The Role of Helicobacter Pylori in Microalbuminuria in Type 2 Diabetic Patients

Helicobacter pylori, previously known as Campylobacter pylori, is a gram-negative, microaerophilic bacterium usually found in the stomach. It was identified in 1982 by Australian scientists Barry Marshall and Robin Warren, who found that it was present in a person with chronic gastritis, gastric ulcers and conditions not previously believed to have a microbial cause. It is also linked to the development of duodenal ulcers and stomach cancer. However, over 80% of individuals infected with the bacterium are asymptomatic, and it may play an important role in the natural stomach ecology. [1] More than 50% of the world's population have H. pylori in their upper gastrointestinal tract. [2] Infection is more common in developing countries than Western countries. [3] H. pylori's helical shape (from which the genus name derives) is thought to have evolved to penetrate the mucoid lining of the stomach. [4, 5] Microalbuminuria, which is defined as an increased urinary albumin to creatinine ratio (UACR) of 30-300 μg/mg .[15] Has been known to be a strong predictor of the development of diabetic nephropathy. [16] It has also been demonstrated that microalbuminuria is a risk factor for cardiovascular disease in the general and diabetic populations. [17-19] and the increased urinary leakage of albumin reflects vascular damage, i.e., endothelial dysfunction or low grade chronic inflammation. [20] In addition, some studies have reported a relationship between microalbuminuria and metabolic syndrome, suggesting that insulin resistance underlies the pathogenesis of microalbuminuria. [21-23]