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To produce glutathione, a cysteine molecule is required

The existing relationship between preDM and CKD suggests that the deterioration of kidney function does not only depend on a glycemic threshold and that other multiple metabolic pathways of damage are also involved, similar to what occurs with other micro- or macrovascular complications.2 Up to 30% of people with recently diagnosed DM have some degree of kidney damage, which would suggest that, amongst other things, the injury effects of dysglycemia on the kidneys can start very early, before these values reach the glucose threshold of DM criteria.2224 The role of dysglycemia in the development of CKD is not completely understood.25 It could be associated with increased production of reactive oxygen species (ROS), that promote the accumulation of advanced glycation end products, activate intracellular signaling molecules such as protein kinase C, and stimulate the reninangiotensin system.2628 These proposed alterations may favor glomerular hyperfiltration, mesangial expansion, thickening of the glomerular basement membrane, damage to podocytes and generation of glomerular sclerosis, which would favor the development of albuminuria and the progression of CKD.27,28 These alterations have been related to renal functional and structural changes such as glomerulomegaly, expansion of the mesangial matrix, and increased plasma flow, which becomes evident with histological patterns of focal and segmental glomerulosclerosis as it has been seen in obesity-related chronic kidney disease29 (Fig

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