♦ Background: The prognostic value of pulmonary hypertension at the start of peritoneal dialysis (PD) in patient survival is unclear. ♦ Methods: We conducted a retrospective study of incident patients who initiated PD therapy from January 2007 to December 2011, and followed up through June 2013. Pulmonary hypertension was defined as an estimated systolic pulmonary artery pressure (PAP) of ≥ 35 mm Hg using echocardiography. Clinical parameters and laboratory findings were compared between patients with and without pulmonary hypertension and a logistic regression model was elaborated. Patient outcomes (all-cause and cardiovascular mortality) were recorded during follow-up. Survival curves were constructed by the Kaplan-Meier method, and the influences of pulmonary hypertension on outcomes were analyzed by Cox regression models. .1% of them due to cardiovascular disease. Kaplan-Meier survival analysis showed that patients with pulmonary hypertension had worse overall rates of survival and cardiovascular death-free survival than those without pulmonary hypertension. After multivariate adjustment, pulmonary hypertension was independently associated with increased risk for both all-cause and cardiovascular mortality, with hazard ratios (HRs) of 2.10 (95% CI: 1.35 -3.27) and 2.60 (95% CI: 1.48 -4.56), respectively. ♦ Conclusions: The prevalence of pulmonary hypertension at the start of PD was common and associated with increased risk of both all-cause and cardiovascular mortality in incident PD patients. KEY WORDS: End-stage renal disease; peritoneal dialysis; pulmonary hypertension; survival. P ulmonary hypertension is a devastating disorder, characterized by a progressive increase in pulmonary vascular resistance and pulmonary artery pressure (PAP), leading to right heart failure or even death (1,2). Recently, pulmonary hypertension has been increasingly recognized as a novel threat in patients with end-stage renal disease (ESRD), with an estimated prevalence range of 0 -68.8% (3-7). The mechanisms involved in pulmonary hypertension development are still under investigation. However, it has been suggested that some factors responsible for this pathogenesis include pulmonary artery calcifications secondary to hyperparathyroidism, volume overload, severe anemia, hemodynamic modifications due to the size or the location of an arteriovenous fistula, and exposure to dialysis membranes. In contrast, pulmonary hypertension improves after successful kidney transplantation (8).Previous studies have demonstrated that pulmonary hypertension, either pre-existing before initiating hemodialysis (HD) or developing incident after regular HD treatment, is related to increased mortality rates (5,7,9). Further, enhanced PAP has a poor survival rate extending to a period beyond dialysis. In a study regarding renal transplant recipients, severe pulmonary hypertension, defined as mean PAP > 50 mmHg, conferred a hazard ratio (HR) of 3.75 (95% confidence