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2017 ; 32
(6
): 1077-1080
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Urinary NGAL deficiency in recurrent urinary tract infections
#MMPMID28210838
Forster CS
; Johnson K
; Patel V
; Wax R
; Rodig N
; Barasch J
; Bachur R
; Lee RS
Pediatr Nephrol
2017[Jun]; 32
(6
): 1077-1080
PMID28210838
show ga
INTRODUCTION: Children with recurrent urinary tract infections (rUTI) often show
no identifiable cause of their infections. Neutrophil gelatinase-associated
lipocalin (NGAL) is known to be upregulated within the uroepithelium and kidney
of patients with UTI and exhibits a localized bacteriostatic effect through iron
chelation. We hypothesize that some patients with rUTI without an identifiable
cause of their recurrent infections have locally deficient NGAL production. We
therefore explored whether a lack of NGAL production may be a factor in the
pathogenesis of rUTI. MATERIALS AND METHODS: Patients seen in the urology clinic
for rUTI who were <21 years of age were enrolled. Patients were excluded if they
had UTI at the time of enrollment, evidence of renal disease, decreased renal
function, known anatomic abnormality of the genitourinary tract, or other reasons
that predispose to UTI, such as neurogenic bladder, the need for intermittent
catheterization, or unrepaired posterior urethral valves. Control patients were
healthy children enrolled from the emergency department with no history of UTI or
renal dysfunction, normal urinalysis at the time of enrollment, and presenting no
diagnosis associated with increased NGAL levels, such as acute kidney injury or
infection. NGAL was measured by immunoblot. RESULTS: Fifteen cases and controls
were enrolled. Median urinary NGAL levels were significantly decreased in rUTI
patients compared with controls [15 (14-29) ng/ml vs 30 (27-61) ng/ml;
p?=?0.002)] Although comparatively diminished, measurable NGAL levels were
present in all patients with rUTI. CONCLUSIONS: Urinary NGAL is significantly
decreased in patients with compared with patients without rUTI. These data
suggest that some patients with rUTI may be predisposed to UTI because of a
relative local deficiency in urinary NGAL production.
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