Abstract Background and Aims Emphysematous pyelonephritis (EPN) denotes a severe infection of renal parenchyma resulting in necrosis and gas accumulation in the renal and perirenal tissue. Risk factors for urinary tract infections in renal transplant recipients include advanced age, female gender, reflux nephropathy prior to transplantation, diabetes mellitus, deceased donor kidney, kidney–pancreas transplant, retransplantation, antibody induction for immunosuppression, urinary bladder catheterisation, history of allograft rejection with subsequent escalation of immunosuppressive therapy and use of ureteral stents. There are no definite guidelines for management of EPN in renal allografts. If unstable and deteriorating, graft nephrectomy should be undertaken as soon as possible. Any delay in surgical intervention, be it percutaneous drainage or nephrectomy may result in death. Method A 25-year old male, diagnosed with IgA Nephropathy (IgAN) received a living donor renal transplant from his mother in 2013 after a dialysis vintage of 3 years. He received Basiliximab induction followed by maintenance immunosuppression with Tacrolimus, Mycophenolate mofetil and Prednisolone. He had no history of UTI in the immediate post-transplant period. His blood glucose levels were within normal limits and he had not had any urological intervention. In 2019, patient was diagnosed with IgAN recurrence as a cause of chronic renal allograft injury. His Creatinine at last follow up in July 2022 was 4.1 mg/dL. He presented in September 2022 with fever, chills, vomiting, pain in the right iliac fossa and inability to extend his right leg. At presentation, his BP was 86/60mmHg, with pyrexia and tachycardia. Ultrasonography revealed an ill-defined collection superomedial to the graft kidney with doubtful posterior extension and air foci. Non-contrast CT study revealed a large subcapsular collection, extending posteriorly into the right iliac fossa involving the right psoas major and inferiorly into the pelvis, with air foci and no evidence of any urinary tract obstruction suggestive of Acute Emphysematous pyelonephritis with ruptured abscess. He was started on broad-spectrum iv antibiotics- Meropenem and Levofloxacin. Immunosuppression was reduced. Laboratory investigations revealed total leucocyte count of 37,000 cells/mm3, Creatinine of 11 mg/dL, urine routine microscopy revealed field full of pus cells. Blood and urine cultures grew ESBL Escherichia coli. He was taken up for urgent urological intervention in the form of percutaneous drain insertion. Frank pus was aspirated and 200mL drained instantaneously, cultures of which demonstrated the same organism. Within 24 hours of pus drainage, patient became afebrile and had pain relief. He was given 3 weeks of culture-appropriate iv antibiotics, to continue another 3 weeks of oral Carbapenem. However, his graft dysfunction persisted, with no recovery and he became dialysis-dependent. Discussion EPN of the renal allograft is a rare occurrence. A study of EPN in renal transplant recipients by Alexander et al from 2012 revealed 18 out of 22 patients were diabetics, 9 necessitated graft nephrectomy and 7 required percutaneous drainage in addition to antibiotics4. Till date, up to 30 cases of graft EPN have been reported in English literature. The striking feature is that more than 90% of these cases were diabetic. Conclusion The complete pathogenesis of renal allograft EPN, especially in patients with no apparent traditionally described risk factors remains yet to be understood. A high degree of suspicion and early intervention may help to save the allograft.
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