Schoenenberger G A, Buser S, Hagmaier V, Locher J T, Mihatsch M, Rist M, Rutishauser G, Scheidegger A M, Städtler K
Curr Probl Clin Biochem. 1979(9):122-34.
From previous investigations with nephroptotic patients increased urinary LDH was assumed to be a reliable marker indicating a renal tissue defect due to the organs descent in erect position. Animal experiments now allowed correlation of this enzymatic activity with controlled changes of anatomical and physiological parameters. Changes of the renal hemodynamics or urinary flow induced in acute experiments in dogs simulated kidney displacement in nephroptotic patients. Both ureters were cannulated for separate urine collection and one kidney was manipulated. The renal arterial or venous flow was reduced or the ureter was occluded under electromagnetic blood-flow control. Arterial constriction alone (30%/15 min) selectively caused a drastic decrease (approximately 80%) of Xenon wash-out (= nutrient-flow) in the renal cortex. Under the same conditions radio-labeled microspheres injected intracardially showed a centralization of the renal capillary blood flow from the outer cortex to the juxtamedullary zone. Urinary LDH activities increased up to 800% immediately after arterial constriction. In accordance with total LDH activity the percentage distribution of isoenzymes changed: LDH-I increased and the LDH-V decreased. Neither constriction of the renal vein nor ureteral occlusion had similar effects. In long-term experiments backward fixation of one kidney in rats would reflect the effects of kidney displacement over years in nephroptotic patients: animals were unilaterally nephrectomized and the remaining kidney was dislocated backwards (approximately 2,5 vertebrae) and fixed to the lateral pelvic wall. "Ptotic" rats showed during the following examinations a constant increase of urinary LDH up to 50% by 26 weeks postoperatively. In accordance with increased LDH the isotope nephrogram was pathological and arteriographies showed a stretched and narrowed renal artery. In a number of rats "ptotic" fixation was not effective enough. All these animals showed normal LDH, isotope nephrograms and arteriographies. Both animal experiments documented that reduced flow/hypoxia is essentially responsible for the tissue damage in the kidney manifested by increased release of urinary LDH.
以往对肾下垂患者的研究认为，尿乳酸脱氢酶（LDH）升高是肾组织因器官在直立位下移而出现缺损的可靠标志物。现在，动物实验使得这种酶活性与解剖学和生理学参数的可控变化之间建立了关联。在犬类急性实验中诱导的肾血流动力学或尿流变化模拟了肾下垂患者的肾脏移位。双侧输尿管插管以便分别收集尿液，并对一侧肾脏进行操作。在电磁血流控制下，减少肾动脉或静脉血流，或阻断输尿管。仅动脉收缩（30%/15分钟）就选择性地导致肾皮质中氙清除率（=营养物质流）急剧下降（约80%）。在相同条件下，心内注射放射性标记微球显示肾毛细血管血流从肾皮质外层向近髓质区集中。动脉收缩后，尿LDH活性立即增加高达800%。与总LDH活性一致，同工酶的百分比分布发生了变化：LDH-I增加，LDH-V减少。肾静脉收缩和输尿管阻塞均未产生类似效果。在长期实验中，大鼠一侧肾脏向后固定可反映肾下垂患者多年来肾脏移位的影响：动物单侧肾切除，剩余肾脏向后移位（约2.5个椎体）并固定于侧腹壁。“下垂”大鼠在术后26周的后续检查中显示尿LDH持续增加，最高可达50%。随着LDH升高，同位素肾图呈病理性，动脉造影显示肾动脉拉长变窄。在一些大鼠中，“下垂”固定效果不佳。所有这些动物的LDH、同位素肾图和动脉造影均正常。两项动物实验均证明，血流减少/缺氧是肾脏组织损伤的主要原因，表现为尿LDH释放增加。
