Recker F, Hofmann W, Bex A, Tscholl R
Urological Clinic, Kantonsspital Aarau, Switzerland.
J Urol. 1992 Sep;148(3 Pt 2):1000-6. doi: 10.1016/s0022-5347(17)36800-3.
To detect the source of relevant acute intrarenal side effects after extracorporeal piezoelectric lithotripsy and its impact on repeat treatment, urinary excretion of highly specific marker proteins was determined before (day-1) and after (days 0, 1, 4, 7, 14 and 21) treatment. Marker proteins included high molecular weight alpha-2-macroglobulin, immunoglobulin G, albumin, alpha-1-microglobulin as well as the enzyme N-acetyl-beta-glucosaminidase. Of 50 patients who underwent 4,000 shock waves to caliceal stones (group 1) 15 were identically retreated after 5 (group 2) or 15 (group 3) days, respectively, to determine the shortest safe interval to repeat extracorporeal piezoelectric lithotripsy. The course of lithotripsy damage was also evaluated in 15 pre-damaged kidneys (group 4). The alpha-2-macroglobulin enhancement found in all groups on day 0 (p less than 0.005 to p less than 0.05) documented intrarenal bleeding from ruptured vessels. Ratios of alpha-2-macroglobulin/albumin greater than 2.00 on days 0 and 1 exclude a glomerular source of gross hematuria (groups 1 to 4). There was only slight acute tubular damage after extracorporeal piezoelectric lithotripsy (N-acetyl-beta-glucosaminidase increase, p less than 0.05 for groups 1 to 4). Retreatment after 5 days did not enhance the amount of proteinuria compared to the same patients from group 1 (statistically significant at p less than 0.45 to p less than 0.10). Group 3 also showed a similar elevation of proteinuria as the identical patients pretreated 15 days previously. Thus, the data seem to suggest that early repeat sessions of extracorporeal piezoelectric lithotripsy are as safe as delayed retreatments. The course of proteinuria in group 4 did not suggest enhancement of extracorporeal piezoelectric lithotripsy damage in pre-injured kidneys. The urinary marker alpha-2-macroglobulin detects intrarenal vessel ruptures, which are responsible for intrarenal hematomas, as evidenced by animal and human histology. A model is offered to understand and detect the most important parenchymal bioeffects to minimize the risk of injury.
为了检测体外压电碎石术后相关急性肾内副作用的来源及其对重复治疗的影响,在治疗前(第 -1 天)和治疗后(第 0、1、4、7、14 和 21 天)测定了高特异性标记蛋白的尿排泄量。标记蛋白包括高分子量α-2-巨球蛋白、免疫球蛋白 G、白蛋白、α-1-微球蛋白以及酶 N-乙酰-β-氨基葡萄糖苷酶。在 50 例接受 4000 次针对肾盏结石的冲击波治疗的患者中(第 1 组),分别在 5 天(第 2 组)或 15 天(第 3 组)后对其中 15 例进行了相同的再次治疗,以确定重复体外压电碎石术的最短安全间隔。还对 15 个预先受损的肾脏(第 4 组)评估了碎石损伤的过程。所有组在第 0 天发现的α-2-巨球蛋白增加(p 小于 0.005 至 p 小于 0.05)证明了血管破裂导致的肾内出血。第 0 天和第 1 天α-2-巨球蛋白/白蛋白比值大于 2.00 排除了肉眼血尿的肾小球来源(第 1 至 4 组)。体外压电碎石术后仅存在轻微的急性肾小管损伤(N-乙酰-β-氨基葡萄糖苷酶增加,第 1 至 4 组 p 小于 0.05)。与第 1 组的相同患者相比,5 天后再次治疗并未增加蛋白尿的量(p 小于 0.45 至 p 小于 0.10 时有统计学意义)。第 3 组也显示出与 15 天前接受预处理的相同患者相似的蛋白尿升高。因此,数据似乎表明早期重复进行体外压电碎石术与延迟再次治疗一样安全。第 4 组蛋白尿的过程并未表明体外压电碎石术对预先受损的肾脏损伤有加重。尿标记物α-2-巨球蛋白可检测到肾内血管破裂,动物和人体组织学证明这是肾内血肿的原因。提供了一个模型来理解和检测最重要的实质生物效应,以尽量减少受伤风险。