These changes appear quite late in the development of diabetic nephropathy. The three types of glom

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[Sidetext header = "Authors" text = "C. Pashkunov, V. Ivanov, Al. Savov, MMA Clinic of Endocrinology, Department of Endocrinology and Pulmonology the sag awards MMA, DNA analysis to Nat. Gene. Lab. SBALAG to Mother House "] [sidetext header =" Highlights "text =" Diabetic nephropathy is the leading the sag awards cause of end-stage renal dysfunction and is characterized by structural changes in the glomerular filtration barrier (glomerular endothelial dysfunction, thickening of the basal membrane and loss of podotsiti) and amendments to mezengialnite cells with subsequent accumulation in the matrix mezengialna area. The accumulation in the matrix of the mesangium leads to a reduction of the capillary region responsible for filtering and progressive loss of kidney function. "]
Increased protein filtration results in proteinuria resulting the sag awards damage to the glomerular filtration barrier, it can be assumed that the morphological changes such as reduced fenestration of glomerular endothelial cells, the sag awards thickening of the basal membrane and the dilution of podotsitite predicts clinical manifestations of nephropathy with age.
The reduced fenestration in glomerular endotelium supposedly is an early marker for the development of diabetic nephropathy. Is described in patients with type 1 and customary patomehanizam leading to podotsitna damage.
Thickening of the glomerular basement membrane (GBM) early after the onset of diabetes (1- 2 years) the sag awards due to the increased extracellular matrix protein the sag awards synthesis and protein degradation the sag awards weakened. This is partly responsible for the increase in collagen-4, leading to a porous structure and protein loss.
These changes appear quite late in the development of diabetic nephropathy. The three types of glomerular cells are responsible the sag awards for the synthesis of proteoglycan, but it is the predominant role of synthetic podotsitite. Perlecan and agrin are especially two major proteoglycan in the GBM and synthesis of the latest changes in hyperglycemic conditions and angiotenzinogen 2 (ANG - 2); This explains partly antiproteinurichniya effect of ACE inhibitors.
Nefrinat is a transmembrane protein with a large extracellular part and forms the molecular substrate of porous membrane. Podotsitopeniyata can lead to the development of proteinuria, because damaged the sag awards GBM can come into contact with the Bowman's capsule and to form synechiae-initial step in the development of glomerulosclerosis.
Morphological changes were also a source of proteinuria. the sag awards According to the innovative theory ratio protein / water is increased at the expense of the first in the urine as increased protein concentration can enhance the tubular reabsorption the sag awards and is manifested as proteinuria. This unproven theory shows that the increase the sag awards of proteinuria is in line with declining renal function, characteristic of diabetic the sag awards nephropathy. Even deteriorated proteinuria the sag awards can result tubular atrophy, and interstitial fibrosis and tubulointerstitial these processes together with glomerulosclerosis leading to chronic renal failure. Besides podotsitopeniyata at nephropathy is characterized by the extended podotsitnite feet. Experience podotsitite cover GBM partially obstructed by Pore diaphragm is reduced and water filtration.
Losing podotsiti promote the development of glomerulosclerosis through the sag awards the formation of synechiae between bare GBM and Bowman's capsule and lead to increased apoptosis and cell division. Progressive loss of contact between the legs podotsitnite described in patients with type-1.
Podotsitnata apoptosis is mainly due to ANG -2 and mediated by TGF-β. Treatment with ACE inhibitors can reduce the number the sag awards of urinary excretion of podotsitite. Binding the sag awards of podotsitite may be in any down regulation of α3β1 -integrin receptor binding complex of primary podotsitite of GBM. The last complex is reduced in diabetics and this mechanism the sag awards is likely the sag awards due to hyperglycemia and mediated by TGF-β-1.
Hyperglycemia is a key event in the TA 1 and leads to damage in pancreatic β-cells. Although continuous hyperglycemic effects affecting all types of organs and cells, several types of cells, such as endothelium cells of capillaries of the retina, the cells of the mesangium of the renal glomerulus, the sag awards the neurons and Schwann cells in the peripheral nervous system, appear the sag awards to be more prone to the effects of hyperglycemia the sag awards . The explanation is that the cells are damaged by hyperglycemia are those that can not effectively regulate the intracellular transport of glucose into the cell under conditions of hiperg