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Herein, we report a rare case of severe respiratory syncytial virus pneumonia after kidney transplant in a 46-year-old woman. The patient was diagnosed with end-stage renal disease and underwent living-donor kidney transplant. Direct flow cytometry crossmatch testing yielded positive results, and desensitization treatment with rituximab, plasmapheresis, and im-munoglobulin was performed before transplant. There were no complications. Five days after discharge, the patient was readmitted with a 2-day history of fever and diagnosed with bilateral pneumonia. The patient was placed on mechanical ventilation and given renal replacement therapy. Respiratory syncytial virus in the bronchial washings was detected via polymerase chain reaction. Broad-spectrum antibiotics, intravenous methylprednisolone, and immunoglobulin were admin-istered. Over-immunosuppression strategies, such as desensitization therapy, may result in severe respiratory syncytial virus pneumonia, even in kidney transplant recipients.
Subject(s)
Desensitization, Immunologic/adverse effects , Kidney Failure, Chronic/surgery , Kidney Transplantation/adverse effects , Opportunistic Infections/virology , Pneumonia, Viral/virology , Respiratory Syncytial Virus Infections/virology , Respiratory Syncytial Virus, Human/pathogenicity , Female , Humans , Immunocompromised Host , Immunoglobulins, Intravenous/adverse effects , Immunosuppressive Agents/adverse effects , Living Donors , Middle Aged , Opportunistic Infections/diagnosis , Opportunistic Infections/immunology , Opportunistic Infections/therapy , Plasmapheresis/adverse effects , Pneumonia, Viral/diagnosis , Pneumonia, Viral/immunology , Pneumonia, Viral/therapy , Respiratory Syncytial Virus Infections/diagnosis , Respiratory Syncytial Virus Infections/immunology , Respiratory Syncytial Virus Infections/therapy , Respiratory Syncytial Virus, Human/immunology , Rituximab/adverse effects , Severity of Illness Index , Treatment OutcomeABSTRACT
BACKGROUND: α1-Antitrypsin (AAT) is an important protein in the anti-inflammatory response that functions to regulate the activity of serine proteinases. We aimed to evaluate the protective effect of AAT on ischemia-reperfusion injury (IRI) in a mouse model. METHODS: We investigated the effects of AAT in a C57BL/6 mouse model of IRI by dividing them into 4 groups: normal control, sham operated, ischemia-reperfusion (IR), and IR after AAT pretreatment (IR-AAT). In the IR-AAT group, mice were pretreated with AAT (80 mg/kg/d) for 3 days before renal ischemia was induced by clamping the bilateral renal vascular pedicles for 30 minutes. At 24 hours after IRI, biochemistry, histology, inflammatory cytokines, and apoptosis were assayed. RESULTS: Blood urea nitrogen and serum creatinine levels were significantly lower in the IR-AAT group than in the IR group. Neutrophil gelatinase-associated lipocalin and kidney injury molecule 1 protein levels were significantly lower in the IR-AAT group than in the IR group. In addition, there were fewer tubular injuries and less interstitial fibrosis in the IR-AAT group than in the IR group, and the expression levels of transforming growth factor ß, interleukin 1ß, and interleukin 6 were significantly lower in the IR-AAT group than in the IR group. When compared with the IR group, there were fewer terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) assay-positive cells, lower caspase 3 activity and B-cell lymphoma 2-associated X protein (Bax), and higher B-cell lymphoma 2 (Bcl-2) in the IR-AAT group. CONCLUSIONS: α1-Antitrypsin preserved renal function, attenuated tubular injuries and interstitial fibrosis, and inhibited inflammation and apoptosis after renal IRI. Our results suggest that AAT has protective effects against renal IRI by inhibiting inflammatory and apoptosis pathways.
Subject(s)
Kidney Diseases/prevention & control , Kidney/blood supply , Reperfusion Injury/prevention & control , Serine Proteinase Inhibitors/therapeutic use , alpha 1-Antitrypsin/therapeutic use , Animals , Apoptosis/drug effects , Blood Urea Nitrogen , Creatinine/blood , Cytokines/metabolism , Disease Models, Animal , Inflammation/pathology , Kidney Diseases/pathology , Male , Mice , Mice, Inbred C57BL , Reperfusion Injury/pathology , Serine Proteinase Inhibitors/pharmacology , alpha 1-Antitrypsin/pharmacologyABSTRACT
BACKGROUND: Phospholipase A2 receptor (PLA2R) has been identified as a major autoantigen in primary membranous nephropathy (MN). We evaluated the association between anti-PLA2R antibodies and clinical outcome in Korean patients with primary MN. METHODS: A total of 66 patients with biopsy-proven MN were included. Serum level of anti-PLA2R antibodies was measured by enzyme-linked immunosorbent assay. Biochemical parameters were estimated initially and at follow-up. RESULTS: Anti-PLA2R antibodies were detected in 52.1% and 27.8% of patients with primary and secondary MN, respectively. Forty-eight patients with primary MN were grouped based on presence or absence of anti-PLA2R antibodies. Proteinuria was more severe in anti-PLA2R-positive patients than in anti-PLA2R-negative patients (urine protein/creatinine ratio 7.922 ± 3.985 g/g vs. 4.318 ± 3.304 g/g, P = 0.001), and anti-PLA2R antibody level was positively correlated with proteinuria. The incidence of chronic kidney disease stage ≥ 3 was higher in anti-PLA2R-positive patients compared with anti-PLA2R-negative patients (P = 0.004). The probabilities of spontaneous remission were higher in anti-PLA2R-negative patients compared with anti-PLA2R-positive patients (P < 0.001). Multivariate analysis demonstrated that anti-PLA2R antibodies are an independent risk factor for developing chronic kidney disease stage ≥ 3 and for not reaching spontaneous remission. CONCLUSION: Detection of anti-PLA2R antibodies at diagnosis in patients with primary MN can predict prognosis and guide treatment decisions.
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[This corrects the article on p. 248 in vol. 37, PMID: 30254849.].
