Lack of Hepcidin Ameliorates Anemia and Improves Growth in an Adenine-induced Mouse Model of Chronic Kidney Disease.

Lack of Hepcidin Ameliorates Anemia and Improves Growth in an Adenine-induced Mouse Model of Chronic Kidney Disease. Am J Physiol Renal Physiol. 2016 Jul 20;:ajprenal.00089.2016 Authors: Akchurin O, Sureshbabu A, Doty SB, Zhu YS, Patino E, Cunningham-Rundles S, Choi ME, Boskey AL, Rivella S Abstract Growth delay is common in children with chronic kidney disease (CKD), often associated with poor quality of life. The role of anemia in uremic growth delay is poorly understood. Here we describe an induction of uremic growth retardation by 0.2% adenine diet in wild type (WT) and hepcidin gene (Hamp) knock-out (KO) mice, compared with their respective littermates fed a regular diet. Experiments were started at weaning (3 weeks). After 8 weeks, blood was collected and mice were euthanized. Adenine-fed WT mice developed CKD (BUN 82.8±11.6 mg/dL, creatinine 0.57±0.07 mg/dL) and were 2.1 cm shorter compared to WT controls. WT adenine-fed mice were anemic, had low serum iron, elevated Hamp, elevated IL6 and TNF-alpha. WT adenine fed mice had advanced mineral bone disease (serum phosphorus 16.9±3.1 mg/dL, FGF23 204.0±115.0 ng/mL) with loss of cortical and trabecular bone volume seen on micro-CT. Hamp disruption rescued the anemia phenotype resulting in improved growth rate in mice with CKD, thus providing direct experimental evidence of the relationship between Hamp pathway and growth impairment in CKD. Hamp disruption ameliorated CKD-induce...
Source: Am J Physiol Renal P... - Category: Urology & Nephrology Authors: Tags: Am J Physiol Renal Physiol Source Type: research