ArticleRenal failure2020
Biomarker evidence for distal tubular damage but cortical sparing in hospitalized diabetic patients with acute kidney injury (AKI) while on SGLT2 inhibitors.
Article in Renal failure, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 28 citations in OpenAlex.
- Acute kidney injury over the past decade: from definition evolution to pathogenesis insights and innovative therapeutic strategies.Cellular and molecular life sciences : CMLS · 2026Review
- The Impact of Sodium Glucose Transporter 2 Inhibitors on Renal Parenchymal Oxygenation: An Unsettled Issue?Kidney360 · 2026Article
- SGLT2 Inhibitors in the Management of Cardio-Renal-Metabolic Syndrome: A New Therapeutic Era.Medicina (Kaunas, Lithuania) · 2025Review
- New Markers for the Assessment of Microvascular Complications in Patients with Metabolic Syndrome.Metabolites · 2025Review
- The impact of short-term administration of dapagliflozin on contrast-induced acute kidney injury in patients with type 2 diabetes and renal insufficiency undergoing percutaneous coronary intervention.Frontiers in medicine · 2025Article
- SGLT2 Inhibitors and the Risk of Contrast-Associated Nephropathy Following Angiographic Intervention: Contradictory Concepts and Clinical Outcomes.International journal of molecular sciences · 2024Review
- Changes in Cardiovascular and Renal Biomarkers Associated with SGLT2 Inhibitors Treatment in Patients with Type 2 Diabetes Mellitus.Pharmaceutics · 2023Review
- Renal Oxygen Demand and Nephron Function: Is Glucose a Friend or Foe?International journal of molecular sciences · 2023Review
- Role of abnormal energy metabolism in the progression of chronic kidney disease and drug intervention.Renal failure · 2022Article
- Renal tubular gen e biomarkers identification based on immune infiltrates in focal segmental glomerulosclerosis.Renal failure · 2022Article
- Review
- Detection of Renal Injury Following Primary Coronary Intervention among ST-Segment Elevation Myocardial Infarction Patients: Doubling the Incidence Using Neutrophil Gelatinase-Associated Lipocalin as a Renal Biomarker.Journal of clinical medicine · 2021Article
- Kidney physiology and susceptibility to acute kidney injury: implications for renoprotection.Nature reviews. Nephrology · 2021Review
- Angiotensin-(1-7)-A Potential Remedy for AKI: Insights Derived from the COVID-19 Pandemic.Journal of clinical medicine · 2021Review
- Sodium-Glucose Co-transporter-2 Inhibitors and Nephroprotection in Diabetic Patients: More Than a Challenge.Frontiers in medicine · 2021Review
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundInhibitors of sodium-glucose co-transporter-2 (SGLT2i) were found to improve renal outcome in diabetic patients in large prospective randomized trials. Yet, SGLT2i may acutely reduce kidney function through volume depletion, altered glomerular hemodynamics or intensified medullary hypoxia leading to acute tubular injury (ATI). The aim or this study was to prospectively assess the pathophysiology of acute kidney injury (AKI) in patients hospitalized while on SGLT2i, differing ATI from pre-renal causes using renal biomarkers.
methodsSerum and urine Neutrophil Gelatinase-Associated Lipocalin (NGAL) and Kidney Ischemia Molecule (KIM)-1, markers of distal and proximal tubular injury, respectively, were determined in 46 diabetic patients who were on SGLT2i upon hospitalization with an acute illness.
resultsSerum and urine NGAL, but not KIM-1, were significantly increased in 21 of the patients who presented with AKI upon admission, as compared with 25 patients that maintained kidney function. Both serum and urinary NGAL correlated with the degree of impaired renal function, which in many cases was likely the result of additional acute renal perturbations, such as sepsis.
conclusionsIncreased urinary and serum NGAL indicates that ATI, principally affecting distal tubular segments, may develop in some of the patients hospitalized with an acute illness and AKI while on SGLT2i. It is suggested that intensified medullary hypoxia by SGLT2i might be detrimental in this injury. By contrast, concomitantly unaltered KIM-1 might reflect improved cortical oxygenation by SGLT2i, and may explain an overall reduced risk of AKI with SGLT1i in large series. The independent potential of SGLT2i to inflict medullary hypoxic damage should be explored further.
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