On the contribution of immune 42 mechanisms to the pathogenesis of diabetic nephropathy
Diabetic nephropathy (NF) came first among all the specified causes of end-stage renal failure. Patients with type 1 diabetes mellitus (DM) make up more than half of all patients treated with chronic hemodialysis in the United States and Western Europe. Among patients with diabetes with terminal renal failure, 60% are people over 50 years old, so hemodialysis is not always prescribed. However, hemodialysis is increasingly used in elderly and senile patients; therefore, the proportion of patients with diabetes, especially type II diabetes, in hemodialysis centers will increase, significantly increasing the cost of treating diabetes. Currently, along with metabolic, hemodynamic and genetic theories, the role of immune disorders in the formation and progression of DNs is being discussed. The prerequisites for the formation of a hypothesis about the immune genesis of DNs were the frequent detection of increased levels of circulating immune complexes (CICs) and immunoglobulins in the blood, as well as deposits of immunoglobulins and complement in the kidney structures of patients with diabetes. However, among researchers there is no unanimity in the explanation of these facts. Many consider indisputably existing immune abnormalities inherent in DN as non-specific epiphenomes. The immune hypothesis of the pathogenesis of DN was formulated back in the 70s. The currently accumulated data suggest the participation of the immunocomplex mechanism in the development of DN. Immunofluorescence examination of the kidney tissue of patients with diabetes almost always reveals a luminescence of IgG, IgM, less often IgA, SZ and other complement fractions along the basal membranes of the glomeruli (BMC) and tubules of focal granular and linear in nature.