Lerch M M, Hoppe-Seyler P, Gerok W
Department of Medicine I, Ulm University Medical School, Germany.
Gut. 1994 Mar;35(3):401-7. doi: 10.1136/gut.35.3.401.
Chronic renal failure affects the physiological function of many organ systems. One of them is the exocrine pancreas. Although varying degrees of pancreatic insufficiency are the dominating clinical characteristic of uraemic pancreatic disease, it remains unclear whether this disease should be regarded as a manifestation of chronic pancreatitis, arising from recurring attacks of acute pancreatitis, or represents a distinct entity. The exocrine pancreas was studied in a model of experimental renal failure. The pancreas was removed from each rat at selected time points over eight weeks after subtotal nephrectomy and from a standard rat model of pancreatitis for comparison. The data show that the in vitro secretory response is considerably changed in renal failure (increased during early acute and decreased during chronic renal failure). While the pancreatic content of digestive enzymes progressively declines, DNA and protein synthesis increase over time. Acinar cell deletion is increased and accompanied by an increased rate of mitosis. This increased cellular turnover is not associated with tissue oedema, pancreatic fibrosis, inflammatory changes, autophagocytosis or subcellular redistribution of lysosomal hydrolases, all of which are characteristic for pancreatitis. The ultrastructural changes of uraemic pancreatic disease bear no resemblance to the changes seen in pancreatitis. It is concluded that the morphological and biochemical changes in early uraemic pancreatic disease are quite distinct, correspond with toxic damage of the pancreas, and are dominated by functional impairment and an increased cellular turnover.
慢性肾衰竭会影响多个器官系统的生理功能。其中之一是外分泌胰腺。尽管不同程度的胰腺功能不全是尿毒症胰腺疾病的主要临床特征，但这种疾病究竟应被视为由急性胰腺炎反复发作引起的慢性胰腺炎的一种表现，还是代表一种独特的病症，仍不明确。我们在实验性肾衰竭模型中对外分泌胰腺进行了研究。在大鼠肾大部切除术后的八周内，于选定时间点从每只大鼠身上取出胰腺，并从标准胰腺炎大鼠模型中取出胰腺作比较。数据显示，肾衰竭时体外分泌反应发生了显著变化（在急性早期增加，在慢性肾衰竭时减少）。虽然胰腺消化酶含量逐渐下降，但随着时间推移，DNA和蛋白质合成增加。腺泡细胞缺失增加，并伴有有丝分裂率上升。这种细胞更新增加与组织水肿、胰腺纤维化、炎症变化、自噬作用或溶酶体水解酶的亚细胞重新分布均无关，而这些都是胰腺炎的特征。尿毒症胰腺疾病的超微结构变化与胰腺炎所见变化毫无相似之处。结论是，早期尿毒症胰腺疾病的形态学和生化变化截然不同，与胰腺的毒性损伤相符，且以功能损害和细胞更新增加为主。
