Schepers Marieke S J, Duim Ronald A J, Asselman Marino, Romijn Johannes C, Schröder Fritz H, Verkoelen Carl F
Department of Urology, Erasmus MC, Rotterdam, The Netherlands.
Kidney Int. 2003 Aug;64(2):493-500. doi: 10.1046/j.1523-1755.2003.00107.x.
Crystal retention in the kidney is caused by the interaction between crystals and the cells lining the renal tubules. These interactions involve crystal attachment, followed by internalization or not. Here, we studied the ability of various renal tubular cell lines to internalize calcium oxalate monohydrate (COM) crystals.
Crystal-cell interactions are studied by light-, electron-, and confocal microscopy with cells resembling the renal proximal tubule [porcine kidney (LLC-PK1)], proximal/distal tubule [Madin-Darby canine kidney II (MDCK-II)], and distal tubule and/or collecting ducts [(Madin-Darby canine kidney I (MDCK-I), rat cortical collecting duct 1 (RCCD1)]. Crystal-binding strength and internalization are characterized and quantified with radiolabeled COM.
Microscopy studies showed that crystals were firmly embedded in the membranes of LLC-PK1 and MDCK-II cells to be subsequently internalized. On the other hand, crystals bound only loosely to MDCK-I and RCCD1 and were not taken up by these cells. Crystal uptake by LLC-PK1 and MDCK-II, expressed in microg/10(6) cells, is temperature-dependent and gradually increases from 0.88 and 0.15 in 30 minutes, respectively, to 4.70 and 3.85, respectively, after five hours, whereas these values never exceeded background levels in MDCK-I and RCCD1 cells.
The adherence of COM crystals to renal cells with properties of the proximal tubule is inevitable and actively followed by their uptake, whereas crystals attached to cells resembling the distal tubule and/or collecting duct are not internalized. Since crystal formation usually occurs in segments beyond the renal proximal tubule, crystal uptake may be of less importance in the etiology of idiopathic calcium oxalate stone disease.
晶体在肾脏中的潴留是由晶体与肾小管内衬细胞之间的相互作用引起的。这些相互作用包括晶体附着，随后可能发生内化或不发生内化。在此，我们研究了各种肾小管细胞系内化一水草酸钙（COM）晶体的能力。
通过光学显微镜、电子显微镜和共聚焦显微镜研究晶体与细胞的相互作用，所使用的细胞分别类似于肾近端小管[猪肾（LLC-PK1）]、近端/远端小管[Madin-Darby犬肾II型（MDCK-II）]以及远端小管和/或集合管[Madin-Darby犬肾I型（MDCK-I）、大鼠皮质集合管1（RCCD1）]。用放射性标记的COM对晶体结合强度和内化进行表征和定量。
显微镜研究表明，晶体牢固地嵌入LLC-PK1和MDCK-II细胞的膜中，随后被内化。另一方面，晶体仅松散地结合到MDCK-I和RCCD1上，未被这些细胞摄取。以微克/10⁶细胞表示的LLC-PK1和MDCK-II对晶体的摄取是温度依赖性的，分别在30分钟时从0.88和0.15逐渐增加到5小时后的4.70和3.85，而这些值在MDCK-I和RCCD1细胞中从未超过背景水平。
COM晶体与具有近端小管特性的肾细胞的粘附是不可避免的，随后会被主动摄取，而附着在类似于远端小管和/或集合管的细胞上的晶体不会被内化。由于晶体形成通常发生在肾近端小管以外的节段，因此晶体摄取在特发性草酸钙结石病的病因学中可能不太重要。
