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Response to: Correspondence on ‘Call for action in ANCA-associated vasculitis and lupus nephritis: promises and challenges of SGLT-2 inhibitors’ by Säemann and Kronbichler
  1. Marcus Säemann1,2,
  2. Andreas Kronbichler3
  1. 16th Medical Department, Nephrology and Dialysis, Clinic Ottakring, Vienna, Austria
  2. 2Medical School, Sigmund Freud University, Vienna, Austria
  3. 3Department of Medicine, University of Cambridge, Cambridge, UK
  1. Correspondence to Dr Marcus Säemann, 6th Medical Department, Nephrology and Dialysis, Clinic Ottakring, VIENNA, Austria; SAEMANNMARCUS{at}GMAIL.COM

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We thank our colleague Dr Patoulias1 for pointing out that sodium glucose transporter (SGLT)-2 inhibition (SGLT-2i) could mediate nephroprotection in patients with lupus nephritis (LN) and ANCA-associated vasculitis (AAV) via specific mechanisms within the tubular cell compartment independent of the presence of diabetes mellitus.2 As discussed by Dr Patoulias, kidney injury molecule-1 (KIM-1) is affected by SGLT-2i correlating with improvements in albuminuria, a hallmark of chronic kidney damage. KIM-1, however, is not only a mere marker of tubular injury, but it is actively involved in diverse pathogenic actions. Hence, its expression, for example, in diabetic kidney disease accelerates kidney injury via fatty acid uptake coupled with tubular glucose reabsorption in renal proximal tubular cells, resulting in various detrimental stress responses.3 Upregulation of KIM-1 and the ensuing tubular cell responses illustrate the close relationship between diseased glomeruli and subsequent tubulointerstitial fibrosis in response to increased tubular workload, thereby diseases traditionally considered primarily of glomerular origin such as diabetic kidney disease, and also inflammatory diseases such as LN and AAV, illustrate the therapeutic potential of innovative therapies such as SGLT-2i by limiting permanent and progressive damage especially to the tubulointerstitial tissue. The concept of nephron overload has been very recently proposed to be the final result of various and diverse pathogenic insults in most forms of chronic kidney disease.4 Since SGLT-2i substantially reduce tubular workload, they belong to the most efficient therapeutic interventions impacting nephron overload, suggesting also significant nephroprotective effects in LN and AAV.

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  • Handling editor Josef S Smolen

  • Contributors MS wrote and submitted the draft. AK edited the first draft of the manuscript.

  • 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 Commissioned; internally peer reviewed.

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