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. 1994 Mar;35(3):401–407. doi: 10.1136/gut.35.3.401

Origin and development of exocrine pancreatic insufficiency in experimental renal failure.

M M Lerch 1, P Hoppe-Seyler 1, W Gerok 1
PMCID: PMC1374599  PMID: 7512063

Abstract

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.

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Selected References

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