Diabetic nephropathy, by far, is the most common cause of end stage renal disease in the US and many other countries. In type 1 diabetes, the natural history of diabetic nephropathy is tightly linked to evolution of classic lesions of the disease, namely glomerular basement membrane thickening, increased mesangial matrix, and reduced glomerular filtration surface density. These lesions progress in parallel and correlate with increased albumin excretion rate and reduced glomerular filtration rate across a wide range of renal function. In fact, the vast majority of the variances of albumin excretion and glomerular filtration rates can be explained by these glomerular lesions alone in type 1 diabetic patients. Although, classic lesions of diabetic nephropathy, indistinguishable from those of type 1 diabetes, also occur in type 2 diabetes, renal lesions are more heterogeneous in type 2 diabetic patients with some patients developing more advanced vascular or chronic tubulointerstitial lesions than diabetic glomerulopathy. More research biopsy longitudinal studies, especially in type 2 diabetic patients, are needed to better understand various pathways of renal injury in diabetic nephropathy.
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Acknowledgments This work was in part supported by grants from the National Institutes of Health (NIH) (DK13083) and 2P01DK013083 and National Center for Research Resources (MO1-KK00400). Behzad Najafian has received a subaward of N001447101 from NIH.
Behzad Najafian is a PI and co-PI of grants supported by the Genzyme and Roche.
- Diabetic nephropathy
- Structural-functional relationships
- Type 1 diabetes
- Type 2 diabetes