Fatal Threat of Bacteremia Caused by Urinary Tract Infection in Renal Transplant Recipients

To the Editor:

Urinary tract infections (UTI) are the most common infections in renal transplant recipients. In this population, 23%–41.9% of recipients experienced at least one urinary tract infection, which was identified by morning mid-stream urine specimen culture [1-3]. The combined risk of graft loss and death after post-transplant pyelonephritis within the first six months is 45% [4]. In one series, the pathogens of gram-negative bacteremia in renal transplant recipients according to their frequency were Escherichia coli (23%), Klebsiella pneumoniae (19%), Pseudomonas aeruginosa (11%), Staphylococcus epidermidis (11%), Acinetobacter baumannii (7.7%), and Enterococcus faecalis (7.7%) [5]. Extended-spectrum β-lactamase (ESBL)-producing E. coli and K. pneumoniae blood stream infections were linked to a high mortality rate [6-8], with the in-hospital mortality rate reaching 20.6%–24% [6].

Last year, we had two cases of bacteremia caused by UTI after renal transplants from deceased donors. In a 34-year old female, the urine culture showed a gram-negative bacterium (8,000 colony-forming units/mL) 10 days after renal transplant, and she began to have fever 20 days later when a ureteral stent was removed. In this case, ESBL-producing E. coli was identified as the pathogen in blood culture specimens, and the immunosuppressant dose was reduced. Because of the weak response to antibacterial agents chosen according to the susceptibility test and her continuous high fever, immunosuppressant was suspended for 10 days. The serum creatinine concentration increased, and blood flow through the graft disappeared two days later. The graft was removed. Again, ESBL-producing E. coli was identified in the specimen. After graft removal, the temperature went back to normal gradually, and the blood and urine culture samples became negative. She was discharged from the hospital 18 days later.

In a 63-year-old woman, pan-drug-resistant strains of K. pneumoniae and P. aeruginosa were identified in urine samples three months after renal transplant and presented very weak responses to antibiotics. The same strains were detected in the blood 17 days later. Tigecycline and gentamicin were used according to the susceptibility tests, and graft function was well maintained with reduced immunosuppressant doses. The K. pneumoniae and P. aeruginosa appeared in phlegm and bronchoalveolar lavage fluid 10 days later and showed inadequate responses to the aggressive treatment. Because of continuous high fever and positive blood cultures, immunosuppressant was suspended for 10 days, and the creatinine concentration increased. The SpO₂ decreased a week later, and she was admitted to the intensive care unit for invasive mechanical ventilation. She finally succumbed to multiple organ failure caused by the refractory drug-resistant infection.

We reported these two bacteremia cases in renal transplant recipients with weak responses to antibacterial agents chosen according to the susceptibility tests. The treatment strategy of immunosuppressant reduction is recommended when bacteremia appears, but aggressive treatment, including the withdrawal of immunosuppressant and removal of the graft, should be considered if the therapeutic effect is limited. We suggest that immunosuppressant should be suspended when the treatment of immunosuppressant reduction and aggressive antibacterial therapy proves to be inadequate within no more than 10 days. The graft should be removed as soon as possible when all of the treatments are proved to be insufficient before septic shock appears, especially if there are refractory drug-resistant bacteria, because the infected graft is a main source of infection, and it is a threat to life.