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Authors’ response ARTICLE
  1. A Smyth1,
  2. C Bertenshaw2,
  3. S Lewis3,
  4. I Choonara1,
  5. A Watson2
  1. 1
    Division of Child Health, University of Nottingham, Nottingham, UK
  2. 2
    Nottingham University Hospitals NHS Trust, Nottingham, UK
  3. 3
    Division of Epidemiology and Public Health, University of Nottingham, Nottingham, UK
  1. Dr A Smyth, Clinical Sciences Building, University of Nottingham, Nottingham City Hospital, Hucknall Road, Nottingham NG5 1PB, UK; alan.smyth{at}nottingham.co.uk

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We welcome Dr Tai’s comments on our paper. We described a case control study of acute renal failure in cystic fibrosis (CF)1 and not a study designed to measure the prevalence, severity or risk factors for renal impairment. Patients with acute renal failure (ARF) were reported to us from 20 UK CF centres and clinical data were extracted retrospectively from the case notes. We therefore adopted a pragmatic definition of ARF (raised plasma creatinine for age with or without oliguria). We agree that substantial renal impairment may occur before a rise in creatinine is seen. However, our intention was to investigate those patients with renal failure requiring dialysis (needed in 13/24 cases) or close monitoring of renal function.2

In an earlier paper, we have published the maximum plasma creatinine values seen in patients with ARF, recorded after gentamicin, where this was administered (median creatinine 674 mmol/l (range 124–1972)).2 At follow-up, 22 of 24 patients had made a full recovery, with a normal plasma creatinine. One patient required long term dialysis (biopsy evidence of diabetic nephropathy prior to ARF) and another long term antihypertensive treatment.

The design of this study did not allow us to assess whether renal impairment was present prior to ARF. The prevalence of renal impairment in adults with CF is reported as 31–42% but the prevalence in children is unknown.3 We agree that a well designed study of the prevalence and risk factors for renal impairment in children with CF would be useful. We would suggested measuring GFR, using the chromium 51 ethylene diamine tetra acetate (EDTA) test.4

Six patients with ARF in our series had biopsy evidence of acute tubular necrosis and two had hypomagnesaemia, which suggests tubular damage.2 We have previously shown that there is a smaller elevation in proximal tubular enzymes with once daily tobramycin administration than with traditional three times daily treatment.5 Measures of proximal tubular impairment could be included in a future study of renal impairment in children with CF.

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  • Competing interests: None.

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