# Weekly Liraglutide for the Management of Intractable Polydipsia and Interdialytic Weight Gain in a Patient on Hemodialysis: A Case Report

**Authors:** Franklin Mora-Bravo, Pamela T Morales, Gabriela Pincay, Samantha Pineda, Brayan Morales

PMC · DOI: 10.7759/cureus.102197 · Cureus · 2026-01-24

## TL;DR

A patient on hemodialysis with severe thirst and fluid retention showed improvement after weekly liraglutide treatment, suggesting a new approach to managing fluid balance.

## Contribution

This case report introduces the novel use of GLP-1RAs for managing intractable polydipsia and interdialytic weight gain in non-diabetic hemodialysis patients.

## Key findings

- Weekly liraglutide reduced interdialytic weight gain from 5.72% to 2.72% and significantly decreased thirst in a hemodialysis patient.
- Liraglutide improved hemodynamic stability and blood pressure in a patient with chronic hypotension and fluid overload.
- The treatment suggests GLP-1RAs may modulate thirst via neuroendocrine pathways independent of glycemic control.

## Abstract

Volume status management is a critical challenge in hemodialysis. Water transgression usually results from intractable polydipsia, for which there are no approved pharmacological treatments. Given the emerging evidence on the role of glucagon-like peptide-1 receptor agonists (GLP-1RAs) in modulating neurological pathways that regulate dipsogenic behavior and satiety, their use is proposed as an unprecedented therapeutic opportunity. A 66-year-old woman with end-stage renal disease (ESRD) secondary to glomerulonephritis was in a chronic hemodiafiltration program without residual diuresis. She started hemodialysis in 2017 and, in 2025, developed refractory hypervolemia driven by intractable polydipsia and interdialytic weight gain (IDWG) of 8% (6 L) on one occasion, and, on average, 5.72%. Management was severely limited by persistent baseline hypotension (90/60 mmHg) and episodes of intradialysis hemodynamic instability that prevented the achievement of dry weight. In this scenario, treatment with liraglutide (1.2 mg weekly) was initiated, resulting in a reduction in IDWG to 2.72% and a significant decrease in thirst (from 10/10 to 3/10 on an analog scale), which stabilized blood pressure and improved tolerance to the treatment. GLP-1RAs can act as potent dipsogenic modulators by modulating neural circuits of osmoreception in the central nervous system, independent of glycemic control. Although gastrointestinal effects require proactive management, the systemic enzymatic degradation of liraglutide positions it as a safe alternative in end-stage renal failure. Pharmacological modulation of the neuroendocrine axis of thirst represents a promising therapeutic frontier to transform the management of refractory hypervolemia and improve hemodynamic stability in patients with no residual diuresis without diabetes. The benefit of GLP-1RAs in this case, a non-diabetic patient on hemodialysis with refractory thirst, extends beyond traditional metabolic control. The clinical success of an intentionally chosen weekly liraglutide regimen indicates that the therapeutic goal was to influence the neuroendocrine system that manages thirst and satiety. This case emphasizes that non-adherence to fluid therapy during dialysis can be viewed as a treatable physiological imbalance rather than a behavioral issue. Although there are no standardized guidelines for weekly dosing, this proof of concept points to a potential new treatment approach. Using incretins as tools to regulate thirst deserves further research through controlled trials to verify their long-term effects on hemodynamic stability and quality of life in patients with ESRD.

## Linked entities

- **Chemicals:** liraglutide (PubChem CID 16134956)
- **Diseases:** end-stage renal disease (MONDO:0004375), glomerulonephritis (MONDO:0002462)

## Full-text entities

- **Genes:** GLP1R (glucagon like peptide 1 receptor) [NCBI Gene 2740] {aka GLP-1, GLP-1-R, GLP-1R}
- **Diseases:** Polydipsia (MESH:D059606), hypotension (MESH:D007022), Weight Gain (MESH:D015430), glomerulonephritis (MESH:D005921), ESRD (MESH:D007676), diabetes (MESH:D003920)
- **Chemicals:** Water (MESH:D014867)
- **Species:** Homo sapiens (human, species) [taxon 9606]

## Full text

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## Figures

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## References

13 references — full list in the complete paper: https://tomesphere.com/paper/PMC12831222/full.md

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Source: https://tomesphere.com/paper/PMC12831222