泌尿道結石，又稱為尿路結石，是影響全人口約10%的重要疾病，近年來全球盛行率上升。尿路結石手術與時精進，然而結石形成的機轉始終未能有答案，許多成因都可能導致結石的行程，包括飲食習慣、基因、解剖構造等。所有結石形成的假說中最著名的是Randall plague理論，Randall plague是在腎盂內裸露在外的磷酸鈣斑塊，在含鈣結石病患腎臟內非常常見。近年來，許多研究發現在Randall plague的位置上氧化壓力和發炎反應都上升，此外，Randall plague的成分與血管鈣化的成分相同，許多研究結果更是支持血管鈣化和尿路結石形成的過程有很高的相似性。此外，很多流行病研究都指出腎結石病患較容易有頸動脈粥狀動脈硬化、冠狀動脈疾病和中風; 血管鈣化和粥狀動脈硬化都有很高的致病率和致死率，然而腎結石和粥狀動脈硬化的關聯性仍舊未知。近年來，氧化型低密度脂蛋白已成為粥狀動脈硬化的最重要角色，許多研究也指出代謝症候群、糖尿病、慢性腎臟病的病患都會有較高的氧化型低密度脂蛋白，而這些疾病也都與腎結石形成相關，因此我們推論氧化型低密度脂蛋白可能是串連腎結石和粥狀動脈硬化的關鍵，本研究的研究目的就是探討巨大含鈣類腎結石病患的血液和尿液中是否有較高濃度的氧化型低密度脂蛋白。
與無尿路結石的對照組相比，結石組有較高的十年心血管風險分數，不過沒有統計上的差異，結石組也有較嚴重的頸動脈粥狀動脈硬化，超過70%的結石病人有程度不一的主動脈鈣化，60%的結石病人有中度到嚴重度的主動脈鈣化。儘管在本篇研究中無法發現結石病患血液中有較高的氧化型低密度脂蛋白，但是卻發現有較高的高敏感度C反應蛋白，並且是和結石體積呈現有統計學上有意義的線性相關。最重要的是，結石組尿液中的氧化型低密度脂蛋白在統計學上有顯著的高於對照組的尿液檢體，而且含鈣成份越高的病患其尿液中的氧化型低密度脂蛋白濃度越高。從結石組的腎臟切片檢體中可以發現顯著的過度表現氧化型低密度脂蛋白，主要堆積在腎臟集尿管細胞的細胞質及間質細胞中。最後，我們用實驗性誘發腎結石的大鼠動物模式與實驗性誘發腎結石同時食用高脂肪食物的大鼠比較，發現同時有食用高脂肪食物的大鼠腎臟中有顯著的草酸鈣沉積。綜合以上，巨大含鈣類腎結石病患潛在較高的心血管疾病風險，過度堆積在腎臟的氧化型低密度脂蛋白可能暗示脂肪代謝的異常會進一步促使含鈣類結石堆積。

Urinary tract stone, also known as urolithiasis, is a major disease that affects approximately 10% population, and its prevalence has been increasing worldwide. Though the advance of urolithiasis surgical techniques are great, the mechanism of urolithiasis formation is still an unanswered mystery. Multiple factors involve in kidney stone formation, including dietary habits, genetic factors, and anatomical factors, and so forth. One of the most famous and most accepted mechanism of urolithiasis is Randall plague theory. The Randall plague is located in renal papilla with exposed calcium phosphate (CaP), and this plaque can be frequently seen in calcium stone formers. In the recent decade, many studies revealed increased oxidative stress (OS) and inflammation were associated with the Randall plague formation. Composition of Randall plague is same as those of vascular calcification. Many studies also support the similarity between the vascular calcification process and urinary stone formation. Moreover, many epidemiological researches have revealed that kidney stone is related to increased risks of carotid atherosclerosis, coronary artery disease and stroke. Both vascular calcification and atherosclerosis are related to high morbidity and mortality. However, the connection between kidney stones and cardiovascular disease is still unclear. Oxidized low-density lipoprotein (oxLDL) has become the most crucial role in atherosclerosis formation. Growing evidence shown the circulating oxLDL increases under the conditions of metabolic syndrome, dyslipidemia, diabetes and chronic kidney disease, and all these diseases are associated with developing kidney stones. Therefore, we hypothesized that oxLDL may be the connection between cardiovascular disease and kidney stone. The aim of this project was to investigate whether circulating or excretion of oxLDL increases in large calcium kidney stone formers.
Compared with stone-free controls (n = 21), large calcium stone formers (n = 29), defined as larger than 2 cm in maximal length, had insignificantly higher Framingham risk scores. Stone formers had increased carotid intima-media thickness and carotid scores compared to normal reference from previous literature. Up to 71.4% of stone formers had different degrees of abdominal aorta calcification found from CT scan study, and over 60% of all stone formers had moderate-to-severe calcification in this study. Although stone formers didn’t have significantly higher serum oxLDL, serum high-sensitive C-reactive protein (hsCRP) was significantly higher and it was positively correlated to the stone volume. Most notably, urinary oxLDL and, LOX-1 (oxLDL specific receptor) levels were significantly higher in stone formers. Urinary oxLDL was particularly higher in harder kidney stones (high CT scan HU), which calcium component is higher than those with low urinary oxLDL levels. By immunohistochemical stains of kidney biopsy, oxLDL obviously accumulated in the cytoplasm of renal collecting tube and interstitial cells in over 80% stone formers. In vivo study, hydroxyproline (HP)-treated rats, which are the animal models of kidney calcium oxalate (CaOx) stone formation, had much CaOx crystals accumulating in the kidney, but rats fed with HP and high fat diets had even more CaOx crystals accumulated in the kidney. To sum up, our results demonstrated that large calcium stone formers carry higher risks in cardiovascular disease, and higher urinary oxLDL and accumulation in renal collecting duct may indicate that lipid dysmetabolism promotes calcium stone formation.

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