She was treated with IVIG 0.1 mg/kg (total

10 doses).She made gradual recovery over few weeks and she cleared the adenovirus by PCR after 5 weeks of therapy with well-functioning graft with creatinine of 126 μmol/L. The patient is a 60-year-old woman with ESRF secondary to polycystic kidney disease. She had been on PD for 4 months prior to undergo deceased-donor renal transplantation with a single HLA mismatch Selleck R788 in 2013. The donor was CMV and EBV positive. Standard induction therapy was administered with basiliximab, prednisolone, mycophenolate mofetil and tacrolimus (0.05 mg/kg). Immediate postoperative care was unremarkable and a creatinine nadir of 49 μmol/L was seen within the first week. Protocol biopsy on day 12 revealed borderline cellular rejection with variable lymphocytic infiltrate see more and mild-moderate tubulitis with no change in serum creatinine. Immunofluorescence failed to show staining for c4d. She was treated with three doses of 500 mg IV methylprednisolone and repeat biopsy at day 29 showed no further evidence of rejection with a creatinine of approximately 50 μmol/L. Immunosuppressant dosage remained unchanged. Around 4 weeks post-transplant she began complaining of dysuria and frequency and fever of 40°C. She was treated empirically with amoxicillin/clavulanic acid but failed to grow a bacterial pathogen. After one week of oral antibiotics

her symptoms did not improve and thus immunosuppression was reduced and a single dose of gentamicin (4 mg/kg) was administered, and a 7 day course of ciprofloxacin was commenced to cover protocol removal of the ureteric stent. After 3 further days of antibiotics and second negative urine culture, the patient developed diarrhoea and was admitted for inpatient management. Stool, plasma and urine specimens were positive for adenovirus confirming suspicion of systemic adenovirus. Given the well-matched donor, and concern for progressive and high risk adenovirus infection, immunosuppression was reduced further. Adenylyl cyclase With severe, almost half-hourly urinary frequency and dysuria, in spite of being systemically well with a normal white cell count, cidofovir was commenced at 1 mg/kg thrice-weekly intravenous infusions. The dysuria

and diarrhoea slowly improved after one week of therapy. Serum and plasma adenovirus was undetectable by PCR after the fourth infusion although the virus continued to shed through the urine and stool albeit reduced by 2–3 logs in semi-quantitative analysis. Subsequently her clinical condition deteriorated with the development of high grade temperatures and severe malaise and worsening renal transplant function. This had not been a feature of her initial presentation and raised concern about cidofovir toxicity necessitating immediate cessation. Over the subsequent 3 days, she developed a renal tubular acidosis and her creatinine rose sharply to 170 μmol/L. Abdomino-pelvic CT showed evidence only of mild perinephric stranding and no obstruction.