Four days after initiating PEP, he developed mild fever and malaise. On day 5, he developed bilateral flank pain and macroscopic haematuria. On day 6, creatinine was 266mmol/l, urea 8.8 mmol/l, and creatine kinase within normal range. Renal ultrasound showed normal size kidneys and no evidence of nephrolithiasis. On day 7, he stopped the LPV/r as he suspected this drug to be the cause of his renal impairment, whereas zidovudine and lamivudine were continued. His symptoms resolved within 2 days of stopping LPV/r and his creatinine improved to 209mmol/l on day 8, 123mmol/l on day 36 and 108mmol/l on day 77. HIV serology (combination p24 antigen and HIV-1/HIV-2 antibody assay) was negative on days 36 and 77.

We believe LPV/r to be the cause of acute kidney injury (AKI) in this case which, to our knowledge, has not previously been reported [1]. The protease inhibitors that have been associated with AKI include atazanavir, indinavir, ritonavir and saquinavir [2]. AKI associated with ritonavir has only been described with full doses, and not with low doses used for boosting [1, 3]. We suspect acute interstitial nephritis as the cause of AKI because of the short latency period relative to PEP initiation, presence of systemic symptoms, haematuria and a positive response following dechallenge of LPV/r [4]. Acute interstitial nephritis has been described with the protease inhibitors indinavir and atazanavir, but there are no studies implicating LPV/r [1, 5, 6]. However, we are unable to confirm this diagnosis in the absence of a renal biopsy.