Emphysematous pyelonephritis of transplant and native polycystic kidneys; Эмфизематозный пиелонефрит трансплантата и собственных поликистозно изменённых почек

Introduction Emphysematous pyelonephritis is a rare necrotizing form of purulent-destructive infection involving the collecting system, renal parenchyma, paranephric and perinephric space [1]. The main risk factors are diabetes mellitus, especially with poor glycemic control, urinary tract obstruction and immunosuppression [2]. Kidney transplant EP is an extremely rare condition. Less than 40 cases of EP have been documented in Englishand Russian-language literature until now [3]. This form of EP combines multiple risk factors: immunosuppressive therapy, frequent diabetes mellitus, and bacterial colonization of the urinary tract. These factors contribute to a more severe course and a higher mortality risk compared to general population [3, 4]. We present a clinical case of EP where the infectious process affected both the renal transplant and the patient's own polycystic kidneys. Clinical case Patient S., 64 years old, female, was admitted in August 2024 for renal transplant dysfunction. She had suffered from end-stage renal failure due to polycystic kidney disease since 2008 and underwent kidney transplantation from a deceased donor in 2009. Since 2023, she had been diagnosed with post-transplant diabetes mellitus managed pharmacologically. Over the past 6 months, she had been hospitalized multiple times for recurrent urinary tract infections caused by ureterocystoanastomosis stricture. Seven days before hospitalization, the patient suffered severe general weakness, nausea and vomiting without fever. On admission, she presented with acute graft dysfunction (oliguria, Pcr 435 μmol/l), hyperglycemia 30,8 mmol/l, systemic inflammatory reaction syndrome (leukocytosis 15.15*109/l, C-reactive protein 106 mg/l, procalcitonin 5.52 ng/ml). CT of the urinary system with contrast revealed gas in the renal pelvis and cysts of the native polycystic kidneys, impaired urodynamics of the renal allograft, and gas in its collecting system (Fig. 1). Based on clinical, laboratory, and imaging data, EP of both renal allograft and the native polycystic kidneys was diagnosed. According to the Huang-Tseng classification (2000), this represents a class IV EP case (involvement of both kidneys or single functioning kidney in the infectious process) [5]. While urgent nephrectomy is typically recommended in such cases, this approach carried a high mortality risk due to the patient's critical condition and the expected surgical volume. Therefore, a minimally invasive approach combined with intensive conservative therapy was selected. The patient underwent percutaneous puncture nephrostomy of the graft (Fig. 2). Empirical antibacterial therapy was initiated (piperacillin/tazobactam and colistin intravenously, taking into account the previous colonization with E. coli sensitive to these antibiotics). Despite this, systemic inflammation markers remained elevated, and subfebrile fever developed. Microbiological analysis of surgical material and blood cultures identified E. coli resistant to cephalosporins, with PCR detection of BLATEM and BLACTX-M genes (indicating extended-spectrum beta-lactamase production). Therapy was adjusted to biapenem and fosfomycin. The patient was stabilized, but fever and elevated markers of systemic inflammation persisted. MRI of the urinary system showed ЕР predominantly in the left native kidney, with large cysts containing inflammatory material, while the transplant showed improving pyelonephritis (Fig. 3). A multidisciplinary team decided to remove the non-functioning polycystic kidneys in order to eliminate the infection source. Bilateral nephrectomy was performed (Fig. 4). Histopathology confirmed polycystic kidneys with variably sized cysts, leukocyte detritus in some cyst lumens, leukocyte infiltration of cyst walls, and focal purulent necrosis (Fig. 5A, 5B). Postoperatively, antibacterial therapy was continued, along with extracorporeal detoxification (continuous venovenous hemodiafiltration, 3 sessions of therapeutic plasma exchange). The patient's condition stabilized, body temperature returned to normal, systemic inflammatory signs resolved, and Pcr decreased to 237 μmol/l. The patient was discharged on day 17. At the six-month follow-up, the transplant function remained stable (creatinine 213.9 μmol/l, urea 19 mmol/l, the graft nephrostomy was functioning well, and no recurrences of UTIs were recorded. Conclusion The case illustrates a rare presentation of emphysematous pyelonephritis involving both native polycystic kidneys and a renal transplant. Two key risk factors were present: immunosuppressive therapy and diabetes mellitus. The multidisciplinary approach, combining drug therapy, extracorporeal detoxification, and surgical intervention, successfully preserved the renal allograph. This case rises important consideration regarding the potential role of pre-transplant period bilateral nephrectomy to eliminate sources of recurrent UTIs. © 2025 Elsevier B.V., All rights reserved.