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INTRODUCTION: Recurrence of anti-glomerular basement membrane (anti-GBM) glomerulonephritis in the kidney graft is a rare event, described in limited reports. The aim of this study was to evaluate, in a large cohort of patients with long follow-up, the risk of recurrence of anti-GBM disease, the risk factors associated with clinical recurrence, and the long-term patient and graft survival. METHODS: This was a multicenter retrospective study. Inclusion criteria were patients with anti-GBM glomerulonephritis who underwent transplantation of a kidney between 1977 and 2015. Exclusion criteria were systemic vasculitis, lupus erythematosus, and cryoglobulinemia. Recurrence was defined as reappearance of clinical signs of glomerulonephritis along with histological signs of proliferative glomerulonephritis and linear IgG staining on kidney biopsy, with or without anti-GBM antibodies. RESULTS: A total of 53 patients were included. Recurrence of anti-GBM glomerulonephritis in a first kidney transplant occurred in only 1 patient 5 years after transplantation (a prevalence rate of 1.9%) in the context of cessation of immunosuppressive drugs, and resulted in graft loss due to recurrence. Linear IgG staining on kidney biopsy in the absence of histological signs of proliferative glomerulonephritis was observed in 4 patients, in the context of cellular rejection. Patient survival was 100%, 94%, and 89% at 5, 10, and 15 years, respectively. Death-censored first-graft survival rates were 88%, 83%, and 79% at 5, 10, and 15 years, respectively. CONCLUSION: The recurrence rate of anti-GBM glomerulonephritis after transplantation is very low but is associated with graft loss. The long-term patient and graft survival rates are excellent.
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Background: Pneumocystis jirovecii associated pneumonia is a potentially life-threatening opportunistic infection, occurring most frequently in the first year after renal transplantation, and may be associated with hypercalcemia. Clinical presentation:We report the case of a renal transplant recipient presenting with Pneumocystis jirovecii associated pneumonia and hypercalcemia due to ectopic production of 1,25-dihydroxyvitamin D, 6 years after renal transplantation. Calcemia and 1-25 hydroxyvitamin D levels normalized after our patient was treated by trimethoprim-sulfamethoxazole. Discussion: We review similar cases to delineate the clinical and biological profile of patients with Pneumocystis jirovecii pneumonia associated hypercalcemia. Conclusion:Physicians should evoke this diagnosis in renal transplant recipients presenting with pulmonary infection associated with hypercalcemia.