Pyroglutamic acidosis in a renal transplant patient

Metabolic acidosis is a common acid–base disorder in critically ill patients. Elucidation of the cause usually commences with the calculation of the anion gap. Increased anion gap metabolic acidosis is commonly due to lactic acidosis, renal failure, ketoacidosis as well as a multitude of drugs including toxic alcohols. Pyroglutamic acidosis (5-oxoprolinuria) is a rare cause of increased anion gap acidosis and has not previously been reported in a renal transplant patient. A 57-year-old married female presented to the hospital with a two day history of lethargy, anorexia and increasing dyspnoea. Her past medical history was extensive. Four years ago she had a renal transplant for medullary sponge kidneys which was failing despite ongoing immunosuppression. Her baseline creatinine was 0.22 mmol/l [reference range (RR) 0.05–0.1]. She had experienced recurrent urinary tract infections, the most recent episodes due to Klebsiella and Enterococcus species, respectively. A ureteric re-anastomosis procedure had been required two years previously for stenosis, which subsequently required insertion of a stent for management of renal calculi in the collecting system the following year. She had moderately severe mitral valve regurgitation associated with mitral valve prolapse, preserved left ventricular function and mild left atrial dilatation. An adhesion-related small bowel obstruction required an ileostomy eight months before presentation, which was reversed six months after this. This was complicated by wound breakdown and sinus formation. She was colonized with methicillin-resistant Staphylococcus aureus (MRSA). Her regular medications were tacrolimus, mycophenolate, prednisolone, amlodipine, sodium bicarbonate, calcitriol, caltrate and multivitamins. Her husband admitted that she also regularly self-administered unknown quantities of analgesics for chronic abdominal pain including preparations containing aspirin, codeine and paracetamol (acetaminophen).