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GLP-1 RAs induced an early dip in eGFR, suggesting decreased intraglomerular pressure and decreased glomerular hyperfiltration, followed by slower eGFR loss in the overall population of GFR subgroups compared with placebo [13, 20], a feature shared with all currently known nephroprotective drugs ranging from renin–angiotensin blockers to mineralocorticoid receptor antagonists to SGLT2is to tolvaptan [67]
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