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2.
Transpl Immunol ; 81: 101943, 2023 12.
Article in English | MEDLINE | ID: mdl-37866670

ABSTRACT

BACKGROUND: The presence of anti-Glutathione S-transferase T1 (GSTT1) antibodies (abs) has been hypothesized as a pathogenic contributor in antibody-mediated rejection (AMR). METHODS: We aimed to evaluate the relationship between genetic variants of GSTT1, anti-GSTT1 abs and AMR in a cohort of 87 kidney transplant (KTx) patients using Immucor's non-HLA Luminex assay. Patients were classified according to biopsy-proven AMR and HLA-DSA status: AMR with positive anti-HLA-DSAs (AMR/DSA+, n = 29), AMR but no detectable anti-HLA-DSAs (AMR/DSA-, n = 28) and control patients with stable allograft function and no evidence of rejection (n = 30). RESULTS: At an MFI cut-off of 3000, the overall prevalence of anti-GSTT1 abs was 18.3%. The proportion of patients with anti-GSTT1 abs was higher in the AMR/DSA- group (25%), compared to the control (13.3%) and AMR/DSA+ group (3.4%) (p = 0.06). Among patients with anti-GSTT1 abs, the MFI was higher in AMR/DSA- and GSTT1-Null patients. Of 81 patients who underwent GSTT1 genotyping, 19.8% were homozygotes for the null allele (GSTT1-Null). GSTT1-Null status in the transplant recipients was associated with the development of anti-GSTT1 abs (OR, 4.49; 95%CI, 1.2-16.7). In addition, GSTT1-Null genotype (OR 26.01; 95%CI, 1.63-404) and anti-GSTT1 ab positivity (OR 14.8; 95%CI, 1.1-190) were associated with AMR. Within AMR/DSA- patients, the presence of anti-GSTT1 abs didn't confer a higher risk of failure within the study observation period. CONCLUSION: The presence of anti-GSTT1 abs and GSTT1-Null genotype is associated with AMR, but do not appear to lead to accelerated graft injury in this cohort of early allograft injury changes, with a limited period of follow-up.


Subject(s)
Kidney Transplantation , Humans , HLA Antigens/genetics , Graft Rejection/genetics , Antibodies , Genotype , Isoantibodies , Tissue Donors
4.
Clin Nephrol ; 94(4): 212-214, 2020 Oct.
Article in English | MEDLINE | ID: mdl-32893813

ABSTRACT

The glomerulonephritis (GN) of granulomatosis polyangiitis is described as "pauci immune" because the glomeruli show little or no evidence of immune complex deposition by immunofluorescence or electron microscopy. Here we describe a severe crescentic GN in which the patient was myeloperoxidase-antineutrophil cytoplasmic antibodies (MPO-ANCA) positive, and on renal biopsy the glomeruli were pauci immune (there were only a few electron-dense deposits). However, by immunofluorescence the glomeruli showed "full-house" staining (the glomeruli stained positive for C1q, C3, IgG, IgA, and IgM). The latter staining pattern would be consistent with that seen in patients with lupus-like GN or with severe crescentic GN as a result of bacterial infection. So, should this patient receive high-dose immunosuppressive therapy and steroid therapy to treat presumed autoimmune GN, or should the patient receive intensive antibiotic therapy to treat a presumed underlying severe infection? This dilemma was soon resolved because the patient's blood culture returned positive for Streptococcus mutans and cardiac echo showed evidence of bacterial endocarditis. This report provides further detail regarding the patient's clinical issues.


Subject(s)
Bacteremia , Glomerulonephritis , Streptococcal Infections , Aged , Diagnosis, Differential , Humans , Kidney/chemistry , Kidney/pathology , Lupus Nephritis , Male , Streptococcus mutans
6.
Cureus ; 10(9): e3289, 2018 Sep 11.
Article in English | MEDLINE | ID: mdl-30443459

ABSTRACT

Typical hemolytic uremic syndrome (HUS) in adults is an uncommon clinical occurrence and has been rarely reported in the literature. Typical HUS is mainly caused by Shiga toxin-producing Escherichia coli (STEC) and is typically a pediatric disease. Worldwide outbreaks have been reported, one of the largest and most recent being in Germany. We are reporting a case of a 55-year-old male who presented with acute diarrhea. His laboratory parameters were suggestive of HUS and molecular testing was positive for STEC in stools. The patient received supportive therapy, and he recovered clinically with an improvement in his laboratory parameters. We hereby highlight the importance of timely diagnosis of typical HUS in guiding management and avoiding unnecessary testing and treatment. The mainstay of therapy is aggressive and prompt intravenous hydration to help alleviate the acute kidney injury and improve the clinical outcomes.

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