ArticleFrontiers in pharmacology2021
Empagliflozin Reduces Renal Hyperfiltration in Response to Uninephrectomy, but Is Not Nephroprotective in UNx/DOCA/Salt Mouse Models.
Article in Frontiers in pharmacology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers, 1 of them a synthesis that pooled it.
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Who cites it
17 citing papers in PubMed, 1 synthesis or guideline pooled it, 24 citations in OpenAlex.
- Application of SGLT2 inhibitors in kidney diseases: a bibliometric analysis.Frontiers in medicine · 2026Pooled it
- Post-nephrectomy outcomes in COVID-19 and non-COVID-19 Patients using ACEi, ARB and SGLT2i: a N3C database study.International urology and nephrology · 2026Article
- Empagliflozin preserves cardiac function and modulates metabolism in a mouse model of Duchenne muscular dystrophy.bioRxiv : the preprint server for biology · 2026Article
- Dual Inhibition of the Renin-Angiotensin-Aldosterone System and Sodium-Glucose Cotransporter-2: Mechanistic and Clinical Evidence for Cardiorenal Protection.Biomedicines · 2026Review
- Microbes and GFR in Health and CKD in Mice.Journal of the American Society of Nephrology : JASN · 2026Article
- Investigating the Role of Empagliflozin in the Pathological Progress of Ischemia-Reperfusion Injury in Rat Kidneys: The Involvement of Nitric Oxide.Advanced pharmaceutical bulletin · 2025Article
- The sodium/glucose cotransporter 2 inhibitor empagliflozin is a pharmacological chaperone of cardiac NaAmerican journal of physiology. Heart and circulatory physiology · 2025Article
- Renal and Vascular Effects of the Allosteric Transglutaminase 2 Modulator LDN-27219 in One-Kidney DOCA-Salt Mice.International journal of molecular sciences · 2025Article
- Effects of sotagliflozin on kidney and cardiac outcome in a hypertensive model of subtotal nephrectomy in male mice.Physiological reports · 2025Article
- Sodium Glucose Cotransporter-2 Inhibitors in Non-Diabetic Kidney Disease: Evidence in Experimental Models.Pharmaceuticals (Basel, Switzerland) · 2024Review
- Empagliflozin treatment rescues abnormally reduced NaAmerican journal of physiology. Heart and circulatory physiology · 2024Article
- Mechanisms of Diabetic Nephropathy Not Mediated by Hyperglycemia.Journal of clinical medicine · 2023Review
- Impact of Impaired Kidney Function on Arrhythmia-Promoting Cardiac Ion Channel Regulation.International journal of molecular sciences · 2023Review
- The immunology of heart failure with preserved ejection fraction.Clinical science (London, England : 1979) · 2023Review
- Combination of canagliflozin and puerarin alleviates the lipotoxicity to diabetic kidney in mice.The Korean journal of physiology & pharmacology : official journal of the Korean Physiological Society and the Korean Society of Pharmacology · 2023Article
- Renoprotective effects of empagliflozin are linked to activation of the tubuloglomerular feedback mechanism and blunting of the complement system.American journal of physiology. Cell physiology · 2023Article
- Empagliflozin increases kidney weight due to increased cell size in the proximal tubule S3 segment and the collecting duct.Frontiers in pharmacology · 2023Article
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Large-scale clinical outcome studies demonstrated the efficacy of SGLT2 inhibitors in patients with type II diabetes. Besides their therapeutic efficacy in diabetes, significant renoprotection was observed in non-diabetic patients with chronic kidney disease (CKD), suggesting the existence of glucose-independent beneficial effects of SGLT2 inhibitors. However, the relevant mechanisms by which SGLT2 inhibition delays the progression of renal injury are still largely unknown and speculative. Previous studies showed that SGLT2 inhibitors reduce diabetic hyperfiltration, which is likely a key element in renoprotection. In line with this hypothesis, this study aimed to investigate the nephroprotective effects of the SGLT2 inhibitor empagliflozin (EMPA) in different mouse models with non-diabetic hyperfiltration and progressing CKD to identify the underlying diabetes-independent cellular mechanisms. Non-diabetic hyperfiltration was induced by unilateral nephrectomy (UNx). Since UNx alone does not result in renal damage, renal disease models with varying degrees of glomerular damage and albuminuria were generated by combining UNx with high NaCl diets ± deoxycorticosterone acetate (DOCA) in different mouse strains with and without genetic predisposition for glomerular injury. Renal parameters (GFR, albuminuria, urine volume) were monitored for 4-6 weeks. Application of EMPA via the drinking water resulted in sufficient EMPA plasma concentration and caused glucosuria, diuresis and in some models renal hypertrophy. EMPA had no effect on GFR in untreated wildtype animals, but significantly reduced hyperfiltration after UNx by 36%. In contrast, EMPA did not reduce UNx induced hyperfiltration in any of our kidney disease models, regardless of their degree of glomerular damage caused by DOCA/salt treatment. Consistent with the lack of reduction in glomerular hyperfiltration, EMPA-treated animals developed albuminuria and renal fibrosis to a similar extent as H
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