Diabetic stages of disease progression have been reduced to five distinct stages of beta-cell destruction leading to diabetes. The article, by Gordon C. Weir and Susan Bonner-Weir of the Joslin Diabetes Center, outlines changes to beta-cell mass, phenotype, and function. Stage one is compensation: the body increases insulin secretion to counter insulin resistance and/or decreasing beta-cells. This is most commonly found in relation to obesity. Stage two is marked by rising glucose levels that reach 5.0-6.5 mmol/L signifying beta-cell adaptation and loss of beta-cell mass. Stage three is marked by rapidly rising glucose levels leading to stage four characterized by stable decompensation with severe beta-cell dedifferentiation. Stage five is severe decompensation with severe reduction of beta-cell mass and onset of ketosis. The researchers stated that the movement between the stages goes both ways with properly treated diabetes moving towards smaller numbers (http://diabetes.diabetesjournals.org/content/53/suppl_3/S16.full).
Diabetic Retinopathy Stages
There are four diabetic stages of retinopathy. Stage one is mild nonproliferative retinopathy marked by microaneurysms in the blood vessels of the retina. Stage two is moderate nonproliferative retinopathy, signifying blockages in the blood vessels of the retina. Severe nonproliferative retinopathy is the third stage. In this stage the blocked blood vessels of the retina cause new, weaker blood vessels to grow. Proliferative retinopathy, the fourth, and most severe form is marked by new, weaker blood vessels growing along the retina and vitreous, often leaking and causing severe vision loss and blindness. Retinopathy is preventable however it may be into advanced stages before symptoms become apparent. Frequent eye exams and tight blood glucose control are both strong preventative measures.
Diabetic Nephropathy Stages
There are five stages of diabetic nephropathy (kidney disease). The first stage is charactereized by an increased glomerular filtration rate (GFR) and renal volume brought on by high glucose levels. Stage one can be reversed with insulin treatment. In stage two, urinary albumin excretion rate (UAER) is at normal levels (less than 20µg/min or 30 mg/24 hours). Glomerulus displays structural changes with elevated GFR matching elevated glycated hemoglobin greater than 9.5%. At this point patients may display clinical diabetic nephropathy. Stage three is considered early-stage diabetic nephropathy, with UAER at 20-200µg/min and can be marked by a slight increase in blood pressure. Stage four is considered clinical diabetic nephropathy or dominant diabetic nephropathy. It is characterized by proteinuria of more than 3.5 g/day, edema, and hypertension. The end stage of diabetic nephropathy is renal failure with increased urinary proteins and decreased renal filter function. First-line preventative measures include treating hyper- and hypoglycemia, and quitting smoking. Secondary measures may be lowering cholesterol, treatment with angiotensin-converting enzyme inhibitors, and dietary protein restriction.
