We examined a group of SPK recipients that had early (<90 d post-transplant) pancreas graft failure caused by a technical complication, and looked at outcomes of the kidney graft in these recipients. Of 289 SPK transplants, 36 (12.5%) had early pancreas graft failure because of a technical complication: thrombosis (n = 16), leak (n = 5), infection (n = 14), and pancreatitis (n = 1). Once the pancreas was lost, there was a high incidence of subsequent kidney graft failure. Kidney graft survival in these 36 recipients was 71.4% at one yr and 59.5% at three yr, significantly inferior compared to recipients that did not have early failure of the pancreas (86% at one yr and 82% at three yr, p < 0.001). Of the 36 recipients with early pancreas loss, 18 have gone on to failure of the kidney graft. Causes included thrombosis (n = 3), infection (n = 1), death with function (n = 6), chronic rejection (n = 4), ischemia (n = 1), and other (n = 3). Of the 18 kidney graft failures, nine occurred within three months after loss of the pancreas graft, usually either because of graft thrombosis, or patient death (usually from systemic sepsis). Multivariate analysis showed technical failure of the pancreas to be the most significant risk factor for kidney graft loss (HR = 2.08, p = 0.006).

Conversion from a twice-daily to a once-daily tacrolimus formulation is a safe, effective strategy in the management of stable liver transplant patients.

Background: Although organizing pneumonia (OP) is a common pathological finding, studies including a substantial number of patients with idiopathic forms from a unique center and a long follow-up are rare. Objectives: To determine patients with cryptogenic forms of organizing pneumonia (COP), in order to characterize their clinical course, to identify predictive factors for relapse and to assess their effect on outcome. Methods: For a 19-year period, all histopathological reports from a community teaching hospital were reviewed, and OP was found in 210 lung specimens belonging to 197 patients. Results: Thirty-three (17%) patients presented cryptogenic forms and 32 of them (97%) responded to steroid therapy. At follow-up, 14 patients presented no relapses (no-relapse group, NR) and 18 (56%) presented relapses (relapsing group, RG) that resolved with ulterior treatment. Multifocal opacities on chest X-ray (RG 83% vs. NR 36%, p = 0.02) appeared to be a predictor for relapse. Patients with relapses showed a shorter time span to chest X-ray normalization (RG 8 ± 8 weeks vs. NR 13 ± 9 weeks, p = 0.09) that became significant in patients with 3 or more relapses (multiple-relapse group, MR, 4 ± 2 weeks vs. NR 13 ± 9 weeks, p < 0.04). Although the initial prednisone dose was similar in patients with relapsing forms, its maintenance was shorter than in patients without relapses, showing a trend to significance (RG 4 ± 3 weeks, NR 7 ± 6 weeks, p = 0.09). Lower levels of lactate dehydrogenase and γ-glutamyltransferase, although always within the normal range, were found in patients with relapsing forms. Conclusion: COP is a specific but infrequent form of OP with a good response to steroid therapy. Relapses are frequent and typical characteristics of COP which resolved with ulterior treatment. Multifocal opacities on chest X-ray and a shorter maintenance of the initial steroid dose may increase the risk of relapse.

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In spite of finding a gradient that linked socioeconomic deprivation to an increased risk of hospitalisation, there were no differences in mortality regarding SES in a universal healthcare coverage system.

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Fabry disease is a rare X-linked lysosomal storage disorder caused by mutations in the alpha-galactosidase gene. The most frequent cardiac presentation of Fabry disease is cardiomyopathy characterized by left ventricular (LV) hypertrophy, usually concentric. Heart disease in affected females tends to be clinically recognized later than in males and cardiac complications are the most frequently reported cause of death in females with Fabry disease. There are few data regarding the association between Fabry disease and LV noncompaction. We report a case of a 30-year-old asymptomatic woman, heterozygous for a nonsense alpha-galactosidase gene mutation (p.R220X), who presented LV noncompaction on cardiac magnetic resonance imaging, without LV wall hypertrophy. Histopathological examination of myocardial fragments showed marked deposition of glycosphingolipids in cardiomyocytes, confirming the diagnosis of Fabry cardiomyopathy. Based on this finding, the patient was proposed for enzyme replacement therapy. This case illustrates the role of endomyocardial biopsy in the clarification of doubtful or atypical findings related to cardiac Fabry disease, even in heterozygous women, and corroborates the contention that Fabry disease should be included in the differential diagnosis of LV hypertrabeculation/noncompaction.

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