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Abstract: FR-PO656

TolvaThirst: Is Thirst Triggered to Adapt to an Acute Natremia Increase in Chronic Hyponatremic Patients?

Session Information

Category: Fluid and Electrolytes

  • 902 Fluid and Electrolytes: Clinical

Authors

  • Bertocchio, Jean-philippe, AP-HP European George Pompidou Hospital, Paris, France
  • Bureau, Côme, AP-HP European George Pompidou Hospital, Paris, France
  • Cohen, Raphael Rc, AP-HP European George Pompidou Hospital, Paris, France
  • Houillier, Pascal, AP-HP European George Pompidou Hospital, Paris, France
  • Blanchard, Anne, AP-HP, European George Pompidou Hospital, Paris, France
Background

Water body content is tightly controlled by both input (mostly, thirst-driven intake) and output (mostly, renal aquaresis). The osmotic-driven thirst threshold is 10 mOsm/kgH2O higher than that of arginine vasopressin (AVP) secretion; it takes over when AVP-induced antidiuresis fails to limit water loss. In chronic hyponatremic patients, both AVP release and/or thirst could be impaired. However, their ability to maintain natremia within a narrow range in response to acute water loss has never been reported.

Methods

We submitted chronic hyponatremic patients (n=31) to acute water loss through a single oral 15 mg tolvaptan administration, a type 2 AVP-receptor antagonist. We then monitored hourly plasma sodium and osmolality, urine output and osmolality, and water intake, as well as thirst scales.

Results

Overall, tolvaptan induced a significant weight loss (-1.2±1.2%, p<0.001) and natremia increase (+3.0±2.9mM, p<0.001). In 18 “isonatric” patients, natremia remained steady (+1.1±1.6 mM) during the first 6 hours (cf. Figure 1), whereas in 13 “dysnatric” patients, it significantly increased (+5.8±1.7 mM, p<0.001). Even if all patients had no difference in minimum urine osmolality (i.e. no difference regarding to the pharmacological intervention), “isonatric” patients had a better water balance (+1.22±7.2 vs.-16.4±7.0 mL/kg, p<0.001), mostly driven by a better water intake during the first hour (13.4±7.5 vs.8.8±10.0 mL/min, p=0.009).

Conclusion

Acute aquaresis-triggered water intake prevented changes innatremia in about 60% of the reported patients, whereas in 40% this mechanism was impaired. Further studies are needed to address the (patho)physiology of thirst adaptation and acute water intake in chronic hyponatremic patients, then to develop tools for identifying patients at risk for wide changes in natremia.

Figure 1. Evolution of natremia after a single tolvaptan administration during the first 6 hours (H1 to H6): 13 "dysnatric" patients significantly increased their natremia, when 18 "isonatric" did not.