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Correspondence on ‘Call for action in ANCA-associated vasculitis and lupus nephritis: promises and challenges of SGLT-2 inhibitors’ by Säemann and Kronbichler
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  1. Dimitrios Patoulias
  1. Second Propedeutic Department of Internal Medicine, Aristoteleio Panepistemio Thessalonikes, Thessaloniki, Greece
  1. Correspondence to Dr Dimitrios Patoulias, Second Propedeutic Department of Internal Medicine, Aristoteleio Panepistemio Thessalonikes, 54642 Thessaloniki, Greece; dipatoulias{at}gmail.com

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Säemann and Kronbichler provided in their published article an excellent perspective on the potential place of sodium–glucose cotransporter-2 (SGLT-2) inhibitors in the treatment armamentarium against antineutrophil cytoplasmic antibodies (ANCA)-associated vasculitis and lupus nephritis (LN).1 Besides the described mechanisms of action, it seems that their effect against tubular damage and atrophy could also be crucial for the mediated nephroprotection in LN. It has been previously shown that interstitial fibrosis and tubular atrophy are strongly associated with the risk for progression to end-stage renal disease in subjects with LN, also increasing the overall mortality burden.2 In a previously published trial by Dekkers et al, it was shown that 6-week treatment with dapagliflozin led to a significant decrease in urinary kidney injury molecule-1 (KIM-1) excretion, a marker of tubular injury, which strongly correlated with the change in albuminuria.3 Recently, in a post-hoc analysis of the VERTIS RENAL trial, it was shown that ertugliflozin was associated with a sustained lowering of the plasma levels of KIM-1 regardless of baseline kidney function.4 Such an effect has also been shown in other trials of smaller sample size.5 Thus, it seems that there are more benefits than expected with the use of SGLT-2 inhibitors in patients with LN. Based on the significant cardiovascular and renal burden of those patients, SGLT-2 inhibitors appear to be a promising treatment option, even in the absence of concomitant diabetes mellitus.

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All data relevant to the study are included in the article. na.

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This study does not involve human participants.

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Footnotes

  • Contributors DP wrote the draft.

  • Funding The author has 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 Commissioned; internally peer reviewed.

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