ABSTRACT
This chapter reviews the evidence for excess consumption of Advanced glycation end products (AGEs) contributing to the development and progression of Chronic kidney disease (CKD). Kidney damage is determined by markers such as proteinuria and abnormalities in urine and blood chemistry, while decreased kidney function is determined by a decline in estimated glomerular filtration rate. End-stage renal disease (ESRD) describes patients who are at Stage 5 of CKD and are being treated with dialysis or kidney transplantation. A number of clinical studies reported that circulating AGEs accumulate with a progressive decline in renal function, even in the absence of diabetes, and with markers of inflammation and oxidative stress in uremic patients. Dietary modulation of AGEs may be a simple, cost-effective, and complementary treatment option for CKD. Indeed, a low-AGE diet, which lowered serum and kidney AGE levels, protected against diabetic nephropathy in spontaneous mouse models of both type 1 and type 2 diabetes.
