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A 17-year-old girl with a few years' history of declining vision, photophobia, and dry eye symptoms was referred to our clinic. She noted that the vision in the right eye declined significantly over the past several months. On her last year examination, her uncorrected distance visual acuity (UDVA) was recorded as 20/25 in both eyes with a corrected distance visual acuity (CDVA) of 20/20 in both eyes with minimal refractive error, with a diagnosis of bilateral Salzmann nodular degeneration. The patient was given artificial tears and was encouraged to wear sunglasses. On examination now, UDVA was 20/70 in the right eye and 20/40 in the left eye. The manifest refraction was -2.00 + 1.25 × 96 in the right eye and -1.00 + 2.00× 34 in the left eye, with a CDVA of 20/50 and 20/30, respectively. Slitlamp examination revealed superficial reticular stromal scar with clear intervening spaces involving the anterior 75 μm of the stromal cornea in the central 6.0 mm optical zone (Figure 1).JOURNAL/jcrs/04.03/02158034-202104000-00021/figure1/v/2021-04-19T183640Z/r/image-tiffJOURNAL/jcrs/04.03/02158034-202104000-00021/figure2/v/2021-04-19T183640Z/r/image-tiff The rest of the anterior and posterior segment examination was completely normal and noncontributory. Anterior segment optical coherence tomography (AS-OCT) revealed subepithelial lesion involving the central aspect of the cornea in the right eye more than that in the left eye (Figure 2). Family history was significant for an older sister with a similar problem who never required medical attention. She also has mild photophobia and dry eye symptoms. What is your differential diagnosis? What diagnostic test will help you in your diagnosis and clinical decision-making? What is the most likely diagnosis in this case? Do you recommend medical and/or surgical intervention in the right eye, realizing that there has been exacerbation of her ocular condition in the most recent year? What is the long-term prognosis and future plan for a patient with this potential condition?Histologic antibody-mediated rejection (hAMR) is defined as a kidney allograft biopsy satisfying the first 2 Banff criteria for diagnosing antibody-mediated rejection (AMR) tissue injury and evidence of current/recent antibody interaction with the endothelium. In approximately one-half of such cases, circulating HLA donor specific antibodies (DSA) are not detectable by current methodology at the time of biopsy. Some studies indicated a better prognosis for HLA-DSA-negative cases of hAMR compared to those with detectable HLA-DSA, whereas others found equally poor survival compared to hAMR-negative cases. We reviewed the literature regarding the pathophysiology of HLA-DSA-negative hAMR. We find 3 nonmutually exclusive possibilities 1) HLA-DSA are involved, but just not detected; 2) non-HLA DSA (allo- or autoantibodies) are pathogenically involved; and/or 3) antibody-independent NK cell activation is mediating the process through "missing self" or other activating mechanisms. These possibilities are discussed in detail. Recommendations regarding the approach to such patients are made. Clearly, more research is necessary regarding the measurement of non-HLA antibodies, recipient/donor NK cell genotyping, and the use of antibody reduction therapy or other immunosuppression in any subset of patients with HLA-DSA-negative hAMR.

Noninvasive detection of primary graft dysfunction (PGD) remains a major challenge. SERCA2a plays an important role in cardiac homeostasis and its dysregulation has been associated with ventricular dysfunction and rejection. This study aimed to determine the potential utility of plasma levels of SERCA2a as a biomarker of PGD.

135 plasma samples were collected from adult recipients 2-6 hours prior to heart transplantation (HT). Selleck AR-A014418 Plasma concentrations of SERCA2a were determined using a specific sandwich enzyme-linked immunosorbent assay. Variables related to the recipient, the donor, and the periprocedural were collected in order to determine a multivariate predictive model of PGD.

Levels of SERCA2a were decreased in patients who developed PGD (median 0.430 ng/mL [IQR 0.260 - 0.945] versus 0.830 ng/mL [IQR 0.582 - 1.052]; p = 0.001). Receiver operating characteristic (ROC) curve analysis revealed that SERCA2a discriminated between patients with and without PGD (AUC = 0.682, p = 0.001), and a cutoff point ≥ 0.60 ng/ml was a protective independent predictor of PGD (odds ratio 0.215 [p = 0.004]). Three independent predictors of PGD in this study were reduced levels of pre-HT SERCA2a, increased bilirubin levels, and short-term mechanical circulatory support bridge to transplantation. The analysis of the ROC curve of the model obtained a significant AUC 0.788, p = 0.0001.

Our findings suggest that assessment of SERCA2a plasma levels may improve risk prediction for the occurrence of PGD, and could be considered as a novel noninvasive biomarker in patients undergoing HT.

Our findings suggest that assessment of SERCA2a plasma levels may improve risk prediction for the occurrence of PGD, and could be considered as a novel noninvasive biomarker in patients undergoing HT.

There is little evidence regarding the use of organs from deceased donors with infective endocarditis. We performed a retrospective analysis of the utilization, safety, and long-term survival of transplants from donors with infective endocarditis in the UK.

We studied deceased donor transplants over an 18-year period (2001 to 2018) using data from the UK Transplant Registry. We estimated the risk of infection transmission, defined as a microbiological isolate in the recipient matching the causative organism in the donor in the first 30 days posttransplant. We examined all-cause allograft failure up to 5 years in kidney and liver recipients, comparing transplants from donors with endocarditis with randomly selected matched control transplants.

We studied 88 transplants from 42 donors with infective endocarditis. We found no cases of infection transmission. There was no difference in allograft failure between transplants from donors with infective endocarditis and matched control transplants, among either kidney (HR 1.