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Acute tubular injury, oxalate nephropathy and kidney allograft injury : case report A 55-year-old woman developed acute tubular injury and oxalate nephropathy leading to kidney allograft injury during treatment with ascorbic acid and norepinephrine for septic shock [not all routes and dosages stated; durations of treatments to reactions onsets not stated]. The woman was hospitalised with abdominal distress. Her medical history included two kidney transplantations (7 years apart) secondary to IgA nephropathy. The first allograft was lost because of chronic allograft rejection, and the current allograft was functioning with an estimated glomerular filtration rate of approximately 60 mL/min per 1.73m2. The CT scan showed sigma perforation, which was treated with sigma resection and protective ileostomy. Within due course, she required 2 more surgical interventions, once because of a burst abdomen and later for presumed peritonitis. Initial blood cultures were found to be positive with Alistipes onderdonkii, whereas the intraoperative cultures showed Klebsiella oxytoca. She eventually developed respiratory insufficiency, fever and showed signs of haemodynamic compromise. Considering septic shock, she was switched to mechanical ventilation, and norepinephrine was necessitated to maintain a mean arterial pressure above 60mm Hg. Antibiotic therapy was escalated, and as supportive sepsis therapy, she was administered IV ascorbic acid [vitamin C] 1.5g four times a day for 4 sequential days (one dose missed, total dose of 22.5 g) along with thiamine [vitamin B1] for 3 sequential days. However, in the following days, her urine output progressively declined with increase in plasma creatinine. Immunosuppression included unspecified corticosteroids, tacrolimus and mycophenolate. Urinalysis showed tubular proteinuria. As a result of further aggravation of renal function, the woman was initiated on citrate-based continuous renal replacement therapy. The possible causes of acute kidney injury were discussed, and acute tubular damage in the context of sepsis was favoured. Allograft rejection was considered to be unlikely, as resistance indices were normal, and the current kidney allograft was a complete HLA match organ although, she had already received one kidney allograft in the past and was HLA sensitised, thus the possibility of acute rejection was suspected. Thereafter, a kidney allograft biopsy was performed and it showed severe signs of acute tubular epithelial injury with multifocal intratubular calcium oxalate depositions. One glomerulus was globally sclerosed, and moderate peritubular capillaritis and a discrete glomerulitis were observed. Kidney biopsy showed oxalate nephropathy and acute tubular injury secondary to ascorbic acid administration that eventually resulted in acute kidney allograft injury. Following the diagnosis, she was continued on citrate-based continuous renal replacement therapy. In due course, her urinary output was restored, and continuous renal replacement therapy was discontinued. In the weeks