Each kidney is made of more than a million units called nephrons. Each nephron has a tuft of blood vessels called a glomerulus. The glomerulus filters blood and forms urine, which drains down into collecting ducts to the ureter.

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. This stage is called "microabuminuria" (micro refers to the small amounts of 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.

Protein may appear in the urine for 5 to 10 years before other symptoms develop. High blood pressure often accompanies diabetic nephropathy. Over time, the kidney's ability to function starts to decline. Diabetic nephropathy may eventually lead to chronic kidney failure. The disorder continues to progress toward end-stage kidney disease, usually within 2 to 6 years after the appearance of high protein in the urine (proteinuria).

Diabetic nephropathy is the most common cause of chronic kidney failure and end-stage kidney disease in the United States. People with both type 1 and type 2 diabetes are at risk. The risk is higher if blood-glucose levels are poorly controlled. However, once nephropathy develops, the greatest rate of progression is seen in patients with poor control of their blood pressure.

Diabetic nephropathy is generally accompanied by other diabetes complications including hypertension, retinopathy, and vascular (blood vessel) changes, although these may not be obvious during the early stages of nephropathy. Nephropathy may be present for many years before high protein in the urine or chronic kidney failure develop.