Kes P
Department of Internal Medicine, University Hospital, Sestre Milosrdnice, Zagreb, Croatia.
Acta Med Croatica. 1992;46(1):47-58.
On the basis of the existing experimental and clinical studies about the factors affecting the appearance of hypergastrinemia in renal failure, it can be concluded that the kidney plays an important, but not the only, role in the degradation of endogenous gastrin in humans. In this process the key role is played by the blood flow through the kidney, the preservation of the peritubular capillary system, and the functional kidney mass. Glomerular filtration has no particular importance in the extraction of gastrin from the circulation, while through the urine only a small amount of gastrin is excreted. In the decomposition of a part or at least some molecular gastrin forms, an important role is played by the capillary systems of extra-renal tissue. One further conclusion is that hypergastrinemia in patients with renal failure is the result of the combined effects of the reduced catabolism of gastrin in the kidney and its increased synthesis which is for the most part connected with hypochlohydria and secondary hyperparathyroidism. In patients with renal failure there exists the inhibition of the gastrin acid secretion which is the cause of the weakening of the mechanism of the feedback connection between HCl and gastrin, while because of a permanent stimulation of G-cells, the hyperplasia of these cells develops, as well as the increased secretory activity, and hypergastrinemia. Parietal cells become less sensitive to a permanently increased serum gastrin concentration but still capable of reacting to the maximal stimulus. In patients with renal failure, especially those with extreme hypergastrinemia, there develops the increased concentration of large, mainly biologically inactive (big big gastrin, component I) molecular forms of gastrin.
基于现有的关于影响肾衰竭患者高胃泌素血症出现因素的实验和临床研究，可以得出结论：肾脏在人体内源性胃泌素的降解过程中起着重要作用，但并非唯一作用。在这个过程中，流经肾脏的血流量、肾小管周围毛细血管系统的保存以及功能性肾实质起着关键作用。肾小球滤过在从循环中提取胃泌素方面没有特别重要的意义，而通过尿液仅排出少量胃泌素。在部分或至少一些分子胃泌素形式的分解过程中，肾外组织的毛细血管系统起着重要作用。另一个结论是，肾衰竭患者的高胃泌素血症是肾脏中胃泌素分解代谢减少及其合成增加共同作用的结果，而合成增加在很大程度上与胃酸过少和继发性甲状旁腺功能亢进有关。在肾衰竭患者中，存在胃泌素酸分泌的抑制，这是盐酸与胃泌素之间反馈联系机制减弱的原因，而由于对G细胞的持续刺激，这些细胞会发生增生，分泌活性增加，进而导致高胃泌素血症。壁细胞对血清胃泌素浓度持续升高的敏感性降低，但仍能对最大刺激做出反应。在肾衰竭患者中，尤其是那些患有极端高胃泌素血症的患者，胃泌素的大分子形式（主要是生物活性较低的大胃泌素、成分I）的浓度会升高。
