Hess B
Nephrologische Station, Medizinische Klinik, Universitätsspital Zürich.
Schweiz Med Wochenschr. 1989 Jul 1;119(26):929-34.
Urinary supersaturation with stone-forming ions is the driving force of crystallization in renal tubules. Based on concentration measurements of the majority of ions, supersaturation can be calculated by means of a computer program. Assessments of 24-hour urine excretions of lithogenic substances do not necessarily detect intermittent supersaturation which may induce crystallization processes. Even the most elaborate metabolic evaluations fail to detect metabolic abnormalities in 10-30% of unselected patients with nephrolithiasis ("idiopathic" nephrolithiasis). Apart from supersaturation, crystal aggregation seems to be a most important factor in kidney stone formation whose pathophysiologic relevance has so far been underestimated. New studies demonstrate excellent inhibition of calcium oxalate monohydrate crystal aggregation by nephrocalcin and Tamm-Horsfall glycoprotein, 2 glycoproteins produced by the kidneys. In recurrent "idiopathic" calcium oxalate stone formers both proteins are structurally and functionally defective crystal aggregation inhibitors.
尿液中形成结石的离子过饱和是肾小管中结晶的驱动力。基于大多数离子的浓度测量值，可通过计算机程序计算过饱和度。对致石物质24小时尿液排泄量的评估不一定能检测到可能引发结晶过程的间歇性过饱和。即使是最精细的代谢评估，也无法在10%至30%未经挑选的肾结石患者（“特发性”肾结石）中检测到代谢异常。除过饱和外，晶体聚集似乎是肾结石形成中一个极其重要的因素，其病理生理相关性迄今一直被低估。新的研究表明，肾钙蛋白和Tamm-Horsfall糖蛋白（肾脏产生的两种糖蛋白）对一水合草酸钙晶体聚集具有出色的抑制作用。在复发性“特发性”草酸钙结石形成者中，这两种蛋白质在结构和功能上都是有缺陷的晶体聚集抑制剂。
