Injury of renal epithelial cell and the formation of Randall's plaque in kidney stones

doi:10.16352/j.issn.1001-6325.2022.09.1454

Abstract

Abstract: Kidney stone has a high incidence and recurrence rate, which is one of the common diseases in urology.At present, Randall's plaque theory is a widely accepted mechanism for the formation of kidney stones. Studies on Randall's plaque are of great significance for the prevention and treatment of kidney stones. Renal epithelial cell damage promotes the formation of Randall's plaque.In this paper, the research progress of osteogenic changes in renal epithelial cells, reactive oxygen species and oxidative stress, phagocytosis of macrophages, and non-coding RNA changes are reviewed.

Key words: Randall's plaque, osteoblastic changes, macrophages, reactive oxygen species, inflammation

CLC Number:

R320.2

YANG Xiong, JIN Xiao-xiao, HE Wen-qiang. Injury of renal epithelial cell and the formation of Randall's plaque in kidney stones[J]. Basic & Clinical Medicine, 2022, 42(9): 1454-1458.

References 25

[1]	Sorokin I, Mamoulakis C, Miyazawa K, et al. Epidemiology of stone disease across the world[J]. World J Urol, 2017, 35: 1301-1320.
[2]	Sancak EB, Reorlu M, Akbas A, et al. Do Hyperten-sion, diabetes mellitus and obesity increase the risk of severity of nephrolithiasis?[J]. Pak J Med Sci, 2015, 31: 566-671.
[3]	Miller NL, Gillen DL, Williams JC Jr, et al. A formal test of the hypothesis that idiopathic calcium oxalate stones grow on Randall's plaque[J]. BJU Int, 2009, 103: 966-971.
[4]	Moor MB, Bonny O. Ways of calcium reabsorption in the kidney[J]. Am J Physiol Renal Physiol, 2016, 310: 1337-1350.
[5]	Breiderhoff T, Himmerkus N, Drewell H, et al. Deletion of claudin-10 rescues claudin-16-deficient mice from hypomagnesemia and hypercalciuria[J]. Kidney Int, 2018, 93: 580-588.
[6]	Khan SR, Pearle MS, Robertson WG, et al. Kidney stones[J]. Nat Rev Dis Primers, 2017, 3: 1700-1710.
[7]	Convento M, Pessoa E, Arago A, et al. Oxalate induces type Ⅱ epithelial to mesenchymal transition (EMT) in inner medullary collecting duct cells (IMCD) in vitro and stimulate the expression of osteogenic and fibrotic markers in kidney medulla in vivo[J]. Oncotarget, 2019, 10: 1102-1118.
[8]	Joshi S, Clapp WL, Wang W, et al. Osteogenic changes in kidneys of hyperoxaluric rats[J]. Biochim Biophys Acta, 2015, 1852: 2000-2012.
[9]	Priante G, Ceol M, Gianesello L, et al. Human proximal tubular cells can form calcium phosphate deposits in osteogenic culture: role of cell death and osteoblast-like transdifferentiation[J]. Cell Death Discov, 2019, 5: 57-65.
[10]	Alelign T, Petros B. Kidney stone disease: an update on current concepts[J]. Adv Urol, 2018, 6: 306-325.
[11]	Liu Y, Li D, He Z, et al. Inhibition of autophagy-attenuated calcium oxalate crystal-induced renal tubular epithelial cell injury in vivo and in vitro[J]. Oncotarget, 2018, 9: 4571-4582.
[12]	Chaiyarit S, Thongboonkerd V. Mitochondrial dysfunction and kidney stone disease[J]. Front Physiol, 2020, 11: 566-576.
[13]	Sun XY, Zhang H, Liu J, et al. Repair activity and crystal adhesion inhibition of polysaccharides with differ-ent molecular weights from red algae Porphyra yezoensis against oxalate-induced oxidative damage in renal epithelial cells[J]. Food Funct, 2019, 10: 3851-3867.
[14]	Taguchi K, Hamamoto S, Okada A, et al. Genome-wide gene expression profiling of Randall's plaques in calcium oxalate stone formers[J]. J Am Soc Nephrol, 2017, 28: 333-347.
[15]	Okada A, Nomura S, Higashibata Y, et al. Successful formation of calcium oxalate crystal deposition in mouse kidney by intraabdominal glyoxylate injection[J]. Urol Res, 2007, 35: 89-99.
[16]	Taguchi K, Okada A, Hamamoto S, et al. M1/M2-macrophage phenotypes regulate renal calcium oxalate crystal development[J]. Sci Rep, 2016, 6: 351-367.
[17]	Liu Q, Liu Y, Guan X, et al. Effect of M2 macrophages on injury and apoptosis of renal tubular epithelial cells induced by calcium oxalate crystals[J]. Kidney Blood Press Res, 2019, 44: 777-791.
[18]	Wang J, Cao B, Han D, et al. Long non-coding RNA H19 induces cerebral ischemia reperfusion injury via activation of autophagy[J]. Aging Dis, 2017, 8: 71-84.
[19]	Liu H, Ye T, Yang X, et al. H19 promote calcium oxalate nephrocalcinosis-induced renal tubular epithelial cell injury via a ceRNA pathway[J]. EBioMedicine, 2019, 50: 366-378.
[20]	Wang Z, Zhang JW, Zhang Y, et al. Analyses of long non-coding RNA and mRNA profiling using RNA sequencing in calcium oxalate monohydrate-stimulated renal tubular epithelial cells[J]. Urolithiasis, 2019, 47: 225-234.
[21]	Song Z, Zhang Y, Gong B, et al. Long noncoding RNA LINC00339 promotes renal tubular epithelial pyroptosis by regulating the miR-22-3p/NLRP3 axis in calcium oxalate-induced kidney stone[J]. J Cell Biochem, 2019, 120: 10452-10462.
[22]	Wahl P, Ducasa GM, Fornoni A. Systemic and renal lipids in kidney disease development and progression[J]. Am J Physiol Renal Physiol, 2016, 310: 433-445.
[23]	Cohen AJ, Adamsky MA, Nottingham CU, et al. Impact of statin intake on kidney stone formation[J]. Urology, 2019, 124: 57-61.
[24]	Dominguez-Gutierrez PR, Kwenda EP, Khan SR, et al. Immunotherapy for stone disease[J]. Curr Opin Urol, 2020, 30: 183-189.
[25]	Zhu W, Zhao Z, Chou F, et al. Loss of the androgen receptor suppresses intrarenal calcium oxalate crystals deposition via altering macrophage recruitment/M2 polarization with change of the miR-185-5p/CSF-1 signals[J]. Cell Death Dis, 2019, 10: 275-284.