Gastric physiological and microbial changes in chronic renal failure patients under dialysis

ABSTRACT

Patients with chronic renal failure have been reported to have an increased incidence of gastric disease, 50 patients with renal failure [25 under haemo dialysis and 25 under peritoneal dialysis] and 12 controls, all suffering of gastritis were subjected to this study with the aim to characterise changes in the gastric physiology and microbial ecology, in end stage renal failure. Symptomatic gastritis was found in 45 of 50 uraemic patients as detected by endoscopic study. Gastric juice urea concentration, blood urea and serum creatinine are all significantly high in haemodialysis and peritoneal dialysis cases than controls. Also gastric juice pH is higher in cases than controls [3.7, 2.5, P<0.01 respectively]. In spite of more alkaline pH values, renal failure cases have high serum gastrin level detected by RAST method than controls [215.2, 185.1 compared to 136 pg/ml, P<0.05 respectively]. High gastric juice urea was expected to encourage urease-producing organisms especially H. pylori to colonise the stomach, yet culturing H. pylori from gastric aspirate and biopsy recovered it to nearly the same prevalence values from renal failure cases and controls [44%, 41.7%]. Serum Ig[G] anti H. pylori antibodies were also detected to nearly same incidence level in cases and controls [42 - 41.7%]. In spite of high urea level in all patients yet H. pylori was detected in only 46% of them. Now the prime mechanism in gastritis is not certain species of bacteria but it is the uraemic state that destruct the gastric mucosa and pump out hydrogen ions. This alkalinisation favours growth of many aerobes, anaerobes and candida species