Prostatic abscess is an uncommon but clinically significant infectious complication in immunocompromised hosts, particularly renal transplant recipients. Its nonspecific symptomatology often results in delayed diagnosis, with potential adverse impact on allograft function and patient outcomes.

We report the case of a 41-year-old male who received a living-related kidney transplant from his 66-year-old mother. Induction immunosuppression consisted of anti-thymocyte globulin (ATG), followed by maintenance with tacrolimus, mycophenolate mofetil (MMF), and corticosteroids. Baseline serum creatinine was 1.7 mg/dL. At 3 months post-transplant, the patient developed acute bacterial cystitis and vesicoureteral reflux involving the graft ureter, with serum creatinine rising to 2.3 mg/dL. At 19 months, he was diagnosed with graft ureteral stricture and underwent ureteral stenting (double-J catheter insertion). Despite intervention, progressive allograft dysfunction ensued. At 25 months post-transplant, he was diagnosed with acute antibody-mediated rejection and treated with plasma exchange. One month later, serum creatinine increased to 5.2 mg/dL. At 38 months post-transplant, a protocol biopsy confirmed chronic active antibody-mediated rejection. At 38 months post-transplant, the patient presented with fever, dysuria, and obstructive lower urinary tract symptoms. Digital rectal examination revealed a tender, enlarged prostate. Multiphasic contrast-enhanced CT of the abdomen and pelvis demonstrated a prostatic abscess.

The patient underwent transurethral resection of the prostate with abscess drainage. Postoperative clinical improvement was observed, with resolution of fever and urinary symptoms, as well as normalization of inflammatory markers.

This case highlights the importance of considering atypical and occult infectious etiologies, such as prostatic abscess, in renal transplant recipients with unexplained urinary symptoms and graft dysfunction. Prompt radiological evaluation and timely surgical intervention can result in rapid clinical improvement and may contribute to stabilization of allograft function.