Introduction. Diabet Melitus is a complex and heterogeneous sindrom caused by an innate or acquired disorder of insulin secretion or resistance of peripheral tissues to the insulin produced, it produces profound disturbances in carbohydrate, protein and mineral metabolism. All these leads to the appearance of cronic complications it has become one of the most common metabolic disease .In the world there are 449,3 mln people with diabetes. In the Republic of Moldova there are 90.000 people with diabetes. Studying the role of the: hyperglicaemia final glycation products, inflammation, oxidative stress, the rennin angiotensin aldosterone system, could serve as information markers involved in the production of late complications of diabet mellitus. Aim of the study.  In these review, I will describe the pathogenetic factors involved in the production of late complications of diabet mellitus. Materials and methods. The material was searched using the PubMed engine along with the psycarticles database. The following keywords joined the search for titles/ abstracts via PubMed: Pathogenesis of late complications of diabet mellitus. Results. Hyperglycaemia is the basis for chronic lesions in diabet mellitus. In hyperglycemia the body is trying to metabolize glucose in an accelerated way, to decrease the amount of glucose in the same time is formed a series of intermediate toxic products which lead to training advanced glycation end products(AGE). The most important pathological effect of AGE is that many cells have surface receptors for AGE called (RAGE), by binding AGE to receptors(RAGE) are stimulated the inflammation and oxidative stress. The inflammation is involved, the source which produce the inflammation is the adipos tissue trough adipocytes and macrophages which releases pro-inflamatory mediators. TNF alfa, IL-6,IL-1,IL-8, gamma interferon increase the inflammation and aggravate insulin resistance also induces the apoptosis and disfunction of beta pancreatic cells. The oxidative stress means excessive formation of free radicals: reactive oxygen molecules(ROS) and reactive nitrogen molecules(RNS) they alter the structure of proteins, lipids and nucleic acids all leading to vascular damage. ANG II it’s an vasoconstrictor factor involved in vascular remodeling and atherosclerosis. Aldosterone has the effect of stimulating proliferation of fibroblasts and stimulating the inflammation. Conclusions. The control of pathogenetic factors will allow development of pathogenetic therapy of Diabetes and only then we will be able to stopped the occurrence of late