BACKGROUND/AIMS:
As default, Helicobacter pylori infection may cause systemic inflammation and vascular endothelial damage. Therefore, it can be assumed that the glomerular damage as a result may lead to an increase in urinary albumin excretion. In this study, this hypothesis was set, and the relationship between Helicobacter pylori infection and microalbuminuria was examined.
METHODS:
Ninety-three patients with type 2 diabetes were included in the study. These patients were divided into two groups as Helicobacter pylori infection-positive (Group 1) or -negative (Group 2). In all infected and non-infected patients, urinary albumin excretion and other parameters were compared.
RESULTS:
The presence of Helicobacter pylori infection was detected in 53 of 93 diabetic patients (56.98%). Diabetic patients infected by Helicobacter pylori (Group 1; 186.7±24.2 mg/24 h) showed significantly higher microalbuminuria than non-infected patients (Group 2; 131.2±11.6 mg/24 h) (p=0.012). Diabetics infected with Helicobacter pylori had significantly higher inflammation marker levels than non-infected patients (p<0.05). It has been concluded that the relation between microalbuminuria level and Helicobacter pylori infection in diabetics is independent from other study variables.
CONCLUSIONS:
Helicobacter pylori infection, because of the systemic inflammatory response, may play an important role in the progression of diabetic nephropathy or its development. In this study, demonstrating the relationship between Helicobacter pylori infection with diabetic microalbuminuria, due to the small number of patients, is inadequate. Therefore, clinical and molecular studies involving more patients should be supported
