The natural progression of kidney injury in young type 1 diabetic patients.

Diabetes is the most common cause of end-stage renal disease in industrialized countries. This article describes the structural changes in early diabetic nephropathy and the relationship with renal functional parameters, blood pressure, and albumin excretion. The detrimental influence of sustained hyperglycemia and/or glycemic fluctuations on renal structural change has been well documented. Tight glycemic control is paramount to preventing the development, and even the regression, of renal lesions. As much of the renal injury from diabetes occurs in clinical silence before symptoms or laboratory findings of renal injury are evident, finding early markers of risk is imperative so that nephropathy can be prevented. Currently, the only clinical surrogate marker of diabetic renal injury available is microalbuminuria. However, given the reports of regression of microalbuminuria back to normoalbuminuria, the reliability of this tool as an indicator of risk has been questioned. The need for alternative, noninvasive surrogate markers is described in this report.