Clark W F, Naylor C D
Division of Nephrology, Victoria Hospital, London, Ontario, Canada.
Med Hypotheses. 1989 Jan;28(1):51-6. doi: 10.1016/0306-9877(89)90153-9.
Purkerson et al. have hypothesized that platelet aggregation and release reactions contribute to the progressive sclerosis of remnant nephrons. The suggested mechanism for platelet activation is disruption of endothelium by the high hydraulic pressures characteristic of remnant nephrons, with platelet exposure to basement membrane collagen. We herein postulate additional mechanisms whereby platelets might be activated in the microcirculation of remnant nephrons: (i) kinetic activation due to high plasma flow rates; (ii) close cell contact due to concentration of blood cells and platelets in the glomerulus; (iii) concentration of protein macromolecules that act as agonists for platelet release; (iv) glomerular release of saturated and monenoic fatty acids that stimulate platelet synthesis of thromboxane A2; (v) glomerular release of membrane-bound pro-coagulant factor, triggering a chain reaction that activates both platelets and the intraglomerular coagulation cascade. Platelet activation could play a pathogenetic role in many of the known derangements of structure and function in remnant nephrons. This paradigm may also be partially applicable to the glomerulosclerosis of diabetes mellitus.
珀克森等人推测，血小板聚集和释放反应会导致残余肾单位的进行性硬化。血小板激活的假定机制是残余肾单位特有的高液压破坏内皮，使血小板暴露于基底膜胶原蛋白。我们在此提出残余肾单位微循环中血小板可能被激活的其他机制：（i）由于高血浆流速导致的动力学激活；（ii）由于肾小球中血细胞和血小板的聚集而导致的紧密细胞接触；（iii）作为血小板释放激动剂的蛋白质大分子的聚集；（iv）肾小球释放刺激血小板合成血栓素A2的饱和脂肪酸和单烯脂肪酸；（v）肾小球释放膜结合促凝血因子，引发激活血小板和肾小球内凝血级联反应的连锁反应。血小板激活可能在残余肾单位许多已知的结构和功能紊乱中起致病作用。这种模式也可能部分适用于糖尿病性肾小球硬化。
