Objective To investigate the risk factors associated with the development of peritonitis caused by enteral bacteria in peritoneal dialysis patients, including the prescription of gastric acid inhibitors as a potential risk factor. Design Retrospective single-center study. Setting Tertiary university hospital. Patients an d Main Outcome Measures Fifty-five patients who entered into our continuous ambulatory peritoneal dialysis (CAPD) program during the last 6 years were included. Multiple logistic regression analysis was used to establish the best determinants over the development of at least one episode of enteric peritonitis. The predictive variables included in the model were: age, gender, diabetic versus nondiabetic, polycystic versus nonpolycystic kidney diseases, history of constipation, presence or absence of moderate/severe malnutrition, peritoneal transport characteristics, peritoneal protein losses, rate of exit-site infections, rate of total peritonitis, intestinal abnormalities, and treatment with inhibitors of gastric acid secretion. Results The total number of peritonitis episodes during the studied period was 88, which clustered in 34 of 55 patients. Fourteen (16%) were caused by enteric microorganisms in 10 patients: Escherichia coli (6), Klebsiella sp (2), Enterobacter sp (1), and Enterococcus sp (5). Nine of 10 patients who developed enteric peritonitis were on gastric acid inhibitors (3 patients on omeprazole and 6 patients on H2-antagonists), while 15 of 45 patients who did not develop enteric peritonitis were on gastric acid inhibitors (all of them on H2-blockers). There were temporal relationships between the start of gastric acid inhibitors and the development of enteric peritonitis in 6 of 9 patients who were on this medication. Four of 10 patients who developed enteric peritonitis had diverticulosis. Ten of 45 patients who did not develop enteric peritonitis had been diagnosed with diverticulosis of the colon or sigmoid prior to entry to CAPD. The unique patient who was not on gastric acid inhibitors and developed enteric peritonitis, had been diagnosed with chronic atrophic gastritis with achlorhydria. By multiple logistic regression analysis, the treatment with gastric acid inhibitors was the only independent variable that entered into the best predictive equation over the development of enteric peritonitis (Iog likelihood ratio = -26.077, odds ratio = 18; 95% CI odds ratio: 2 - 155). Conclusion Gastric acid inhibitors may increase the risk for developing enteric peritonitis in peritoneal dialysis patients.

Oral phosphorus supplementation led to a significant increase in the PTH concentration of kidney transplant recipients. The mean 1,25(OH)(2)D concentration decreased mainly in recipients with optimal allograft function. The counterbalance effect of PTH on 1,25(OH)(2)D production may account for the relative preservation of 1,25(OH)2D levels in recipients with suboptimal allograft function.

Altered diurnal rhythm should not be considered as a usual complication of renal disease. Inadequate antihypertensive pharmacotherapy could be related to the abnormalities of nighttime BP fall when it is detected.

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