Serum Gastrin in Chronic Renal Failure: Morphological and Physiological Correlations

Abstract

Elevated serum gastrin (SG) has been reported in chronic renal failure (CRF). We studied SG levels in relation to various humoral and gastroduodenal histopathologic findings in 20 controls, 12 uremics under conservative therapy (CT), 27 patients on regular dialysis (RDT) and 8 transplanted patients (Tx). SG and parathyroid hormone (PTH) levels were estimated by radioimmunoassay (RIA), in addition serum BUN, creatinine, Ca ⁺⁺PO₄^---and alkaline phosphatase (predialysis in RDT) were determined. 20 patients (12 on CT and 8 on RDT) underwent pentagastrin (PG) stimulation test and upper gastrointestinal endoscopy with biopsy of gastric and duodenal mucosa. The mucosal samples were stained for mucopolysaccharides (MPS), nucleic acid (NA) and alkaline phosphatase (AP), and divided into intense, normal or faint staining. Mean SG was 688.71 pg/ml (CT cases), 636.2 pg/ml (RDT cases) and 280.6 pg/ml (Tx cases), all values being significantly higher than controls (118.46 pg/ml). SG level had a linear correlation with serum creatinine in CT patients and predialysis creatinine in RDT patients, but not with other parameters studied (BUN, Ca ⁺⁺, PTH, PO₄^---AP). The incidence of gastroduodenal erosions (40%) had a significant negative correlation with SG. They were more frequent with normal MPS stain (p = 0.01) and NA staining (p < 0.001) than faint staining of gastric mucosa biopsy. The acid response to PG stimulation was inversely correlated with SG. We believe that elevated SG is compensatory to a decreased response of the gastroduodenal mucosa to PG. Mere retention of SG does not explain its elevation as its correlation with serum creatinine existed not only in patients on CT, but also in RDT patients. The apparently protective effect of elevated SG against gastric mucosal erosions may be partially related to its effect on gastric motility with diminution of biliary reflux. Gastric mucosal erosions seem to occur in a relatively healthy mucosa with low SG, serum calcium or PTH.

Gastrointestinal Complications in Patients with Chronic Kidney Disease—A 5-Year Retrospective Study from a Tertiary Referral Center

“…Urea causing increased backdiffusion of hydrogen ions across the mucosal barrier and elevated gastrin levels partly due to the decreased renal clearance of gastrin [3][4][5] and partly due to the enhanced gastrin synthesis, 6 which in turn act as an important stimulus for acid secretion are some of the Herpes simplex esophagitis ( Figure 1) 0 1…”

Gastrointestinal Evaluation in Chronic Kidney Diseases

“…Dyspeptic problems were detected in 42.9% of uremic patients undergoing dialysis. The most frequent gastrointestinal symptoms in uremia are the consequence of disequilibria of liquid and electrolytes, mechanical, physical, and emotional problems of patients, and toxins, which cannot be removed by dialysis and, which cause abnormalities in the stomach [12].…”

Hormonal Changes in Hemodialysis

“…The dialysance of these gas trointestinal peptide hormones depends on individual molecular weight and protein binding, but it is anyway negligible from a quantitative and clinical point of view [ 123], In particular, serum gastrin levels continue to be elevated on RDT [6,124,125], with no significant intradialytic removal [126]. How ever, there is no close relationship in dialysis patients between hypergastrinemia on the one hand and baseline or pentagastrin-stimulated gastric acid secretion or peptic ulcer disease on the other [127], Hyperparathy roidism and hypercalcemia can further stim ulate gastrin release.…”