ABSTRACT
BACKGROUND: 25-Hydroxyvitamin D (25OHD) deficiency is common in children with chronic kidney disease (CKD). It has been associated with an increased risk for anemia in both healthy US children and in adults with CKD. This association has not been explored in children with CKD. METHODS: Children aged 1-16 enrolled in the Chronic Kidney Disease in Children (CKiD) study with mild to moderate kidney dysfunction, and with 25OHD measured at baseline (n = 580), were included in the analysis. The cross-sectional associations between 25OHD and hemoglobin (g/dL) and anemia were assessed. Anemia was defined as hemoglobin < 5th percentile for age and sex. RESULTS: Overall 334 (57.59%) children were vitamin D insufficient/deficient and 137 (23.62%) were anemic. Of those who were vitamin D insufficient/deficient, 95 (28.44%) were anemic. In the overall cohort, the odds of being anemic was 1.9 times higher (95% CI, 1.22-3.04, p < 0.01) in vitamin D insufficient/deficient vs sufficient children, when adjusting for covariates (age, sex, race [black, white, or other], body mass index (BMI), iohexol GFR (iGFR), erythropoietin stimulation agent (ESA) use, iron supplementation use, and underlying cause of CKD). Stratified by race, the odds of being anemic was 2.39 times higher (95% CI, 1.41-4.05, p = 0.001) in vitamin D insufficient/deficient vs vitamin D sufficient white children. The association between vitamin D status and anemia was not significant in black children. CONCLUSIONS: The data support our hypothesis that vitamin D insufficiency/deficiency increases the odds of anemia in children with CKD. The effect was strong and significant among white, but not black, children.
Subject(s)
Anemia/epidemiology , Hemoglobins/analysis , Renal Insufficiency, Chronic/blood , Vitamin D Deficiency/epidemiology , Vitamin D/analogs & derivatives , Adolescent , Anemia/blood , Anemia/diagnosis , Anemia/etiology , Child , Cross-Sectional Studies , Female , Humans , Male , Nutrition Surveys , Prospective Studies , Renal Insufficiency, Chronic/complications , Risk Factors , Vitamin D/blood , Vitamin D Deficiency/blood , Vitamin D Deficiency/diagnosis , Vitamin D Deficiency/etiologyABSTRACT
Previous research has shown that basal forebrain cholinergic inputs to the cerebral cortex are necessary for attentional processing. However, the key components of attention-demanding tasks for demonstrating deficits following loss of basal forebrain corticopetal cholinergic neurons are unclear. In the present experiment, rats were trained in a visual cued discrimination task with limited explicit attentional demands and then received intrabasalis infusions of the immunotoxin, 192 IgG-saporin, or saline. Postsurgically, attentional demands were increased by decreasing the signal duration or the intertrial interval or by increasing the variability of these parameters. Subsequently, rats were trained in a task that required discrimination of successively presented signals and "blank" trials with no signal presentation. Again, attentional demands were increased by manipulating signal duration or the intertrial interval. Finally, all rats were trained in a task with both the signal duration and the intertrial interval designed to increase attentional demands. Compared to sham-lesioned animals, lesioned animals exhibited deficits in signal detection only during the successive discrimination task with both the signal duration and intertrial interval shorter and variable. The present data suggest that attentional deficits following loss of cortical cholinergic inputs result from overall attentional task demands rather than being dependent on any single task parameter.
