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Nat. Rev. Nephrol. doi:10.1038/nrneph.2017.182 Figure 1 Effects of SGLT2 inhibition and GLP1 agonism on renal haemodynamics in diabetes mellitus Figure 1 | Effects of SGLT2 inhibition and GLP1 agonism on renal haemodynamics in diabetes mellitus. a | Haemodynamic alterations induced by hyperglycaemia and diabetes mellitus. Glucose and sodium reabsorption in the proximal tubule is maximally activated and reduced amounts of sodium are delivered to the juxtaglomerular apparatus. The macula densa, via tubuloglomerular feedfack (TGF), induces vasodilation of the renal afferent arteriole, leading to an increase in intraglomerular pressure and hyperfiltration. b | Sodium–glucose cotransporter 2 (SGLT2) inhibition induces an increase in afferent arteriole tone and a subsequent decrease in intraglomerular pressure with a transient lowering of glomerular filtration rate (GFR). The integrated effect of glucagon-like peptide 1 (GLP1) agonism on renal haemodynamics seems to be the result of nitric oxide (NO)-induced vasodilation and inhibition of glomerular hyperfiltration. JGA, juxtaglomerular apparatus; NHE3, sodium–hydrogen exchanger isoform 3; RAS, renin–angiotensin system; SNS, sympathetic nervous system. Wanner, C. et al. (2018) A new era in therapeutics for diabetic kidney disease Nat. Rev. Nephrol. doi:10.1038/nrneph.2017.182