Species-Specific Efflux-Associated Transcriptional Patterns in Gram-Negative Uropathogens from Kidney Transplant Recipients: A Companion Molecular Analysis

Multidrug-resistant (MDR) Gram-negative uropathogens pose a significant challenge for kidney transplant (KTX) recipients, yet the relationship between efflux-associated transcription and antimicrobial resistance in isolates from this patient population remains poorly characterized. We quantified species-specific efflux-associated gene expression using TaqMan RT-qPCR in 83 urinary isolates from KTX recipients obtained during the first post-transplant year (Escherichia coli, n = 37; Klebsiella pneumoniae, n = 41; Pseudomonas aeruginosa, n = 5), and then examined its associations with CLSI-interpreted antimicrobial resistance phenotypes, recipient and transplant characteristics, and within-species gene co-expression. Strong correlations were observed between cognate gene pairs, including emrA–emrB and acrE–acrF in E. coli and kpnE–kpnF and acrA–acrB in K. pneumoniae. Nominally higher acrA and acrB expression occurred in ciprofloxacin-resistant K. pneumoniae (Cliff’s δ = +0.40; p = 0.029 and 0.031), and higher mdtA expression was observed in ciprofloxacin-resistant E. coli, whereas emrA, acrA, and emrB showed nominal associations with cephalosporin resistance in E. coli; none of these associations remained significant after Benjamini–Hochberg false-discovery-rate correction (all q > 0.05), and the ciprofloxacin signals were attenuated when intermediate isolates were excluded. In additional analyses, the E. coli emrA, emrB, and acrA signals were stronger for third-generation cephalosporin resistance (Cliff’s δ = +0.52 to +0.53; q = 0.052) and reached q < 0.05 in sensitivity analyses of intermediate results (q = 0.031–0.041), although these analyses remained exploratory. No corrected associations were found with trimethoprim–sulfamethoxazole resistance, MDR status, or clinical characteristics; P. aeruginosa data were descriptive only. These exploratory, associative findings indicate that the measured transcriptional variation itself does not explain the MDR phenotype, supporting further studies integrating functional efflux assays with genomic characterization of other resistance mechanisms.