Case Report: A 56-year-old man was referred for investigation of selleck compound nocturnal polydipsia and an elevated serum creatinine of 130 μmol/L. The patient’s history included GORD, hypertension and

gout. The patient had no history of kidney disease or drug allergies. The patient’s medications consisted of Allopurinol 300 mg daily, Verapamil 180 mg daily, Meclobomide 600 mg daily and Perindopril 7.5 mg nocte. He had also been taking Omeprazole 20 mg mane for four years. PPI-induced AIN was suspected and the patient’s serum creatinine normalised to 80 μmol/L following the replacement of Omeprazole with Ranitidine 300 mg daily. The serum creatinine deteriorated to 175 μmol/L after the Omeprazole was reintroduced because of worsening symptoms of GORD but returned to 80 μmol/L after the Omeprazole was again replaced with Ranitidine. Six months later, whilst taking Ranitidine 300 mg daily,

the serum creatinine unexpectedly deteriorated to 195 μmol/L and the patient developed a normochromic normocytic anaemia and sterile pyuria. A kidney biopsy confirmed a diagnosis of AIN. The Ranitidine was ceased and a four-week course of prednisolone was instituted. Four years later, the serum creatinine was 90 μmol/L. Deteriorating symptoms of GORD and concern regarding worsening oesophagitis prompted a trial of Famotidine 20 mg nocte. The serum creatinine promptly increased to 180 μmol/L and normalised following withdrawal of the Famotidine. Conclusions: As far as we are aware, this Dasatinib cell line is the first reported case of AIN to

both PPIs and H2RAs in a patient. 279 GRAM NEGATIVE SEPSIS POST RENAL TRANSPLANT BIOPSY IN PATIENT WITH ASYMPTOMATIC PYELONEPHRITIS H AL-KHAYYAT, N TOUSSAINT, S HOLT, P HUGHES Department of Nephrology, The Royal Melbourne Hospital, Parkville, Victoria, Australia Background: Pyelonephritis in patients post renal transplantation GBA3 has a reported incidence between 10–25% and nearly half of cases are asymptomatic. Transplant pyelonephritis shares many histopathological changes with cellular rejection (interstitial infiltrate, tubulitis) and may mask detection of rejection. Case Report: 41-year male with end-stage kidney disease secondary to IgA nephropathy (haemodialysis for 6 years) underwent a cadaveric renal transplant in 2004. Other medical history included hypertension, ischemic heart disease, and AF on warfarin. With worsening graft function after 10 years (Cr increased from 140 to 200 μmol/L) a renal biopsy was performed. The patient was asymptomatic and admitted the day before as he was rurally based. Pre-biopsy tests included urine microscopy which was pending at the time of the procedure.