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Curr Opin Nephrol Hypertens ; 31(5): 456-463, 2022 09 01.
Artigo em Inglês | MEDLINE | ID: mdl-35894280

RESUMO

PURPOSE OF REVIEW: Diabetic kidney disease is the most common cause of chronic kidney disease (CKD) and end-stage kidney disease in the world. Risk factor modification, glucose control, and renin-angiotensin-aldosterone system blockade have remained the standard of care for 2 decades. New therapeutic agents have emerged in recent years, demonstrating kidney and cardiovascular benefits, and herein we review recent clinical trials on this topic. RECENT FINDINGS: After the publication of several cardiovascular outcome trials for sodium-glucose cotransporter 2 inhibitors (SGLT-2i), new trials have focused ON primary kidney-specific outcomes demonstrating safety and benefits among patients with proteinuric CKD; patients with or without diabetes, and heart failure with preserved ejection fraction (HFpEF) respectively. Similarly, nonsteroidal mineralocorticoid receptor antagonists (ns-MRAs) and glucagon-like-peptide 1 receptor agonists (GLP-1 RAs) have improved cardiovascular and kidney outcomes. Recently, clinical practice guidelines have also been updated to reflect this new evidence. SUMMARY: In summary, SGLT-2i, GLP-1 RAs, and ns-MRAs have demonstrated cardiovascular and kidney benefits, including all-cause and cardiovascular mortality, progression to end-stage kidney disease, and hospitalizations for heart failure exacerbation among diverse patient population.


Assuntos
Diabetes Mellitus Tipo 2 , Nefropatias Diabéticas , Insuficiência Cardíaca , Falência Renal Crônica , Insuficiência Renal Crônica , Diabetes Mellitus Tipo 2/tratamento farmacológico , Nefropatias Diabéticas/tratamento farmacológico , Receptor do Peptídeo Semelhante ao Glucagon 1/agonistas , Insuficiência Cardíaca/tratamento farmacológico , Humanos , Falência Renal Crônica/tratamento farmacológico , Antagonistas de Receptores de Mineralocorticoides/uso terapêutico , Insuficiência Renal Crônica/complicações , Insuficiência Renal Crônica/tratamento farmacológico , Volume Sistólico
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