Sayer John A, Carr Georgina, Simmons Nicholas L
School of Cell and Molecular Biosciences, Medical School, University of Newcastle upon Tyne, Newcastle upon Tyne NE2 4HH, UK.
Clin Sci (Lond). 2004 Jun;106(6):549-61. doi: 10.1042/CS20040048.
Nephrocalcinosis may be defined as a generalized increase in the calcium content of the kidneys. This renal calcification may occur at a molecular, microscopic or macroscopic level leading to progressive amounts of renal damage. The major causes include those associated with an increase in urinary levels of calcium, oxalate and phosphate. Under these conditions, urine concentration and supersaturation leads to calcium crystal precipitation, which may be an intratubular event or initiate within the renal interstitium. The focus of discussion concerning renal calcification is often limited to factors that lead to renal stones (calculi and nephrolithiasis); however, nephrocalcinosis is a more sinister event, and often implies a serious metabolic defect. This review will discuss the hypotheses concerning initiating lesions of nephrocalcinosis using available laboratory and clinical studies and will examine whether new understanding of the molecular basis of tubulopathies, that lead to nephrocalcinosis, has given further insights.
肾钙质沉着症可定义为肾脏钙含量普遍增加。这种肾脏钙化可发生在分子、微观或宏观层面,导致进行性肾损害。主要原因包括与尿钙、草酸和磷酸盐水平升高相关的因素。在这些情况下,尿液浓缩和过饱和会导致钙晶体沉淀,这可能是肾小管内事件或在肾间质内引发。关于肾钙化的讨论焦点通常局限于导致肾结石(结石症和肾石病)的因素;然而,肾钙质沉着症是一个更严重的事件,通常意味着严重的代谢缺陷。本综述将利用现有的实验室和临床研究讨论关于肾钙质沉着症起始病变的假说,并将探讨对导致肾钙质沉着症的肾小管疾病分子基础的新认识是否提供了进一步的见解。