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      Pulmonary hypertension and post-operative outcome in renal transplant: A retrospective analysis of 170 patients

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          Abstract

          Background and Aims:

          Renal transplant is the best possible treatment for patients suffering with end-stage renal disease (ESRD). Cardiovascular events are the commonest factors contributing to perioperative morbidity and mortality in this population. These patients have a high incidence (up to 60%) of pulmonary hypertension (PH) and that may affect the perioperative outcome.

          Methods:

          In this study, we aimed to study the impact of PH on perioperative outcome after renal transplant. PH was defined as patients with pulmonary artery systolic pressure ≥35 mmHg on pre-operative echocardiography. Medical records of 170 patients who had undergone renal transplantation in the past 3 years were reviewed. Primary outcome was delayed graft functioning and secondary outcomes were perioperative complications such as hypotension, arrhythmias, need of post-operative mechanical ventilation, atelectasis and pulmonary oedema.

          Results:

          We observed 46.5% incidence of PH in ESRD patients. Compared to patients without PH, more patients with PH had postoperative hypotension (26.58% vs. 9.89%, P = 0.004) and delayed graft functioning (8.8% vs. 1.1%, P = 0.026). On multivariate analysis, however, PH was not an independent predictor of delayed graft functioning.

          Conclusion:

          In ESRD patients, although PH is not an independent predictor of delayed graft functioning, patients having PH are more prone for perioperative hypotension and delayed graft functioning after renal transplant.

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          Most cited references18

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          Pulmonary hypertension in patients with end-stage renal disease.

          The aims of this study were to evaluate the incidence of unexplained pulmonary hypertension (PH) among patients with end-stage renal disease (ESRD) and to suggest possible etiologic factors. The incidence of PH was prospectively estimated by Doppler echocardiography in 58 patients with ESRD receiving long-term hemodialysis via arteriovenous access, and in control groups of 5 patients receiving peritoneal dialysis (PD) and 12 predialysis patients without a known other cause to suggest the presence of PH. Clinical variables were compared between patients with and without PH receiving hemodialysis. Changes in pulmonary artery pressure (PAP) values before and after onset of hemodialysis via arteriovenous access, arteriovenous access compression, and successful kidney transplantation were recorded. PH > 35 mm Hg was found in 39.7% of patients receiving hemodialysis (mean +/- SD, 44 +/- 7 mm Hg; range, 37 to 65 mm Hg), in none of the patients receiving PD, and in 1 of 12 predialysis patients. Patients with PH receiving hemodialysis had a significantly higher cardiac output (6.9 L/min vs 5.5 L/min, p = 0.017). PH developed in four of six patients with normal PAP after onset of hemodialysis therapy via arteriovenous access. One-minute arteriovenous access compression in four patients decreased the mean systolic PAP from 52 +/- 7 to 41 +/- 4 mm Hg (p = 0.024). PH normalized in four of five patients receiving hemodialysis following kidney transplantation. Kaplan-Meier survival analysis according to PAP values revealed significant survival differences (p < 0.024). This study demonstrates a surprisingly high incidence of PH among patients with ESRD receiving long-term hemodialysis with surgical arteriovenous access. Both ESRD and long-term hemodialysis via arteriovenous access may be involved in the pathogenesis of PH by affecting pulmonary vascular resistance and cardiac output.
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            Impact of pulmonary hypertension on the outcomes of noncardiac surgery: predictors of perioperative morbidity and mortality.

            We sought to determine the predictors of short-term morbidity and mortality ( or = II (p = 0.02), intermediate- to high-risk surgery (p = 0.04), and duration of anesthesia > 3 h (p = 0.04) were independent predictors of short-term morbidity. There were 10 early deaths (7%). A history of pulmonary embolism (p = 0.04), right-axis deviation (p = 0.02), right ventricular (RV) hypertrophy (p = 0.04), RV index of myocardial performance > or = 0.75 (p = 0.03), RVSP/systolic blood pressure > or = 0.66 (p = 0.01), intraoperative use of vasopressors (p < 0.01), and anesthesia when nitrous oxide was not used (p < 0.01) were each associated with postoperative mortality. In patients with PH undergoing noncardiac surgery with general anesthesia, specific clinical, diagnostic, and intraoperative factors may predict worse outcomes.
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              Pulmonary hypertension in CKD.

              Pulmonary arterial hypertension is a rare disease often associated with positive antinuclear antibody and high mortality. Pulmonary hypertension, which rarely is severe, occurs frequently in patients with chronic kidney disease (CKD). The prevalence of pulmonary hypertension ranges from 9%-39% in individuals with stage 5 CKD, 18.8%-68.8% in hemodialysis patients, and 0%-42% in patients on peritoneal dialysis therapy. No epidemiologic data are available yet for earlier stages of CKD. Pulmonary hypertension in patients with CKD may be induced and/or aggravated by left ventricular disorders and risk factors typical of CKD, including volume overload, an arteriovenous fistula, sleep-disordered breathing, exposure to dialysis membranes, endothelial dysfunction, vascular calcification and stiffening, and severe anemia. No specific intervention trial aimed at reducing pulmonary hypertension in patients with CKD has been performed to date. Correcting volume overload and treating left ventricular disorders are factors of paramount importance for relieving pulmonary hypertension in patients with CKD. Preventing pulmonary hypertension in this population is crucial because even kidney transplantation may not reverse the high mortality associated with established pulmonary hypertension. Copyright © 2013 National Kidney Foundation, Inc. Published by Elsevier Inc. All rights reserved.
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                Author and article information

                Journal
                Indian J Anaesth
                Indian J Anaesth
                IJA
                Indian Journal of Anaesthesia
                Medknow Publications & Media Pvt Ltd (India )
                0019-5049
                0976-2817
                February 2018
                : 62
                : 2
                : 131-135
                Affiliations
                [1]Department of Anaesthesiology and Critical Care, Mahatma Gandhi Medical College and Hospital, Jaipur, Rajasthan, India
                [1 ]Department of Anaesthesiology, Critical Care and Pain, Tata Memorial Centre, Mumbai, Maharashtra, India
                Author notes
                Address for correspondence: Dr. Sohan Lal Solanki, Department of Anaesthesiology, Critical Care and Pain, Tata Memorial Centre, Mumbai, Maharashtra, India. E-mail: me_sohans@ 123456yahoo.co.in
                Article
                IJA-62-131
                10.4103/ija.IJA_529_17
                5827480
                29491519
                0d1c480f-b362-4488-84d9-7b9edd35dc64
                Copyright: © 2018 Indian Journal of Anaesthesia

                This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 License, which allows others to remix, tweak, and build upon the work non-commercially, as long as the author is credited and the new creations are licensed under the identical terms.

                History
                Categories
                Original Article

                Anesthesiology & Pain management
                end-stage renal disease,hypertension,pulmonary,transplantation

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