BackgroundFibroblast Growth Factor-23 (FGF23) and cofactor Klotho are key regulators of mineral metabolism in chronic kidney disease (CKD), but little is known about the mechanisms that regulate their production. This study evaluates longitudinal changes of FGF23 and Klotho levels and their regulatory factors in children on chronic peritoneal dialysis (PD).MethodsFGF23, Klotho, 25(OH) vitamin D, 1,25-dihydroxyvitamin D and parathyroid hormone (PTH) plasma concentrations were measured during 1 year of follow-up in PD children. Anthropometric and dialytical parameters were evaluated in addition to mineral metabolism variables.ResultsThirty-one patients under chronic PD were followed for 12 months. FGF23 mean plasma levels at Month 1 were significantly increased compared with controls, 215.1 ± 303.6 versus 9.4 ± 5.7 pg/mL, respectively (P < 0.001). Baseline Klotho levels were 41% lower in patients compared with controls, 132.1 ± 58 versus 320 ± 119.4 pg/mL, respectively (P < 0.001), and did not correlate with FGF23 and phosphorus levels. At Month 12, FGF23 (195 ± 300 pg/mL) and Klotho levels (130 ± 34 pg/mL) remained similar to baseline values. Log-FGF23 correlated significantly with height/age Z score (r= −0.38) and residual renal function (r = −0.44), but no correlation was found with serum phosphorus, phosphate intake, PTH and vitamin D levels. The log-FGF23 strongly correlated with calcium levels at Months 1, 6 and 12, however, this relationship was blunted if serum phosphorus was >6 mg/dL. By multiple regression analysis, calcium was the strongest variable determining FGF23 levels.ConclusionsIn this longitudinal study, FGF23 levels are markedly increased, and Klotho levels are reduced in PD children compared with controls. FGF23 levels appeared to be regulated primarily by serum calcium, showing a significant correlation at each time of measurement. This relationship was lost in patients with phosphorus >6 mg/dL. These observations may have important consequences to the therapeutic management of phosphate homeostasis in CKD patients.
La hipertensión arterial (HTA) en niños y adolescentes es una patología importante, asociada a factores modificables y no modificables. En la edad pediátrica, la prevalencia de la HTA es de alrededor de un 3,5%, y va aumentando progresivamente con la edad. El método ideal para su diagnóstico es la medición de la presión arterial (PA) con instrumentos auscultatorios. Según lo publicado por la Academia Americana de Pediatría (AAP) la PA debe ser medida en niños mayores de 3 años una vez al año, y en niños menores de 3 años, si presenta factores de riesgo. Una vez confirmada la HTA, la evaluación debe dirigirse hacia la detección de una enfermedad causal y a la búsqueda de factores de riesgo asociados a una HTA primaria. El objetivo del tratamiento de la HTA primaria y secundaria en pediatría es lograr un nivel de PA que disminuya el riesgo de daño de órgano blanco. Las opciones terapéuticas incluyen: tratamiento según etiología específica, no farmacológico y farmacológico. Este documento es producto de un esfuerzo colaborativo de la Rama de Nefrología de la Sociedad Chilena de Pediatría con el objetivo de ayudar a los pediatras y nefrólogos infantiles en el diagnóstico y tratamiento de la HTA en la infancia. En esta primera parte, se presentan las recomendaciones del diagnóstico y estudio.
Background: Steroid use in renal transplant is related to multiple adverse effects.Long-term effects of early withdrawal steroids in pediatric renal transplant were assessed.Methods: Renal transplant children with low immunological risk treated on basiliximab, tacrolimus, and mycophenolate with steroid withdrawal or steroid control were evaluated between 2003 and 2019. Clinical variables, treatment adherence, acute rejection, graft loss, and death were analyzed through hazard ratios, and Kaplan-Meier and multivariate analyses. Results:The study included 152 patients, 71.1% steroid withdrawal, mean follow-up 8.5 years, 64.5% structural abnormalities, and 81.6% deceased donor. At 12 years of transplant, event-free survival analysis for graft loss or death showed no significant difference between steroid withdrawal and control steroid treatment (85.9% vs.
In this study, children with CKD undergoing PD therapy showed an impaired phosphorylation of JAK2/STAT5b signaling in fibroblasts after GH stimulation, as well as impaired IGFBP3 mRNA abundance. Both impairments may be partially responsible for the observed resistance to the growth-promoting actions of GH in chronic kidney failure.
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