In the United States, diabetes is the most common cause of end-stage renal disease, the final stage of nephropathy. Diabetic nephropathy occurs in Type 1 and Type 2 diabetes. About 35% of patients who’ve had Type 1 diabetes for more than 20 years develop end-stage renal disease. Among those with Type 2 diabetes, the risk of end-stage renal disease may be higher or lower, depending on the patient’s ethnic group. African-Americans, Native Americans, and Mexican-Americans are at higher risk than whites. Other risk factors for diabetic nephropathy include hypertension, poor blood glucose control, genetic predisposition, and high protein intake.Diabetic nephropathy develops over many years. Typically, diabetic nephropathy in patients with Type 1 diabetes progresses through five stages . However, patients with Type 2 diabetes may not progress through these five stages in the same manner as patients with Type 1 diabetes.
The exact cause of kidney destruction in diabetic nephropathy isn’t known. What’s known is that kidney damage occurs in the glomerulus, which consists of tufts of capillaries in the renal corpuscle, which is surrounded by Bowman’s capsule. The glomerular capillaries are made up of three layers of cells: the endothelium, basement membrane, and visceral epithelium. Mesangial cells lie between and support the capillaries.
Normally, blood enters the glomerulus through the afferent arteriole and exits by the efferent arteriole. As blood passes through the glomerulus, water, electrolytes, creatinine, urea nitrogen, and glucose filter across the capillary basement membrane into Bowman’s capsule. This filtrate is similar to blood plasma, but it doesn’t normally contain proteins. After the filtrate enters Bowman’s capsule, it flows through the tubules of the kidney and is eventually excreted from the body.
In diabetic nephropathy, kidney destruction results from gradual structural changes in the glomerulus. First, the glomerulus enlarges. Then glomerulosclerosis-the replacement of normal glomerular tissue with fibrous scar tissue occurs. In diffuse glomerulosclerosis, the more common type, the basement membrane of the glomerular capillaries thickens and eventually leaks capillary fluid. Also, the mesangial matrix (the spongy network surrounding the mesangial cells) thickens. In nodular glomerulosclerosis, hyaline nodules (hard masses of glassy, eosinophilic substances) form in the mesangial part of the glomerulus. In both types of glomerulosclerosis, the sclerotic changes disrupt the function of increasing numbers of glomeruli, slowly impairing the patient’s renal function.