Primary prevention includes early detection of diabetes, glycemic control, screening for microalbuminuria, control of hypertension and smoking cessation, while key issues in secondary prevention are glycemic control, reduction of hypercholesterolemia, control of hypertension, smoking cessation, use of ACE inhibitors and possibly restriction of dietary protein (Walling 2000).

             There are several pathologic processes that contribute to diabetic nephropathy, including glomerular hypertrophy, sclerosis and nephron loss (Walling 2000). In the beginning stage, hyperglycemia increases the glomerular filtration rate and causes glomerular hypertrophy, and is already established in 40 percent of patients at the time of diagnosis with diabetes (Walling 2000). The microalbuminuric stage develops roughly five years after diagnosis in patients with type 1 diabetes but may occur earlier in patients with type 2 diabetes (Walling 2000). Up to 300 mg of albumin may be excreted daily (Walling 2000). Good glycemic control and introduction of angiotensin-converting enzyme (ACE) inhibitors can retard progression of nephropathy at this stage, while at more advanced stages of diabetic nephropathy, overt proteinuria, hypertension and reduction in creatinine clearance develop (Walling 2000). At this stage, patients rapidly progress to require dialysis or transplantation (Walling 2000). .

             Nephropathy is a common complication of diabetes and is characterized by the development of proteinuria, culminating in end-stage renal disease with a particular high risk of cardiovascular morbidity and mortality (Thornalley 2003). Tight control of blood glucose (mad blood pressure) decreases the risk of developing nephropathy, however it is not always achievable due to the limitations of current drug therapy (Thornalley 2003). A study published in the August 01, 2003 issue of Diabetes, suggest that "high-dose thiamine repletion suppressed the development of incipient nephropathy in experimental diabetes in which effects on the PKC, glycation, and oxidative stress pathways were involved" (Thornalley 2003).