Nephrocalcinosis in animal models with and without stones.
Nephrocalcinosis in animal models with and without stones.
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DOI：
10.1007/s00240-010-0303-4
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发表时间：
2010-12
影响因子：
--
通讯作者：
Khan SR
中科院分区：
文献类型：
--
作者：
Khan SR
肾钙质沉着症是钙盐在肾实质中的沉积，可以是肾小管内或间质内的。动物模型研究表明，肾小管内钙质沉着症是尿液过饱和度增加的结果。尿液中草酸钙 (CaOx) 和磷酸钙 (CaP) 的过饱和通常在肾小管的不同位置实现。结果，在具有 CaP 沉积物的动物中实验诱导高草酸尿症不会导致 CaOx 超过 CaP 的生长。间质性肾钙质沉着症见于缺乏结晶调节剂 Tamm-Horsfall 蛋白和骨桥蛋白的小鼠。磷酸钠协同转运蛋白或钠氢交换调节因子1缺失小鼠也产生间质性肾钙质沉着症。晶体通过聚集并附着在管腔细胞表面来堵塞小管。肾小管的结构特征也在晶体滞留中发挥作用。当暴露于亚稳态盆腔尿液时，堵塞终末集合管的晶体可能会促进结石的形成。
Nephrocalcinosis is the deposition of calcium salts in renal parenchyma and can be intratubular or interstitial. Animal model studies indicate that intratubular nephrocalcinosis is a result of increased urinary supersaturation. Urinary supersaturation with respect to calcium oxalate (CaOx) and calcium phosphate (CaP) are generally achieved at different locations in the renal tubules. As a result experimental induction of hyperoxaluria in animals with CaP deposits does not lead to growth of CaOx over CaP. Interstitial nephrocalcinosis has been seen in mice with lack of crystallization modulators Tamm–Horsfall protein and osteopontin. Sodium phosphate co-transporter or sodiumhydrogen exchanger regulator factor-1 null mice also produced interstitial nephrocalcinosis. Crystals plug the tubules by aggregating and attaching to the luminal cell surface. Structural features of the renal tubules also play a role in crystal retention. The crystals plugging the terminal collecting ducts when exposed to the metastable pelvic urine may promote the formation of stone.
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影响因子：
19.6
作者：
Bushinsky, DA;Asplin, JR;Coe, FL
通讯作者：
Coe, FL
影响因子：
3
作者：
Evan, Andrew P.
通讯作者：
Evan, Andrew P.
DOI：
10.1073/pnas.95.9.5372
发表时间：
1998-04-28
影响因子：
11.1
作者：
Beck, L;Karaplis, AC;Tenenhouse, HS
通讯作者：
Tenenhouse, HS
影响因子：
19.6
作者：
Evan, A. P.;Lingeman, J.;Worcester, E.
通讯作者：
Worcester, E.
影响因子：
13.2
作者：
de Water, R;Noordermeer, C;Schröder, FH
通讯作者：
Schröder, FH