Patients with cystic fibrosis have an increased risk of hyperoxaluria, and of subsequent
nephrocalcinosis and calcium-oxalate urolithiasis. Oxalate homoeostasis is controlled,
in part, by the intestinal bacterium, Oxalobacter formigenes. The loss of this bacterium
from the gut flora is associated with an increased risk of hyperoxaluria and calcium-oxalate
urolithiasis. We investigated whether the absence of O. formigenes and the presence
of hyperoxaluria are correlated in cystic fibrosis (CF) patients.
Stool specimens from 43 patients with CF aged 3-9 years and from 21 similarly aged
healthy volunteers were examined for O. formigenes by culture and DNA analysis. At
the same time, 24 h urine samples were collected and analysed for oxalate and other
factors that promote or inhibit stone formation.
15 (71%) of 21 healthy volunteers but only seven (16%) of 43 CF patients were colonised
with O. formigenes. Detection of O. formigenes in six of these seven patients required
DNA-based identification, suggesting low numbers of colony-forming units, and the
CF patient with normal numbers of O. formigenes was the only one of the 43 patients
who had not been treated with antibiotics. All seven CF patients colonised with O.
formigenes had normal urinary oxalate levels, but 19 (53%) of 36 patients not colonised
with O. formigenes were hyperoxaluric, with the most severe hyperoxaluria occurring
in young patients.
Absence of O. formigenes from the intestinal tract of CF patients appears to lead
to increased absorption of oxalate, thereby increasing the risk of hyperoxaluria and
its complications (eg, nephrocalcinosis, urolithiasis). Prolonged widespread use of
antibiotics, and alterations of the gastrointestinal tract that occur in CF, may induce
a permanent decolonisation in CF patients.