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Kidney Disease Progression Does Not Decrease Intestinal Phosphorus Absorption in a Rat Model of Chronic Kidney Disease-Mineral Bone Disorder.
Journal of Bone and Mineral Research ( IF 6.2 ) Pub Date : 2019-11-15 , DOI: 10.1002/jbmr.3894
Colby J Vorland 1 , Annabel Biruete 2 , Pamela J Lachcik 1 , Shruthi Srinivasan 2 , Neal X Chen 2 , Sharon M Moe 2, 3, 4 , Kathleen M Hill Gallant 1, 2
Affiliation  

The Cy/+ rat has been characterized as a progressive model of chronic kidney disease-mineral bone disorder (CKD-MBD). We aimed to determine the effect of kidney disease progression on intestinal phosphorus absorption and whole-body phosphorus balance in this model. A total of 48 Cy/+ (CKD) and 48 normal littermates (NL) rats were studied at two ages: 20 weeks and 30 weeks, to model progressive kidney function decline at approximately 50% and 20% of normal kidney function. Sodium-dependent and sodium-independent intestinal phosphorus absorption efficiency were measured by the in situ jejunal ligated loop method using 33 P radioisotope. Our results show that CKD rats had slightly higher sodium-dependent phosphorus absorption compared to NL rats, and absorption decreased from 20 to 30 weeks. These results are in contrast to plasma 1,25OH2 D, which was lower in CKD rats. Gene expression of the major intestinal phosphorus transporter, NaPi-2b, was not different between CKD and NL rats in the jejunum but was lower in CKD rats versus NL rats in the duodenum. Jejunal ligated loop phosphorus absorption results are consistent with percent net phosphorus absorption results obtained from metabolic balance: higher net percent phosphorus absorption values in CKD rats compared with NL, and lower values in 30-week-olds compared with 20-week-olds. Phosphorus balance was negative (below zero) in CKD rats, significantly lower in 30-week-old rats compared with 20-week-old rats, and lower in CKD rats compared with NL rats at both ages. These results demonstrate no reduction in intestinal phosphorus absorption with progression of CKD despite lower 1,25OH2 D status when assessed by an in situ ligated loop test, which is in contrast to the majority of in vitro studies, and if confirmed in further studies, could challenge the physiological relevance of in vitro findings. © 2019 American Society for Bone and Mineral Research.

中文翻译:

在慢性肾病-矿物质骨疾病大鼠模型中,肾病进展不会降低肠道磷吸收。

Cy/+ 大鼠已被定性为慢性肾病-矿物质性骨病 (CKD-MBD) 的进展模型。我们的目的是在该模型中确定肾脏疾病进展对肠道磷吸收和全身磷平衡的影响。对总共 48 只 Cy/+ (CKD) 和 48 只正常同窝 (NL) 大鼠在两个年龄(20 周和 30 周)进行了研究,以模拟肾功能进行性下降,约为正常肾功能的 50% 和 20%。使用 33 P放射性同位素通过原位空肠结扎环法测量钠依赖性和钠非依赖性肠磷吸收效率。我们的结果表明,与 NL 大鼠相比,CKD 大鼠的钠依赖性磷吸收略高,并且吸收在 20 至 30 周期间有所下降。这些结果与血浆 1,25OH2 D 形成鲜明对比,CKD 大鼠的血浆 1,25OH2 D 较低。主要肠道磷转运蛋白 NaPi-2b 的基因表达在 CKD 和 NL 大鼠之间在空肠中没有差异,但在十二指肠中 CKD 大鼠低于 NL 大鼠。空肠结扎环磷吸收结果与代谢平衡获得的净磷吸收百分比结果一致:与NL相比,CKD大鼠的净磷吸收百分比值较高,30周龄大鼠的净磷吸收百分比值低于20周龄大鼠。CKD 大鼠的磷平衡为负值(低于零),30 周龄大鼠的磷平衡显着低于 20 周龄大鼠,两个年龄段的 CKD 大鼠均低于 NL 大鼠。这些结果表明,尽管通过原位结扎环测试评估时 1,25OH2 D 状态较低,但肠道磷吸收并未随着 CKD 的进展而减少,这与大多数体外研究相反,如果在进一步的研究中得到证实,可以挑战体外研究结果的生理相关性。© 2019 美国骨与矿物质研究学会。
更新日期:2019-11-17
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