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SGLT2 inhibitors in lupus nephropathy, a new therapeutic strategy for nephroprotection
  1. Enrique Morales1,
  2. Maria Galindo2
  1. 1 Nephrology, Hospital Universitario 12 de Octubre, Madrid, Spain
  2. 2 Rheumatology, Hospital Universitario 12 de Octubre, Madrid, Spain
  1. Correspondence to Dr Enrique Morales, Nephrology, Hospital Universitario 12 de Octubre, Madrid, Spain, Spain; emoralesr{at}senefro.org

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Systemic lupus erythematosus (SLE) is a chronic autoimmune condition characterised by heterogeneous clinical features. The patients with SLE are known to have an increased risk of cardiovascular events, due to both traditional and disease-specific risk factors, including inflammation, endothelial dysfunction, accelerated atherosclerosis and lupus nephritis (LN). Since chronic kidney disease (CKD) is per se one of the strongest CV risk factors, any manoeuvres to prevent CKD progression, including reduction of albuminuria and prevention of estimated glomerular filtration decline, will likely have profound influences on patient outcomes.1 2

All patients with LN have by definition CKD, since they display albuminuria to varying degrees. While albuminuria is a classical sign of renal damage, a substantial portion of patients will also have structural and functional impairment of their kidney function as hallmark of CKD, that is, glomerular hyperfiltration and albuminuria. In the past, renin–angiotensin–aldosterone system inhibitors (RAASi) has already conferred nephroprotective potential in patients with LN; however, a substantial residual renal risk remains …

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Footnotes

  • Handling editor Josef S Smolen

  • Contributors EM and MG conceived and designed the study, drafted the manuscripts and approval of the final version.

  • Funding The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.

  • Competing interests None declared.

  • Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.

  • Provenance and peer review Not commissioned; externally peer reviewed.

  • Supplemental material This content has been supplied by the author(s). It has not been vetted by BMJ Publishing Group Limited (BMJ) and may not have been peer-reviewed. Any opinions or recommendations discussed are solely those of the author(s) and are not endorsed by BMJ. BMJ disclaims all liability and responsibility arising from any reliance placed on the content. Where the content includes any translated material, BMJ does not warrant the accuracy and reliability of the translations (including but not limited to local regulations, clinical guidelines, terminology, drug names and drug dosages), and is not responsible for any error and/or omissions arising from translation and adaptation or otherwise.