Renal tubular effects of prolonged therapy with the GLP-1 receptor agonist lixisenatide in patients with type 2 diabetes mellitus
Open accessAbstract
Glucagon-like peptide-1 (GLP-1) receptor agonists (RAs) are well-established glucose-lowering drugs for type 2 diabetes mellitus (T2DM) management. Acute GLP-1RA administration increases urinary excretion of sodium and other electrolytes. However, the renal tubular effects of prolonged GLP-1RA treatment are largely unknown. In this secondary analysis of a randomized trial, we determined the renal tubular effects of 8-wk treatment with 20 μg lixisenatide, a short-acting (prandial) GLP-1RA, versus titrated once-daily insulin glulisine in 35 overweight T2DM-patients on stable insulin glargine background therapy (age: 62 ± 7 yr, glycated hemoglobin: 8.0 ± 0.9%, estimated glomerular filtration rate: >60 ml·min−1·1.73 m−2). After a standardized breakfast, lixisenatide increased absolute and fractional excretions of sodium, chloride, and potassium and increased urinary pH. In contrast, lixisenatide reduced absolute and fractional excretions of magnesium, calcium, and phosphate. At week 8, patients treated with lixisenatide had significantly more phosphorylated sodium-hydrogen exchanger isoform 3 (NHE3) in urinary extracellular vesicles than those on insulin glulisine treatment, which suggested decreased NHE3 activity in the proximal tubule. A rise in postprandial blood pressure with lixisenatide partly explained the changes in the urinary excretion of sodium, potassium, magnesium, and phosphate and the changes in urinary pH. In conclusion, lixisenatide affects postprandial urinary excretion of several electrolytes and increases urinary pH compared with insulin glulisine in T2DM patients after 8 wk of treatment. This is most likely explained by a drug-induced rise in blood pressure or direct inhibitory effects on NHE3 in the proximal tubule.
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GLP-1 receptor activation can induce a proximal tubular natriuresis via inhibition of sodium-hydrogen exchanger 3, an effect proposed to activate tubuloglomerular feedback which may reduce glomerular hyperfiltration and GFR.
“Furthermore, GLP-1 receptor activation can induce a proximal tubular natriuresis via inhibition of sodium-hydrogen exchanger 3, an effect proposed to activate tubuloglomerular feedback which may reduce glomerular hyperfiltration and GFR.29”
From The Effect of Retatrutide on Kidney Parameters in Participants With Type 2 Diabetes Mellitus and/or Obesity (2025) · cites this paper as [29]
The Introduction reports that rodent studies suggest GLP-1 receptor stimulation inhibits proximal-tubule NHE3, and the Discussion links lixisenatide-associated sodium excretion to possible NHE3 inhibition. The passages found do not propose the further step of tubuloglomerular-feedback activation or a consequent reduction in hyperfiltration or GFR; searches for those terms found no supporting passage. (LLM, conf=0.85)
Experimental — accuracy not yet measuredIn both rodents and humans, GLP-1 receptor agonist infusion enhances kidney lithium clearance, a marker of proximal tubular sodium reabsorption, as well as urinary pH.
“in both rodents and humans, GLP-1 receptor agonist infusion enhances kidney lithium clearance, a marker of proximal tubular sodium reabsorption, as well as urinary pH.”
From GLP-1 agonists in the treatment of chronic kidney disease in type 2 diabetes and obesity (2025) · cites this paper as [33]
The Discussion reports that acute GLP-1 receptor stimulation increases urinary lithium excretion in rodents and humans, and that GLP-1 or exenatide infusion increases urinary pH in people. It does not establish that infusion was the method in the rodent lithium studies or that urinary pH increased in rodents. Page numbers are unavailable in our copy. (LLM, conf=0.84)
Experimental — accuracy not yet measuredThe effect of GLP-1 receptor agonists on natriuresis involves inhibition of sodium-hydrogen antiporter NHE3.
“This suggests that the effect involves inhibition of sodium-hydrogen antiporter (NHE3) (33).”
From GLP-1 agonists in the treatment of chronic kidney disease in type 2 diabetes and obesity (2025) · cites this paper as [33]
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“This suggests that the effect involves inhibition of sodium-hydrogen antiporter (NHE3) (33).”
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- Authors
- Tonneijck, L., Muskiet, M. H. A., Blijdorp, C. J., Smits, M. M., Twisk, J. W., Kramer, M. H. H., Danser, A. H. J., Diamant, M., Joles, J. A., Hoorn, E. J., & van Raalte, D. H.
- Affiliations
- Amsterdam UMC Location Vrije Universiteit Amsterdam (NL)
- Erasmus MC (NL)
- Amsterdam Public Health (NL)
- Diabetes Center, Department of Internal Medicine, VU University Medical Center, Amsterdam, The Netherlands
- University Medical Center Utrecht (NL)
- Corresponding author
- Tonneijck, Lennart
- ORCID
- Venue
- American Journal of Physiology-Renal Physiology
- Publisher
- American Physiological Society
- Published
- 2019-02-01
- Volume
- 316
- Issue
- 2
- Pages
- F231-F240
- ISSN
- 1522-1466 (ISSN-L)
- 1931-857X
- OpenAlex
- W2898592605
- Cited by
- 57
- References
- 27
- Citations by year
- 2026: 12 · 2025: 9 · 2024: 10 · 2023: 4 · 2022: 6 · 2021: 8 · 2020: 6 · 2019: 2
- FWCI
- 3.18
- Type
- journal article
- Language
- en
- Open access
- green
- pure.amsterdamumc.nl
- Licence
- other-oa
- Locations
- American Journal of Physiology-Renal Physiology (publishedVersion)
- PubMed (publishedVersion)
- EUR Research Repository (Erasmus University Rotterdam) (publishedVersion)
- Pure Amsterdam UMC (submittedVersion, other-oa)
- EUR Research Repository (Erasmus University Rotterdam) (submittedVersion)
- Utrecht University Repository (Utrecht University) (submittedVersion, other-oa)
- Amsterdam UMC (VU Amsterdam) - Institutional Repository (submittedVersion)
- Utrecht University Repository (Utrecht University) (submittedVersion)
- Data Archiving and Networked Services (DANS) (submittedVersion)
- Funders
- Sanofi
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diabetes Treatment and Management
- Health Sciences › Medicine › Nephrology › Chronic Kidney Disease and Diabetes
- Health Sciences › Medicine › Cardiology and Cardiovascular Medicine › Blood Pressure and Hypertension Studies
- Keywords
- lixisenatide, GLP-1 receptor agonists, type 2 diabetes, urinary electrolyte excretion, sodium excretion, urine pH, NHE3, urinary extracellular vesicles, proximal tubule, insulin glulisine, postprandial blood pressure
- MeSH terms
- Glucagon-Like Peptide-1 Receptor, Glucagon-Like Peptide-2 Receptor, Sodium-Hydrogen Exchanger 3, Glucagon-Like Peptide-1 Receptor Agonists, Adult, Aged, Blood Glucose, Diabetes Mellitus, Type 2, Drug Administration Schedule, Female, Glycated Hemoglobin, Humans, Hypoglycemic Agents, Kidney Tubules, Proximal, Male, Middle Aged, Peptides, Phosphorylation, Sodium, Time Factors, Biomarkers, Treatment Outcome, Renal Elimination
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