Abstract: SA-PO1164
A Recurrent Humoral Immune Defect Unmasked by Invasive Extended-Spectrum β-Lactamase (ESBL) Escherichia coli Infection in a Kidney Transplant Recipient
Session Information
- Transplantation: Clinical - Infectious Diseases
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Khalifa, Muhammed, Hennepin Healthcare System Inc, Minneapolis, Minnesota, United States
- Ibrahim, Abdelrahman, Hennepin Healthcare System Inc, Minneapolis, Minnesota, United States
- Gad, Ahmed, Hennepin Healthcare System Inc, Minneapolis, Minnesota, United States
- Kwakye, Kwabena A., Hennepin Healthcare System Inc, Minneapolis, Minnesota, United States
Introduction
Secondary hypogammaglobulinemia is underrecognized in kidney transplant recipients and may predispose to severe multidrug-resistant infections. We report invasive ESBL Escherichia coli infection involving urine, blood, and lung in a kidney transplant recipient with recurrent severe hypogammaglobulinemia.
Case Description
A 61-year-old man with ESRD from diabetic nephropathy status post deceased donor kidney transplant in 2023 on tacrolimus and chronic prednisone, severe steroid-dependent asthma, persistent CMV viremia, and recurrent resistant pulmonary infections including carbapenem-resistant Pseudomonas aeruginosa and MSSA pneumonia in 2025 presented with acute hypoxic respiratory failure requiring intubation. CT chest showed bilateral consolidative opacities consistent with multifocal pneumonia. Urine culture grew >100,000 CFU/mL ESBL E. coli, blood cultures grew ESBL E. coli with CTX-M detected by NAAT, and BAL from the left upper lobe grew E. coli with PMNs on Gram stain. AFB smear, fungal testing, and viral respiratory testing were negative. Serum IgG was 286 mg/dL. He had hypogammaglobulinemia since 2013, with IgG nadir 188 mg/dL in 2013. Prior hematology evaluation in 2014 showed normal IgA/IgM, no CVID, no malignancy on imaging, and unremarkable bone marrow biopsy; however, marrow flow cytometry noted B cells comprising only 2% of lymphocytes. Low IgG was attributed to chronic steroids and kidney disease. IgG later normalized to 1,192 mg/dL in 2025 before declining again. He received IV ertapenem for 10 days and IVIG 0.4 g/kg.
Discussion
This case illustrates recurrent severe hypogammaglobulinemia across two eras: chronic steroid exposure and ESRD predating transplant, followed by post-transplant immunosuppression after DDKT. This culminated in invasive ESBL E. coli infection involving urine, blood, and lung. The low marrow B-cell population identified over a decade before transplant suggests limited humoral reserve beyond steroid effect alone. The transient IgG normalization followed by recurrent severe decline highlights dynamic humoral immunity in immunosuppressed kidney transplant recipients. Patients with recurrent or invasive infections should be evaluated for hypogammaglobulinemia regardless of prior normal IgG levels. Recognition may affect antimicrobial strategy, immunosuppression review, infection prevention, and IVIG consideration.