[Pediatric renal abscesses: a diagnostic challenge]. / Absceso renal en Pediatría: un desafío diagnóstico.

Kidney abscess is an unusual entity in childhood with few studies about its clinical characteris tics. OBJECTIVE: To report the clinical presentation, diagnosis, and therapy used in a cohort of 20 children with kidney abscess. PATIENTS AND METHOD: retrospective study of cases of kidney abscess during a 10-year period at the Hospital Roberto del Río. The analysis of clinical, laboratory, and imaging characteristics were evaluated as well as the treatment usedfor this condition. RESULTS: 20 cases were reported among which 65% were women with a median age of 3.6 years. The most com mon clinical presentation was fever, vomit, and dysuria. Eighty percent of patients presented an increase of inflammatory parameters, 88% presented positive urine culture, and the most common organism identified was Escherichia Coli (77.8%). The diagnosis was mostly made through kidney ultrasound (75%) followed by an abdominal CT scan (35%). 93% of abscesses were unilateral. About 95% of the patients only required antibiotic treatment. Vesicoureteral reflux was diagno sed in 28% of the patients with no sphincter control, and only one of them presented high-grade reflux. In patients with sphincter control, bladder and bowel dysfunction (BBD) was diagnosed in 90% of the cases. Forty four percent of the patients with late DMSA renal scintigraphy presented renal scarring. CONCLUSIONS: In this series, pediatric kidney abscess appears with persistent fever despite the treatment, requiring prolonged antibiotic therapy and rarely surgical drains. We su ggest a study aimed at detecting modifiable factors, such as vesicoureteral reflux in patients with no sphincter control and BBD in patients with sphincter control, as well as identifying renal paren chymal sequels in all patients.

Glucocorticoids Decrease Longitudinal Bone Growth in Pediatric Kidney Transplant Recipients by Stimulating the FGF23/FGFR3 Signaling Pathway.

Renal transplantation (RTx) is an effective therapy to improve clinical outcomes in pediatric patients with terminal chronic kidney disease. However, chronic immunosuppression with glucocorticoids (GCs) reduces bone growth and BMD. The mechanisms causing GC-induced growth impairment have not been fully clarified. Fibroblast growth factor 23 (FGF23) is a peptide hormone that regulates phosphate homeostasis and bone growth. In pathological conditions, FGF23 excess or abnormal FGF receptors (FGFR) activity leads to bone growth impairment. Experimental data indicate that FGF23 expression is induced by chronic GC exposure. Therefore, we hypothesize that GCs impair bone growth by increasing FGF23 expression, which has direct effects on bone growth plate. In a post hoc analysis of a multicentric randomized clinical trial of prepubertal RTx children treated with early GC withdrawal or chronic GC treatment, we observed that GC withdrawal was associated with improvement in longitudinal growth and BMD, and lower plasma FGF23 levels as compared with a chronic GC group. In prepubertal rats, GC-induced bone growth retardation correlated with increased plasma FGF23 and bone FGF23 expression. Additionally, GC treatment decreased FGFR1 expression whereas it increased FGFR3 expression in mouse tibia explants. The GC-induced bone growth impairment in tibiae explants was prevented by blockade of FGF23 receptors using either a pan-FGFR antagonist (PD173074), a C-terminal FGF23 peptide (FGF23180-205) which blocks the binding of FGF23 to the FGFR-Klotho complex or a specific FGFR3 antagonist (P3). Finally, local administration of PD173074 into the tibia growth plate ameliorated cartilage growth impairment in GC-treated rats. These results show that GC treatment partially reduces longitudinal bone growth via upregulation of FGF23 and FGFR3 expression, thus suggesting that the FGF23/Klotho/FGFR3 axis at the growth plate could be a potential therapeutic target for the management of GC-induced growth impairment in children.