Journal ArticleDOI
Pathophysiology-based treatment of urolithiasis.
Takahiro Yasui,Atsushi Okada,Shuzo Hamamoto,Ryosuke Ando,Kazumi Taguchi,Keiichi Tozawa,Kenjiro Kohri +6 more
TLDR
The present article reviews the epidemiology, pathophysiology and potential treatment of urolithiasis and suggests that oxidative stress and reactive oxygen species could be one such mechanistic pathway.Abstract:
Urolithiasis, a complex multifactorial disease, results from interactions between environmental and genetic factors. Epidemiological studies have shown the association of urolithiasis with a number of lifestyle-related diseases, including cardiovascular diseases, hypertension, chronic kidney disease, diabetes and metabolic syndrome. Elucidation of the mechanisms underlying urinary stone formation will enable development of new preventive treatments. The present article reviews the epidemiology, pathophysiology and potential treatment of urolithiasis. Recent literature has shown that oxidative stress and reactive oxygen species could be one such mechanistic pathway. Calcium oxalate crystals adhering to renal tubular cells are incorporated into the cells through the involvement of osteopontin. Stimulation of crystal-cell adhesion impairs acceleration of the mitochondrial permeability transition pore in tubular cells, resulting in mitochondrial collapse, oxidative stress and activation of the apoptotic pathway in the initial steps of renal calcium crystallization. With regard to genetic factors, studies show that single nucleotide polymorphisms in genes encoding calcium-sensing receptor, vitamin D receptor and osteopontin are correlated with urolithiasis. Genome-wide association studies have shown that CLDN14 and NPT2 are associated with urolithiasis in Caucasian and Japanese populations, respectively. Thus, single nucleotide polymorphism analysis would aid in the prediction of urolithiasis risk and recurrence. New diagnostic methods and preventive approaches, along with complete removal of stones, will improve the management of urolithiasis.read more
Citations
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91140960 Evidence for a renal calcium leak in postmenopausal women
TL;DR: It is suggested that estrogens promote tubular reabsorption of calcium and that the rise in bone resorption at the menopause could be accounted for, at least in part, by the effect of estrogen deficiency on the kidney.
Journal ArticleDOI
An International Collaborative Consensus Statement on En Bloc Resection of Bladder Tumour Incorporating Two Systematic Reviews, a Two-round Delphi Survey, and a Consensus Meeting.
Jeremy Yuen-Chun Teoh,Steven MacLennan,Vinson Wai-Shun Chan,Jun Miki,Hsiang-Ying Lee,Edmund Chiong,Lui-Shiong Lee,Yong Wei,Yuhong Yuan,Chun Pong Yu,Wing-Kie Chow,Darren Ming-Chun Poon,Ronald C. K. Chan,Fernand Mac-Moune Lai,Chi-Fai Ng,Alberto Breda,Mario W. Kramer,Bernard Malavaud,Hugh Mostafid,Thomas R. W. Herrmann,Marek Babjuk,Marek Babjuk +21 more
TL;DR: A consensus statement to standardise various aspects of ERBT for clinical practice and to guide future research is developed and ERBT should always be considered for treating non-muscle-invasive bladder cancer.
Journal ArticleDOI
Curcumin ameliorates glyoxylate-induced calcium oxalate deposition and renal injuries in mice
Yinhui Li,Jie Zhang,Haiyun Liu,Ji-hang Yuan,Yupeng Yin,Tian-tian Wang,Bingfeng Cheng,Shuhan Sun,Zhiyong Guo +8 more
TL;DR: Curcumin could significantly alleviate CaOx crystal deposition in the mouse kidney and the concurrent renal tissue injury in mouse kidneys, and make curcumin a good potential choice to prevent and treat new or recurrent nephrolithiasis.
Journal ArticleDOI
LncRNA HOXA11-AS regulates calcium oxalate crystal-induced renal inflammation via miR-124-3p/MCP-1.
Yinhui Li,Guiling Yan,Jie Zhang,Wei Chen,Tao Ding,Yupeng Yin,Minghan Li,Yiqing Zhu,Shuhan Sun,Ji Hang Yuan,Zhiyong Guo +10 more
TL;DR: HexA11‐AS mediated CaOx crystal–induced renal inflammation via the miR‐124‐3p/MCP‐1 axis, and this outcome may provide a good potential therapeutic target for nephrolithiasis.
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