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Immunosuppressants/micafungin Candida krusei urinary tract infection and transient infusion reactions: case report

A 62-year-old man developed chronic symptomatic Candida krusei urinary tract infection following immunosuppressive treatment with tacrolimus, mycophenolate mofetil and prednisone. Additionally, he developed transient infusion reactions during treatment with micafungin for Candida krusei urinary tract infection [not all routes and dosages stated; time to reaction onsets not stated]. The man, who had diabetes mellitus, presented with dysuria, urinary frequency, gross haematuria and poor glycaemic control. His medical history was significant for cirrhosis due to hepatitis C and alcoholic liver disease in addition to end‐stage renal disease because of membranoproliferative glomerulonephritis. Thus, he had undergone simultaneous deceased donor liver and kidney transplant 9 years ago. Six months following the initial transplantation, he had developed allograft failure. He had been receiving immunosuppressive treatment with tacrolimus, mycophenolate mofetil and prednisone along with aciclovir. Following presentation, at the time of symptom onset (day 0), dipstick urinalysis revealed 3+ leucocytes. Thereafter, he received empirical treatment with cefalexin [cephalexin], following which his haematuria resolved. However, dysuria and frequency persisted. On day 9, urinalysis demonstrated 21‐50 WBC/high‐power field (HPF). Urine culture grew 10 000 colony‐forming units(CFU)/mL yeast. A CT angiography of the abdomen and pelvis did not reveal a cause of haematuria. Thereafter, the man started receiving empirical therapy with cotrimoxazole [trimethoprim/sulfamethoxazole] for 10 days without improvement. On day 35, urinalysis showed 51‐100 WBC/HPF and urine culture grew unquantified Candida krusei. On day 46, voiding cystourethrogram showed grade 2 reflux during voiding into the right renal allograft without evidence of filling defect or dilatation, no reflux into the left renal allograft and a small amount of post‐void residual. On day 57, urinalysis showed full-field WBC/HPF and urine culture was sterile. On day 59 and 63, urine cultures for acid‐fast bacilli were negative by smear and culture. On day 161, he was hospitalised with a 7 day history of chills, fatigue, and generalised weakness. Urinalysis revealed full-field WBC/HPF and urine culture grew 10 000 CFU/mL Candida krusei. In vitro antifungal susceptibility testing was susceptible for caspofungin at 0.12 µg/mL, micafungin at 0.06 µg/mL and voriconazole at 0.25 µg/mL. Blood cultures were found to be sterile. Technetium‐99m mercaptoacetyltriglycine renal perfusion‐excretion determination scan with furosemide revealed the following: decreased perfusion, function and clearance of radiotracer within the right renal allograft, but insufficient radioactive urine production to assess obstruction; normal perfusion, mildly impaired function and normal clearance of radiotracer without evidence of obstruction w