Abstract
Diabetic nephropathy (DN) is one of the most perilous side effects of diabetes mellitus type 1 and type 2 (T1DM and T2DM).). It is known that sodium/glucose cotransporter 2 inhibitors (SGLT 2i) and glucagone like peptide-1 receptor agonists (GLP-1 RAs) have renoprotective effects, but the molecular mechanisms are still unknown. In clinical trials GLP-1 analogs exerted important impact on renal composite outcomes, primarily on macroalbuminuria, possibly through suppression of inflammation-related pathways, however enhancement of natriuresis and diuresis is also one of possible mechanisms of nephroprotection. Dapagliflozin, canagliflozin, and empagliflozin are SGLT2i drugs, useful in reducing hyperglycemia and in their potential renoprotective mechanisms, which include blood pressure control, body weight loss, intraglomerular pressure reduction, and a decrease in urinary proximal tubular injury biomarkers. In this review we have discussed the potential synergistic and/or additive effects of GLP 1 RA and SGLT2 inhibitors on the primary onset and progression of kidney disease, and the potential implications on current guidelines of diabetes type 2 management.
Highlights
Diabetic nephropathy (DN) is a complication of diabetes mellitus, both type I and II, caused by changes in microvasculature [1], and which can lead to end-stage renal disease and cardiovascular disease [2,3]
Considering the structural changes in diabetic kidney disease, they are similar in both DM1 and DM2, but are more heterogeneous and less predictable in association with clinical presentation in DM2 [23], probably because DM2 has unreliable onset timing, longer exposure to hyperglycemia before diagnosis, older patients, and patients that are treated with renin-angiotensin inhibitors before the onset of diabetes [24]
Sodium/glucose cotransporter 2 (SGLT2) inhibitors are orally administrated hypoglycemic drugs with a novel mechanism of action that is useful across a continuum of diabetes regardless of duration of diabetes, baseline Hba1c or concomitant antidiabetic therapy [73,74]
Summary
Diabetic nephropathy (DN) is a complication of diabetes mellitus, both type I and II, caused by changes in microvasculature [1], and which can lead to end-stage renal disease and cardiovascular disease [2,3]. Considering the structural changes in diabetic kidney disease, they are similar in both DM1 and DM2, but are more heterogeneous and less predictable in association with clinical presentation in DM2 [23], probably because DM2 has unreliable onset timing, longer exposure to hyperglycemia before diagnosis, older patients, and patients that are treated with renin-angiotensin inhibitors before the onset of diabetes [24]. These structural alterations encompass modifications of several kidney departments. Glomerular filtration, albuminuria, and hypertension in DM1 are strongly correlated with mesangial expansion, but to a less degree with glomerular basement membrane width [25]
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