Pathophysiology of gastric acid secretion in patients with chronic renal failure: influence of Helicobacter pylori infection
Authors: Watanabe H. , Hiraishi H. , Ishida M. , Kazama J. J. , Terano A. 
Published: October 2003

Abstract. Watanabe H, Hiraishi H, Ishida M, Kazama JJ, Terano A (Dokkyo University School of Medicine, Tochigi and Niigata University Medical Hospital, Niigata, Japan). Pathophysiology of gastric acid secretion in patients with chronic renal failure: influence of Helicobacter pylori infection. J Intern Med 2003; 254: 439–446.Objectives. The incidence of gastroduodenal diseases is high in patients with chronic renal failure (CRF). However, gastric acidity in CRF has been reported to range in level from low to high. Moreover, it remains unknown whether Helicobacter pylori infection influences gastric acidity in such patients. Thus, we aimed to clarify the pathophysiological perturbation in gastric acidity and to determine the influence of H. pylori infection in CRF.Design. Case–control study.Setting. A university hospital.Subjects. Twenty‐seven patients with CRF and 24 control patients, presenting with either gastrointestinal symptoms, positive faecal occult blood, or anaemia (haemoglobin <10 g dL−1).Measures. The patients underwent gastroduodenal endoscopy with simultaneous determination of H. pylori infection. Gastric ammonium concen‐tration, serum pepsinogen I and II, and basal gastrin level were measured. Thereafter, gastric acid secretion was monitored by 24‐h intragastric acidity measurement with calculation of pH‐3 holding time (%) (hours showing pH > 3/24 h).Results. In the CRF group, pH‐3 holding time of H. pylori (+) subgroup was significantly greater than that of H. pylori (−) subgroup (71.2 ± 32.4% vs. 32.8 ± 30.0%, mean ± SD; P = 0.03). Pepsinogen I/II ratio was inversely correlated with pH‐3 holding time in the control and CRF groups. Gastric ammonium concentration in CRF/H. pylori (+) subgroup (14.1 ± 9.2 mmol L−1) was significantly higher than in CRF/H. pylori (−) (2.5 ± 2.7 mmol L−1; P = 0.002) and control/H. pylori (+) subgroups (6.1 ± 4.2 mmol L−1; P = 0.01). Serum gastrin level was significantly higher in the CRF group than in the control group (297 ±343 pg mL−1 vs. 116 ± 69 pg mL−1; P = 0.02) as a whole. However, there was no significant correlation between serum creatinine and gastrin levels in the CRF group. Gastrin level in CRF/H. pylori (+) subgroup was significantly higher than in CRF/H. pylori (−), control/H. pylori (+), and control/H. pylori (−) subgroups (423 ±398 pg mL−1 vs. 113 ± 79, 124 ± 78, and 96 ±43 pg mL−1, respectively; P = 0.01–0.03). Significant positive correlations amongst pH‐3 holding time, ammonium and gastrin concentrations were found in the CRF group, but not in the control group.Conclusions. CRF without H. pylori infection primarily shows a tendency for high gastric acidity, but without hypergastrinaemia. Persistent H. pylori infection in CRF leads to decreased acidity and, consequently, to fasting hypergastrinaemia via a feedback mechanism. The hypoacidity in CRF with H. pylori infection appears to result from neutralization of acid by ammonia as well as from gastric atrophy. Thus, H. pylori infection status critically determines perturbation in gastric acidity and fasting gastrin level in CRF.