MP33-15 MITOCHONDRIAL COLLAPSE DEPENDS ON CYCLOPHILIN D IN RENAL TUBULAR CELLS PROMOTES KIDNEY STONE FORMATION

2015 ◽  
Vol 193 (4S) ◽  
Author(s):  
Yasuhiko Ito ◽  
Takahiro Yasui ◽  
Kazuhiro Niimi ◽  
Shoichiro Iwatsuki ◽  
Takashi Hamakawa ◽  
...  
Keyword(s):  
Kidney Stone ◽  
Stone Formation ◽  
Cyclophilin D ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Kidney Stone Formation

scholarly journals Effects of Hyaluronic Acid on Calcium Oxalate Crystallization, Growth, Aggregation, Adhesion on Renal Tubular Cells, and Invasion Through Extracellular Matrix

2020 ◽  
Vol 4 (Supplement_2) ◽  
pp. 13-13
Author(s):  
Chanettee Chanthick ◽  
Visith Thongboonkerd
Keyword(s):  
Extracellular Matrix ◽  
Hyaluronic Acid ◽  
Crystal Growth ◽  
Calcium Oxalate ◽  
Kidney Stone ◽  
Stone Formation ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Kidney Stone Formation

Abstract Objectives Hyaluronic acid (HA), a large non-sulfated glycosaminoglycan, is one of the major components of extracellular matrix (ECM) in connective tissues and other organs. Currently, it is widely used as a dietary supplement, especially for treatment or prevention of aging-related disorders. On the other hand, HA has been reported with an increased risk of kidney stone disease, particularly calcium oxalate (CaOx) type, but with unclear mechanisms. We therefore performed systematic analyses for its modulatory effects on CaOx monohydrate (COM) crystal at various steps of kidney stone formation processes. Methods HA at 1, 10, 100, 1000 and 10,000 ng/ml was tested in various assays for COM crystallization, crystal growth, aggregation, crystal-cell adhesion and invasion through ECM. Results COM crystallization and crystal aggregation were not affected by HA at all concentrations. However, HA significantly promoted COM crystal growth and adhesion onto renal tubular cells in a dose-dependent manner. Interestingly, COM crystal invasion through the ECM was dramatically enhanced by HA even at very low concentration (such as 1 ng/ml). Conclusions Our findings provide evidence for promoting effects of HA on COM crystal growth, adhesion on renal tubular cell surface and invasion through the ECM, all of which are the important steps for kidney stone formation. Funding Sources TRF-IRN grant.

Reduction of Oxidative Stress in Cultured Renal Tubular Cells and Preventive Effects on Renal Stone Formation by the Bioflavonoid Quercetin

2008 ◽  
Vol 179 (4) ◽  
pp. 1620-1626 ◽  
Author(s):  
Hyoung Keun Park ◽  
Byong Chang Jeong ◽  
Mi-Kyung Sung ◽  
Mi-Young Park ◽  
Eun Young Choi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Renal Stone ◽  
Stone Formation ◽  
Tubular Cells ◽  
Renal Tubular Cells ◽  
Renal Tubular ◽  
Preventive Effects

MP20-13 OXYGEN NANO-BUBBLE WATER EXERTS INHIBITORY EFFECTS ON KIDNEY STONE FORMATION BY INHIBITING RENAL TUBULAR CELL INJURY

2014 ◽  
Vol 191 (4S) ◽  
Author(s):  
Yasuhiko Hirose ◽  
Kazumi Taguchi ◽  
Yasuhiro Fujii ◽  
Kazuhiro Niimi ◽  
Shuzo Hamamoto ◽  
...  
Keyword(s):  
Kidney Stone ◽  
Cell Injury ◽  
Stone Formation ◽  
Tubular Cell ◽  
Renal Tubular Cell ◽  
Inhibitory Effects ◽  
Renal Tubular ◽  
Kidney Stone Formation

Mechanisms Underlying Calcium Nephrolithiasis

2021 ◽  
Vol 84 (1) ◽  
Author(s):  
R.T. Alexander ◽  
D.G. Fuster ◽  
H. Dimke
Keyword(s):  
Kidney Stones ◽  
Kidney Stone ◽  
Stone Formation ◽  
Urinary Calcium ◽  
Annual Review ◽  
Publication Date ◽  
Calcium Excretion ◽  
Thick Ascending Limb ◽  
Renal Tubular ◽  
Kidney Stone Formation

Nephrolithiasis is a worldwide problem with increasing prevalence, enormous costs, and significant morbidity. Calcium-containing kidney stones are by far the most common kidney stones encountered in clinical practice. Consequently, hypercalciuria is the greatest risk factor for kidney stone formation. Hypercalciuria can result from enhanced intestinal absorption, increased bone resorption, or altered renal tubular transport. Kidney stone formation is complex and driven by high concentrations of calcium-oxalate or calcium-phosphate in the urine. After discussing the mechanism mediating renal calcium salt precipitation, we review recent discoveries in renal tubular calcium transport from the proximal tubule, thick ascending limb, and distal convolution. Furthermore, we address how calcium is absorbed from the intestine and mobilized from bone. The effect of acidosis on bone calcium resorption and urinary calcium excretion is also considered. Although recent discoveries provide insight into these processes, much remains to be understood in order to provide improved therapies for hypercalciuria and prevent kidney stone formation. Expected final online publication date for the Annual Review of Physiology, Volume 84 is February 2022. Please see http://www.annualreviews.org/page/journal/pubdates for revised estimates.

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