Should we stop using intravenous gentamicin in patients with cystic fibrosis?

Patients with cystic fibrosis (CF) have shown continual annual improvement in survival in many countries.1^–4 The improvements in outcome have been attributed to better treatments and a multidisciplinary approach to care focused in care centres with specific expertise in CF.5^–8 As survival improves, we may start increasingly to see adverse events related to intensive treatments used to battle the chronic airway infections and airway inflammation in CF.

Because of chronic lung infections, patients with CF receive repeated courses of oral, inhaled and intravenous antibiotics, some of which are known to be nephrotoxic drugs such as aminoglycosides. The primary defect in CF, the cystic fibrosis transmembrane regulator protein (CFTR), is expressed in the kidney but its function is unknown.9 In this issue of Thorax, Smyth and colleagues10 present data on the association of intravenous aminoglycosides—particularly gentamicin—and acute renal failure (ARF) in the UK (see page 532). The authors have published a previous report in Thorax in which they established an incidence of ARF in CF of 4.6–10.5 cases per 10 000 patients per year.11 The associated use of aminoglycosides and renal failure in this population seemed clear, and most of the patients with ARF had received intravenous gentamicin treatment. In their current paper the authors have moved forward to assess these associations more formally by conducting a case-control study to determine which factors were associated with an increased risk of ARF in these patients. They found that intravenous aminoglycoside use (particularly gentamicin) was associated with ARF, with an odds ratio of 81.8 (95% CI 4.7 to 1427). When they evaluated aminoglycoside use during the previous year, gentamicin (and not tobramycin) was associated with ARF (gentamicin: 19/24 cases vs 1/42 controls, p<0.001; tobramycin: 9/24 cases vs 15/42 controls, p = 0.9). They also found that …