A 41year old male patient received a Donation after brain death (DBD) kidney transplant from a 27-year-old female patient with a traumatic head injury. The donor had normal kidney function with an estimated glomerular filtration rate (eGFR) greater than 90 ml/min/1.732 m2 with no significant past medical history. The HLA mismatch was 1:1:1 and a cold ischaemic time of 13 hours 42 minutes. His primary renal disease was hypertensive ischaemic nephropathy, which was proven by renal biopsy in year 2016. Patient was on haemodialysis for 3 months via a left brachiocephalic fistula and had a urine output of 1000 to 1200 milliliters (mls) per day. Induction for renal transplant was with Basiliximab and Methylprednisolone. Maintenance immunosuppression therapy consisted of Prednisolone, Tacrolimus and Mycophenolate initiated from the day of surgery. Pneumocystis Carinii Pneumonia (PCP) prophylaxis was provided with co-trimoxazole. His surgery was uncomplicated and no immediate post-operative complications were reported. Immediately following surgery patient had a urine output of 90-100 mls/hour. On the first post-operative day this increased to 200 mls/hour. Despite having a good urine output his eGFR did not improve. Ultrasounds suggested good renal perfusion with no evidence of obstruction. His Tacrolimus levels were within acceptable limits (8-10) and there were no signs of infection. A decision to do a transplant kidney biopsy was made on the fifth day following a multidisciplinary team meeting. Patient's clinical notes and local renal data software (Vital Data) were used to get the details and information. Histological light microscopy images were requested from the Histopathology department.View Large Image Figure ViewerDownload Hi-res image Download (PPT) His transplant kidney biopsy showed florid granulomatous interstitial nephritis with no evidence of infection, rejection or Calcineurin Inhibitor (CNI) toxicity Figure 1. Differential diagnosis were fungal infections, sarcoidosis, adenovirus and tuberculosis, however all results were negative. The status of sister kidney (other kidney from the same donor) was investigated and showed that the recipient was discharged with an eGFR greater than 60 on the seventh day post-transplant. After excluding infection, rejection and any granulomatous disease in the sister kidney, drugs were thought to be a potential causative agent. Co-trimoxazole seemed most likely but there was very limited evidence in support of this. The patients’ Co-Trimoxazole was stopped and Dapsone was initiated for PCP prophylaxis. High dose oral prednisolone 60 mg was also initiated keeping in mind the severe inflammation. His eGFR rose from 7-to 20 ml/min/1.732 m2 in 7 days. Since then it has continually improved and the eGFR is now 46. Demonstrated by Figure 2. Our case report i suggests that in patients with early renal allograft dysfunction clinicians should be mindful about the possibility of AIN secondary to prophylactic antibiotics like Co-Trimoxazole. This case was discussed in American Society of Nephrology at San Diego 2018 in a talk on renal biopsy and clinical correlations. Neither the speakers and nor the audience agreed to have seen a case of granulomatous interstitial nephritis secondary to Co-trimoxazole and suggested to publish this case.