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muscle bulk associated with anabolic steroids can in-crease creatinine levels, but the changes in our patient varied too acutely to be explained in this way. The rise in creatinine was not due to elimination failure as evi-denced by his creatinine clearance being significantly higher than his estimated GFR had implied. This case posed a diagnostic dilemma in the early stages as we were presented with a patient with an ap-parent rapidly progressive rising creatinine without a clear history of ingestion of exogenous substance. It was decided not to conduct a biopsy in view of the ab-sence of proteinuria and negative nephritic screen but meant we had to deal with diagnostic uncertainty while urine tests were performed. This case highlights the im-portance of a high index of suspicion for other causes of raised creatinine rather than the assumption of elimin-ation failure, i.e. renal disease. Diagnostic clues were the disproportionate elevation in creatinine without other markers of renal disease (raised urea, raised phosphate, normal urinary protein–creatinine ratio, low haemoglo-bin, etc.) and the marked fluctuations with falls seen during admission when abuse was not possible and a rapid rise post-discharge. Acknowledgements. Our clinical biochemists were actively involved with this case. They verified the raised creatinine via two methods and suggested that the urine could be set away to be tested for other steroids at the National Reference Laboratory ultimately leading to a diagnosis. We also thank the Drug Control Centre, King's College Hospital, London for processing the urine for anabolic steroids. Conflict of interest statement. None declared

Year: 2016
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