Kidney Stone Disease: An Update on Current Concepts.
Kidney Stone Disease: An Update on Current Concepts.
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DOI：
10.1155/2018/3068365
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发表时间：
2018
影响因子：
1.4
通讯作者：
Petros B
中科院分区：
文献类型：
--
作者：
Alelign T;Petros B
肾结石是一种晶体结核形成通常在肾脏。它是一种日益增加的人类健康泌尿系统疾病，影响约12%的世界人口。它与终末期肾衰竭的风险增加有关。肾结石的病因是多方面的。最常见的肾结石类型是在肾乳头表面的兰德尔斑块处形成的草酸钙。结石形成的机制是一个复杂的过程，其由几个物理化学事件引起，包括尿结石成分在肾小管细胞内的过饱和、成核、生长、聚集和保留。这些步骤受到促进或抑制尿结晶的因素之间的不平衡的调节。还注意到，细胞损伤促进颗粒在肾乳头表面上的保留。肾上皮细胞暴露于草酸盐引起信号级联反应，通过p38丝裂原活化蛋白激酶途径导致细胞凋亡。目前，没有令人满意的药物来治疗和/或预防肾结石复发。因此，进一步了解肾结石形成的病理生理学是使用新药治疗尿石症的研究领域。因此，本文综述了肾结石的病因、发病机制和预防方法。
Kidney stone disease is a crystal concretion formed usually within the kidneys. It is an increasing urological disorder of human health, affecting about 12% of the world population. It has been associated with an increased risk of end-stage renal failure. The etiology of kidney stone is multifactorial. The most common type of kidney stone is calcium oxalate formed at Randall's plaque on the renal papillary surfaces. The mechanism of stone formation is a complex process which results from several physicochemical events including supersaturation, nucleation, growth, aggregation, and retention of urinary stone constituents within tubular cells. These steps are modulated by an imbalance between factors that promote or inhibit urinary crystallization. It is also noted that cellular injury promotes retention of particles on renal papillary surfaces. The exposure of renal epithelial cells to oxalate causes a signaling cascade which leads to apoptosis by p38 mitogen-activated protein kinase pathways. Currently, there is no satisfactory drug to cure and/or prevent kidney stone recurrences. Thus, further understanding of the pathophysiology of kidney stone formation is a research area to manage urolithiasis using new drugs. Therefore, this review has intended to provide a compiled up-to-date information on kidney stone etiology, pathogenesis, and prevention approaches.