The underlying pathophysiology defect in type 2 diabetes is characterized by the following three disorders (1) peripheral resistance to insulin, especially in muscles cells: (2) increased production of glucose by the liver, and (3) altered pancreatic secretion. Increased tissue resistance to insulin generally occurs first and eventually followed by impaired insulin secretions. The pancreas produces insulin, yet insulin resistance prevents its proper use at the cellular level. Glucose cannot enter target cells and accumulates in the blood streams, resulting in hyperglycemia. The high blood glucose levels often stimulate an increase in insulin production by the pancreas: thus. Type 2 diabetic individuals often have excessive insulin production (hyperinsulinemia).
Insulin resistance refers to tissue sensitivity to insulin. Intracellular reaction are diminished, making insulin less effective at stimulating glucose uptake by the tissues and regulating glucose release by the liver.
If blood glucose levels are elevated consistently for a significant period of time, the kidney’s filtration mechanism is stressed, allowing blood proteins to leak into the urine. As a result, the pressure in the blood vessels of the kidney increases. It is thought that the elevated pressure serves as the stimulus the level of nephropathy.
The earliest detectable change in the course of diabetic nephropathy is a thickening in the glomerulus. At this stage, the kidney may start allowing more albumin (protein) than normal in the urine, and this can be detected by sensitive tests for albumin.
As diabetic nephropathy progresses, increasing numbers of glomeruli are destroyed. Now the amounts of albumin being excreted in the urine increases, and may be detected by ordinary urinalysis techniques. At this stage, a kidney biopsy clearly shows diabetic nephropathy and eventually leads to Chronic renal failure.
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