiving treatment with PD. The median prevalence of PAH was 38% (range 8 to 70%) among patients undergoing any type of dialysis, 40% (range 16–70%) among patients undergoing HD, and 19% (range 8–37%) among patients undergoing PD [
32]. In our study the prevalence of PAH (24.2%) was in line with those reported in previous studies [
33‐
35]. Studies from the Middle East and North Africa [
33‐
37] had a pooled prevalence among patients undergoing any type of dialysis of 38% (95% CI 30–45%), among patients receiving HD of 42% (95% CI 35–50%), and among patients receiving PD of 15% (95% CI 9–21%). Studies from East Asia had a pooled prevalence among patients undergoing any type of dialysis of 35% (95% CI 27–44%), among patients receiving HD of 44% (95% CI 38–51%), and among patients receiving PD of 24% (95% CI 14–34%) [
16,
17,
33‐
35,
38‐
46]. Pathogenesis of PAH in ESRD has not been completely elucidated and the mechanisms leading to the disease are still under investigation [
39,
40]. A cross-sectional study by Unal et al. demonstrated a close association between hypervolemia and PAH by using bioimpedance analysis [
17]. Similarly, Agarwal et al. speculated that pulmonary hypertension may occur in response to chronic volume overload [
13]. Interestingly, the study showed that fluid overload was significantly higher in dialysis patients with PAH than those without PAH. Also, sPAP and TBW-ECW levels and the frequency of PAH were significantly reduced after dialysis, and a significant positive correlation was found between sPAP and volume overload. It is possible that chronic fluid overload associated with hyperdynamic circulation causes elevated right atrial pressure, elevated mean pulmonary artery pressure as a consequence of increased pulmonary blood flow. In our study, volume overload was a definite risk factors for PAH and ECHO abnormalities as demonstrated by univariate and multivariant analyses. Other factors that can contribute to the development of PAH by increasing cardiac output are anemia and low albumin, [
17,
28,
42,
47‐
51]. Our analysis, however, did not confirm a relation between serum albumin levels and PAH and this could probably be due to the small sample size and the fact that there were no significant differences in albumin levels between the beginning and end of the study. Contrary to previous reports [
13,
17,
28,
42‐
47] duration of dialysis inversely correlated with the risk of PAH and this was proved by both correlation coefficient (r = − 267,
p = 0.013) and by multivariant analysis (
p = < 0.001), which may not be attributed only to one variable, but getting other factors in light. Reviewing literature showed significant relationship between impaired production and decreased responsiveness of nitric oxide in pulmonary endothelial vascular smooth muscle in patient with high PAP [
47]. Endothelin-1 is a potent vasoconstrictor that had an important role in development of PAH [
48], increase in endothelial activities has been reported in chronic renal failure [
49]. Rubin et al., reported a significant drop of PAP in 19-year-old hemodialysis patient after treatment with Bosentan (an endothelial receptor antagonist) [
50]. The cytokines in particular (tumor necrosis factors alpha, endothelial-1, atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and interleukin-1) have been shown to induce pulmonary angiogenesis, fibroblast proliferation and apoptosis of cardiac myocytes [
51,
52]. High level of BNP has been reported by as poor prognostic factor in patients with PAH [
52‐
56]. There is high body of evidence indicating that PD has the capability to remove small and middle-size molecules [
30]. The molecular weight of TNF alpha is about 17KDa and that of other myocardial depressant factors ranges between 700 and 800 [
55]. Thus, the removal of these small and middle weight cytokines by PD is probably another important factor in prevention of PAH in PD patients. In addition, PD is more or less considered as normal physiological process with no hemodynamic disturbances and no A-V access that can augment PAH in dialysis patients which could explain the low prevalence of PAH in PD patients and the improvement of PAP with time in PD patients [
30]. Risk factors for PAH in our study were found to be age (
> 65), volume overload, cardiovascular disease and low hemoglobin levels (defined as 8 g/dl or less). In the younger than 65 years of age, when adjusting for age, PAH significantly improved at the end of the study. Although RRF in our study did not vary significantly between the beginning and end, we do believe that RRF plays a major role in APD adequacy and outcomes. RRF might have a significant impact on the initial as well as the end volume status in our report. Fluid overload is a common and serious problem that leads to severe complications in HD patients and has a great impact on the pathogenesis of cardiovascular disease and PAH. (76). We think that volume control in our APD patients played a role in reducing PAP. In our report, old age (
> 65) was suggested as a possible risk factor for PAH and demonstrated by analysis. PAH is increasingly recognized in the elderly population; however, its causes and characteristics in those population are not well established [
57‐
61]. A report from a multinational European registry found 63% of patients in a cohort of IPAH were aged ≥65 years [
60‐
62] and an analysis of incident cases of PAH in the United Kingdom and Ireland reported 13.5% of patients were diagnosed with PAH at age ≥ 70 years [
61] and PAH associated with heart disease and vascular calcifications even with preserved ejection fraction is an increasingly recognized cause of PAH in older adults [
62‐
64]. Whatever mechanisms causing PAH in elderly, we suggest that PD is a reasonable and effective option for ESRD elderly patients based on the results in our study. Since PAH is associated with significant morbidity and mortality in ESRD patients, its prevention and early diagnosis and treatment is of great importance. In patients who are at known risk for development of PAH, such as those with pre-existing moderate to severe systolic/diastolic cardiac dysfunction, changing the dialysis type from HD to PD may be a reasonable option to prevent PAH or to prevent further elevation of PAP. The limitations of this study are the small size of study population, and the fact that the peritoneal membrane transport characteristics of the patients were not evaluated. However, the fact that it is a long-term study of incident patients with a minimum time of 1 years and up to 5 years follow-up, the therapy being provided by a single dialysis supplier, and the thorough quality control used for collecting data and handling the database may authenticate our report.