Transplantation For Idiopathic Pulmonary Fibrosis Research Articles

Outcomes of Lung Transplantation for Idiopathic Pulmonary Fibrosis: Glass Half Full or Still Half Empty?

Outcomes of Lung Transplantation for Idiopathic Pulmonary Fibrosis: Glass Half Full or Still Half Empty?

Impact of age and telomere length on circulating T cells and rejection risk after lung transplantation for idiopathic pulmonary fibrosis

Most idiopathic pulmonary fibrosis (IPF) lung transplant recipients (IPF-LTRs) have short telomere (ST) length. Inherited mutations in telomere-related genes are associated with the development of T cell immunodeficiency. Despite this, IPF-LTRs with telomere-related rare variants are not protected from acute cellular rejection (ACR). We set out to determine the impact of both age and telomere length on the circulating T cell compartment and ACR burden of IPF-LTRs. We identified 106 IPF-LTRs who had telomere length testing using flowFISH (57 with short telomeres and 49 with long telomeres) as well as a subset from both cohorts who had cryopreserved PBMC at least 1 time point, 6 months posttransplantation. Circulating T cells from before transplantation and at 6 and 12 months posttransplantation were analyzed using multiparameter flow cytometry to study phenotype and functional capacity, and bulk T cell receptor sequencing was performed to study repertoire diversity. Linear regression was used to study the relationship of age and telomere length on early (within 1 year) and late (between 1 and 2 years) ACR. IPF-LTRs with ST were found to have premature "aging" of their circulating T cell compartment, with age-agnostic elevations in posttransplant terminal differentiation of CD8+ T cells, increased granzyme B positivity of both CD8+ and CD4+ T cells, upregulation of the exhaustion marker, CD57, and chemotactic protein CCR5, and enhanced T cell receptor clonal expansion. Additionally, we found a significant decline in early ACR burden with increasing age, but only in the ST cohort. IPF-LTRs with ST have premature "aging" of their circulating T cell compartment posttransplantation and a clear age-related decline in ACR burden.

Lung transplantation for idiopathic pulmonary fibrosis enriches for individuals with telomere-mediated disease.

Idiopathic pulmonary fibrosis (IPF) is the most common indication for lung transplantation in North America and variants in telomere-maintenance genes are the most common identifiable cause of IPF. We reasoned that younger IPF patients are more likely to undergo lung transplantation and we hypothesized that lung transplant recipients would be enriched for individuals with telomere-mediated disease due to the earlier onset and more severe disease in these patients. Individuals with IPF who underwent lung transplantation or were evaluated in an interstitial lung disease specialty clinic who did not undergo lung transplantation were examined. Genetic evaluation was completed via whole genome sequencing (WGS) of 426 individuals and targeted sequencing for 5 individuals. Rare variants in genes previously associated with IPF were classified using the American College of Medical Genetics guidelines. Telomere length from WGS data was measured using TelSeq software. Patient characteristics were collected via medical record review. Of 431 individuals, 149 underwent lung transplantation for IPF. The median age of diagnosis of transplanted vs non-transplanted individuals was significantly younger (60 years vs 70 years, respectively, p<0.0001). IPF lung transplant recipients (IPF-LTRs) were twice as likely to have telomere-related rare variants compared to non-transplanted individuals (24% vs 12%, respectively, p=0.0013). IPF-LTRs had shorter telomeres than non-transplanted IPF patients (p=0.0028) and >85% had telomeres below the age-adjusted mean. Post-transplant survival and CLAD were similar amongst IPF-LTRs with rare variants in telomere-maintenance genes compared to those without, as well as in those with short telomeres versus longer telomeres. There is an enrichment for telomere-maintenance gene variants and short telomeres among IPF-LTRs. However, transplant outcomes of survival and CLAD do not differ by gene variants or telomere length within IPF-LTRs. Our findings support individual with telomere-mediated disease should not be excluded from lung transplantation and focusing research efforts on therapies directed toward individuals with short-telomere mediated disease.

Delayed Opening of Patent Foramen Ovale in Recipients of Left Single Lung Transplant for Idiopathic Pulmonary Fibrosis

<h3>Introduction</h3> Patent foramen ovale (PFO) is a common cardiac abnormality but rarely causes significant hemodynamic consequences in the absence of elevated right heart pressures. Cases of delayed reopening of PFO with right-to-left shunts have been reported following left single lung transplantation despite normal right heart pressures. This phenomenon occurs by redirection of blood flow through the inferior vena cava toward the PFO due to rightward mediastinal shift toward the fibrotic native lung following transplantation. <h3>Case Report</h3> Case1: A 72 year-old man with left single lung transplantation for idiopathic pulmonary fibrosis (IPF) developed new exertional hypoxemia on post-operative day (POD) 32. Pre-operative transthoracic echocardiogram (TTE) showed only intrapulmonic shunt, but no Valsalva maneuver was performed. Computed tomography (CT) scan of the chest demonstrated normal appearing allograft on the left and rightward mediastinal shift. Transbronchial biopsy showed no acute rejection. Perfusion scan showed the presence of a right-to-left shunt with tracer uptake of brain and kidneys and low likelihood for pulmonary embolism. TTE revealed a moderate PFO and normal right ventricular systolic pressure by echocardiographic criteria. Transesophageal echo (TEE) confirmed the presence of a large PFO. Hypoxemia resolved following percutaneous closure with a septal occluding device. Case 2: A 75 year-old man with PFO on pre-operative TTE underwent left single lung transplant for IPF. Post-operative course was complicated by exertional hypoxemia on POD 67. Workup included transbronchial biopsy without evidence of acute rejection and CT scan of the chest showing normal allograft on the left, new rightward mediastinal shift, and no pulmonary emboli. TTE showed a PFO at rest and TEE confirmed a large PFO with bidirectional flow. Right heart catheterization confirmed normal right-sided heart pressures prior to percutaneous PFO closure, resulting in resolution of hypoxemia. <h3>Summary</h3> Hypoxemia due to right-to-left shunting through a PFO is a possible post-operative complication of left single lung transplant for fibrotic disease even in the absence of elevated right-sided heart pressures. This can occur when a more compliant allograft causes mediastinal shift.

Impaired CD8+ T Cell Proliferation to Alloantigens in Lung Transplant Recipients with Idiopathic Pulmonary Fibrosis is Associated with P53 Upregulation

<h3>Purpose</h3> Telomere dysfunction may persist in the immune system following lung transplantation for idiopathic pulmonary fibrosis (IPF) and impact responses to infections or donor antigens. Mechanistically, critically short telomeres can activate p53 and block cell proliferation. We hypothesized that p53 activation might be associated with the impaired proliferation to alloantigens for IPF lung transplant recipients. <h3>Methods</h3> We analyzed 5 IPF lung transplant recipients with telomere dysfunction and 6 age-matched non-IPF controls, 18 months after transplantation, and 4 healthy donors. We quantified CD8+ T cell proliferation to pooled, donor-derived, stimulated B cells (sBc) with or without treatment with KML001, a reagent that binds and erodes telomeres. Expression of p53 and proportions of Annexin V+ apoptotic cells were quantified by flow cytometry. Statistical comparisons were performed using 2-way ANOVA with Dunnett's post-test. <h3>Results</h3> IPF lung transplant recipients (Fig. A) demonstrated impaired CD8+ T cell proliferation relative to non-IPF patients (Fig. B) and healthy controls (Fig. C&D, P≤0.0002). This proliferation was further impaired by telomere erosion (Fig. C&E, P<0.0001). P53 expression was increased in cells responding to sBc stimulation (MFI change 183, 95% CI 159-207). Among T cells that did not proliferate to allo-stimulation (Fig. F), p53 expression was higher in IPF subjects versus non-IPF (P=0.049) or healthy referents (P=0.002). Apoptotic cells were not different between groups. <h3>Conclusion</h3> P53 upregulation is associated with impaired CD8+ T cell proliferation to alloantigens in lung transplant recipients with IPF and may mediate proliferative arrest in CD8+T cells for IPF lung transplant recipients. These findings may explain sensitivity of some recipients to p53 activators, such as mycophenolic acid, that may synergize with telomere dysfunction to drive cell cycle arrest and leukopenia.

CoQ10 enhances the efficacy of airway basal stem cell transplantation on bleomycin-induced idiopathic pulmonary fibrosis in mice

BackgroundRecent studies have demonstrated that airway basal stem cells (BCs) transplantation can ameliorate bleomycin-induced idiopathic pulmonary fibrosis (IPF) through lung regeneration promotion. However, BCs under oxidative stress in the alveolar microenvironment are poor in survival, causing unsatisfied efficacy of BCs transplantation. In this study, we investigated whether Coenzyme Q10(CoQ10) counteracts oxidative stress in the alveolar microenvironment, thus improved the efficacy of BCs transplantation for IPF treatment.MethodsThe protective effects of CoQ10 on H2O2-induced BCs apoptosis and cytoplasmic reactive oxygen species (ROS) level were tested by flow cytometry in vitro. The therapeutic effects of BCs combined with CoQ10 were compared to a single BCs transplantation protocol in IPF treatment after 2 weeks and were evaluated by parameters including changes of body weight and survival rate, as well as various levels of pulmonary inflammation, α-SMA expression and hydroxyproline (HYP) in IPF mouse lung tissues.ResultsCoQ10 preincubation with BCs (10 mM, 24 h) significantly reduced the late apoptosis of BCs and the number of oxidative stressful BCs as a result of H2O2 stimulation (1 mM, 6 h) in vitro. IPF mouse model was constructed through bleomycin (5 mg/kg) intratracheal instillation. Bleomycin-induced IPF mice showed weight loss continuously and mortality increased progressively during modeling. Serious pulmonary inflammatory cell infiltration, collagen fiber proliferation, and collagen protein deposition were observed in lung tissues of IPF mice. Though BCs transplantation alone improved indicators above in bleomycin-induced IPF mice to some extent, the combination with CoQ10 improved the transplantation efficacy and obtained better therapeutic effects.ConclusionCoQ10 blocked H2O2-induced apoptosis of BCs and ROS production in vitro, and enhanced the efficacy of BCs transplantation against bleomycin-induced IPF in mice.

Acute worsening of native lung fibrosis after single lung transplantation for pulmonary fibrosis: two case reports

BackgroundIn patients receiving single lung transplantation for idiopathic pulmonary fibrosis, worsening of fibrosis of the native lung is usually progressive over time, with no significant effects on gas exchange.Case presentationHere, we describe the cases of two Caucasian male recipients of single lung transplants for idiopathic pulmonary fibrosis, 65 and 62 years of age, who exhibited acute worsening of lung fibrosis after an episode of serious viral infection (cytomegalovirus primo-infection in one case and COVID-19 in the other). In both cases, along with opacification of the native lung over several days, the patients presented acute respiratory failure that required the use of high-flow nasal oxygen therapy. Eventually, hypoxemic respiratory failure resolved, but with rapid progression of fibrosis of the native lung.ConclusionWe conclude that acute worsening of fibrosis on the native lung secondary to a severe viral infection should be added to the list of potential complications developing on the native lung after single lung transplantation for idiopathic pulmonary fibrosis.

Successful Eradication of De Novo C1q-Binding Donor-Specific Antibodies with Rituximab Monotherapy

<h3>Introduction</h3> Antibody-mediated rejection (AMR) is an increasingly recognized cause of lung transplant allograft failure. Treatment of AMR involves combination therapy that is often poorly tolerated or unsuccessful with regimens involving the combination of intravenous immunoglobulins, plasmapheresis, and proteasome inhibitors, complement, or CD20 therapy. The development of DSAs alone, specifically complement activating C1q-binding DSAs, has been identified as an independent risk factor for solid organ transplant allograft dysfunction. Previous studies have examined the efficacy of combination therapy involving the anti-CD20 antibody rituximab to preemptively eliminate DSAs. Here we report on a case of successful eradication of de novo C1q-binding DSAs in a lung transplant recipient using rituximab. <h3>Case Report</h3> Our patient underwent double-lung transplantation for idiopathic pulmonary fibrosis in August 2019. His post-transplant course was notable for multiple episodes of acute cellular rejection (ACR) requiring burst-dose corticosteroids. DSA titers were monitored every three months post-transplant. At six months, de novo DSAs were detected (DQ7 with DQA1*05) at a mean fluorescence intensity (MFI) of 3623 (low-moderate) (Figure 1). These subsequently rose to an MFI of 11281 (strong) with development of C1q positivity that peaked at an MFI of 15038. Given his frequent episodes of ACR, the strong C1q positivity, and concerns regarding his ability to tolerate therapy for potential future AMR, he was preemptively treated with a single infusion of rituximab (375 mg per meter-squared body surface area). Follow-up DSA titers demonstrated near-total elimination of the C1q component (MFI 403). The patient tolerated the treatment without issue and continues to demonstrate improvement in his allograft function. <h3>Summary</h3> Rituximab monotherapy can be considered preemptively in patients with C1q-binding DSAs that may not tolerate traditional treatment of antibody-mediated rejection.

Lung Transplantation for Idiopathic Pulmonary Fibrosis: A Narrative Review

Idiopathic pulmonary fibrosis (IPF) is a debilitating and progressive lung disease without an identifiable cause. It is the most common form of interstitial pneumonias. The prognosis is worst in this disease with median survival of just 2–3 years after diagnosis without a lung transplant. Currently, there are no proven medical therapies to cure IPF. Pharmacological agents such as nintedanib and pirfenidone retard the progression of the disease to an extent but without any survival benefit. The only therapeutic option for IPF is lung transplantation with proven survival benefit. The major concern with lung transplantation is waiting time mortality. Lung allocation score was introduced in 2005 to reduce this mortality. Both single- and double-lung transplantations are used worldwide for IPF. Bilateral lung transplantation has been seen to have better survival rates in some studies, but there are no randomized trials which favor this recent trend. The posttransplant survival is lower than seen in other indications for lung transplantation. Posttransplant follow-up should be vigilant to detect complications as early as possible and treat them accordingly.

Acute myocardial infarction secondary to mucormycosis after lung transplantation

We present a case of a 57-year-old man who underwent bilateral lung transplantation for idiopathic pulmonary fibrosis. His immediately post-operative course was complicated by fever and cardiac arrest. Despite supportive care and broad-spectrum antibiotics, he experienced continued clinical decline. Autopsy results indicated angioinvasive mucormycosis and coronary arteritis resulting in acute myocardial infarction as the cause of death.

Fungki Ulcers

A 61-year-old female with a history of bilateral lung transplantation for idiopathic pulmonary fibrosis presented with shortness of breath, cough and diarrhea. She was on chronic immunosuppressive medications, including Tacrolimus and mycophenolate, and on apixaban for deep vein thrombosis.

Single versus double lung transplantation for fibrotic disease-systematic review.

Lung transplantation has long been the accepted therapy for end-stage pulmonary fibrotic disease. Presently, there is an ongoing debate over whether single or bilateral transplantation is the most appropriate treatment for end-stage disease, with a paucity of high-quality evidence comparing the two approaches head-to-head. This review was performed in accordance with PRISMA recommendations and guidance. Searches were performed on PubMed Central, Scopus and Medline from dates of database inception to September 2019. For the assessed papers, data was extracted from the reviewed text, tables and figures, by two independent authors. Estimated survival was analyzed using the Kaplan-Meier method for studies where time-to-event data was provided. Overall, 4,212 unique records were identified from the literature search. Following initial screening and the addition of reference list findings, 83 full-text articles were assessed for eligibility, of which 17 were included in the final analysis, with a total of 5,601 patients. Kaplan-Meier survival analysis illustrated improved survival in patients receiving bilateral lung transplantation (BLTx) than in those receiving unilateral transplantation for idiopathic pulmonary fibrosis at all time intervals, with aggregated survival for BLTx at 57%, 35.3% and 24% at 5-, 10- and 15-year follow-up, respectively. Survival rates for SLTx were 50%, 27.8% and 13.9%, respectively. Whilst a number of studies present conflicting results with respect to short-term transplantation outcomes, BLTx confers improved long-term survival over SLTx, with large-scale registries supporting findings from single- and multi-center studies. Through an aggregation of published survival data, this meta-analysis identified improved survival in patients receiving BLTx versus SLTx at all time intervals.

Review of Lung Transplantation for Patients 65 Years and Older with Idiopathic Pulmonary Fibrosis in Ireland

Purpose The first lung transplant (LTX) was performed in Ireland in 2005 in the MMUH, Dublin. Since the establishment of this programme there have been 243 LTX. LTX is the only effective treatment for Idiopathic Pulmonary Fibrosis (IPF). IPF has an average age of diagnosis of 66 years (yrs) and a median survival of 2.5 to 3.5 yrs (Ley et al., 2010). This demonstrates the need for LTX not only in this disease but also this age group. Advanced age is reported to negatively affect survival post LTX (Smith et al., 2006). We hypothesized that LTX in patients with IPF aged ≥ 65 yrs could be performed with acceptable outcomes. Methods A retrospective review of patients ≥ 65 yrs of age with IPF who received a LTX in the MMUH between 2008 and 2018. Electronic and paper patient records were reviewed and outcomes were analysed. Results To date 19.3 % (47/243) of LTX recipients in Ireland were ≥ 65 yrs. Of these 85.1% (40/47) had a diagnosis of IPF. The IPF group consisted of 77.5 % males (n=31) and 22.5% females (n=9) with a mean age of 66.7 yrs (range, 65 to 75 yrs). All recipients received single LTX, 50% received a left LTX and 50% received a right LTX. 1 died pre extubation, 3 intubated Conclusion Many lung transplant centres do not assess or transplant patients ≥ 65 yrs of age on the basis of poorer outcomes in this population. However it is evident from the analysed survival data that survival rates of this older IPF transplant recipient population is favourable when compared to the overall lung transplant survival rates reported by the ISHLT in 2017, of 80.47 % at 1 yr, 64.99% at 3 yrs and 53.42% at 5 yrs (ISHLT, 2017). This should encourage other centres to extend their cohort of patients considered for LTX assessment.

Risk of anastomotic dehiscence in patients with pulmonary fibrosis transplanted while receiving anti-fibrotics: Experience of the Australian Lung Transplant Collaborative.

The new anti-fibrotics pirfenidone and nintedanib are now in widespread use for idiopathic pulmonary fibrosis (IPF), but they may have an adverse impact on pathways involved in wound-healing. This study aimed to establish the safety of anti-fibrotic therapy in the peri-transplant period, particularly with regard to healing of the bronchial anastomosis. In this work we assessed a retrospective cohort of patients who had undergone lung transplantation with a diagnosis of pulmonary fibrosis between January 2012 and December 2017. Pre-transplant use of pirfenidone and nintedanib was identified. Anastomotic dehiscence of any extent was determined at bronchoscopy. Known risk factors for anastomotic dehiscence were evaluated in both anti-fibrotic and control groups. Two hundred twenty-six patients (160 males; mean age 59.7 ± 7.8 years) underwent transplantation in Australia for pulmonary fibrosis during the study period. Forty (17.7%) were receiving anti-fibrotics at the time of transplantation (29 with pirfenidone and 11 with nintedanib). There were 7 anastomotic dehiscence events, with overall incidence rates of 7.5% and 2.2% in the anti-fibrotic and control groups, respectively (p = 0.08). All episodes of dehiscence in the anti-fibrotic group and 2 of 4 in the comparator group occurred <6 weeks post-transplant. Survival at 30days was 100% and 96% (p = 0.21) and at 1 year was 93% and 88% (p = 0.01) in the anti-fibrotic and comparator groups, respectively. Two patients with dehiscence died. The other 5 anastomotic defects resolved, with 1 requiring stent insertion. The incidence of bronchial dehiscence after transplantation for IPF is low and is not significantly higher in patients receiving anti-fibrotic therapy at the time of transplantation.

Single Versus Bilateral Lung Transplantation for Idiopathic Pulmonary Fibrosis in the Lung Allocation Score Era

BackgroundIdiopathic pulmonary fibrosis (IPF) is a progressive and fatal disease. Lung transplantation is the only therapy associated with prolonged survival. The ideal transplant procedure for IPF is unclear. Outcomes after single transplantation (SLTx) versus bilateral lung transplantation (BLTx) in IPF patients after introduction of the Lung Allocation Score were examined. MethodsRecords of patients undergoing lung transplantation for IPF at our institution between May 2005 and March 2017 were reviewed to examine the effect of transplant laterality. Primary outcomes were overall, rejection-free, and bronchiolitis obliterans (BOS)-free survival at 1 and 5 years post-transplant. ResultsLung transplantation was performed in 151 IPF patients post-Lung Allocation Score. Most recipients were male with average age 59 ± 8 years. SLTx was performed in 94 patients (62%). In the overall cohort, comparative survival between SLTx and BLTx was similar at 1 and 5 years before and after adjusting for age and pulmonary hypertension (PH). SLTx was associated with shorter ventilator time and intensive care unit stay and trended toward improved survival over BLTx in patients without PH. ConclusionsThe use of SLTx versus BLTx in IPF did not correspond to significantly different survival adjusting for age and PH. BLTx was associated with prolonged postoperative ventilation and length of stay compared with SLTx. Patients without PH, all older patients, and patients with PH and advanced disease should be considered for SLTx for IPF.

Evolution and Risk Factors for Early Mortality After Lung Transplantation for Idiopathic Pulmonary Fibrosis: An Experience of 20 Years

High early mortality after lung transplantation (LT) for idiopathic pulmonary fibrosis (IPF) is still not well controlled, and some aspects remain debated. The aim of this study was to evaluate our experience to identify factors that might improve the early outcomes. Among the 427 patients transplanted from October 1993 to December 2014, 117 IPF patients underwent LT at our department. There was an increasing age of transplant recipients, and the overall early (1-mo_ mortality was 25/117 (21.4%) with a progressive decrease over the years. Logistic regression analysis for early mortality was performed, and multivariate analysis identified recipient age <55 years (P = .042; odds ratio [OR], 2.98), single-lung transplants (P = .001; OR, 5.226), and previous corticosteroid treatment (P = .05; OR, 5.128) as independent risk factors for development of early mortality. In conclusion, despite the increasing age of transplant recipients, we observed a decrease in mortality to almost one-half compared with our initial results. According to our results, the mortality risk in patients <55 years old is independent from the type of transplant (single or double), being higher with a single transplant. In addition, corticosteroid treatment should be reduced to achieve lower early mortality.

Lung Transplantation for Hypersensitivity Pneumonitis

Hypersensitivity pneumonitis (HP) is an inhaled antigen-mediated interstitial lung disease (ILD). Advanced disease may necessitate the need for lung transplantation. There are no published studies addressing lung transplant outcomes in HP. We characterized HP outcomes compared with referents undergoing lung transplantation for idiopathic pulmonary fibrosis (IPF). To identify HP cases, we reviewed records for all ILD lung transplantation cases at our institution from 2000 to 2013. We compared clinical characteristics, survival, and acute and chronic rejection for lung transplant recipients with HP to referents with IPF. We also reviewed diagnoses of HP discovered only by explant pathology and looked for evidence of recurrent HP after transplant. Survival was compared using Kaplan-Meier methods and Cox proportional hazard modeling. We analyzed 31 subjects with HP and 91 with IPF among 183 cases undergoing lung transplantation for ILD. Survival at 1, 3, and 5 years after lung transplant in HP compared with IPF was 96%, 89%, and 89% vs 86%, 67%, and 49%, respectively. Subjects with HP manifested a reduced adjusted risk for death compared with subjects with IPF (hazard ratio, 0.25; 95% CI, 0.08-0.74; P = .013). Of the 31 cases, the diagnosis of HP was unexpectedly made at explant in five (16%). Two subjects developed recurrent HP in their allografts. Overall, subjects with HP have excellent medium-term survival after lung transplantation and, relative to IPF, a reduced risk for death. HP may be initially discovered only by review of the explant pathology. Notably, HP may recur in the allograft.

A Rare Occurrence of Pulmonary Alveolar Proteinosis after Lung Transplantation

We present a case of pulmonary alveolar proteinosis (PAP) initially diagnosed 28 months after left single-lung transplantation for idiopathic pulmonary fibrosis. The diagnosis was based upon the presence of periodic acid-Schiff (PAS)-positive and surfactant immunostain-positive acellular lipoproteinaceous material within alveoli seen on transbronchial biopsy as well as in bronchoalveolar lavage fluid. The patient eventually also displayed a characteristic "crazy paving" pattern on radiographic imaging. Granulocyte macrophage-colony stimulating factor antibodies were negative, consistent with secondary PAP. PAP is a rare interstitial lung disease with only a few reported cases occurring after lung transplantation. The etiology is thought to be related to a defect in macrophage function caused by immunosuppression. Reduced immunosuppression has been associated with stabilization, but not reversal, of the condition in the case reported here. PAP is an exceptionally rare cause of dyspnea and radiographic infiltrates after lung transplantation and may be related to toxicity of immune-suppressive medications.

Bilateral versus single lung transplantation for idiopathic pulmonary fibrosis

Bilateral versus single lung transplantation for idiopathic pulmonary fibrosis

Kayexalate-Induced Esophageal Ulcer in a Patient With Gastroparesis

A 53-year-old man presented with an episode of coffee-ground emesis. He had undergone bilateral lung transplantation for idiopathic pulmonary fibrosis 1 month before admission. On presentation, his vital signs were stable (heart rate, 95/min; blood pressure, 106/80 mm Hg), with a hemoglobin of 11.4 g/dL. He was on tacrolimus immunosuppression, with trough levels within the therapeutic range (10–12 ng/mL). His serum potassium level had been elevated (range, 5.5–5.9 mmol/L) for 1 week before admission, for which he was being treated with sodium polystyrene sulfonate in sorbitol (Kayexalate 30 g/d orally).