Abstract: PUB117
Diet-Associated Hyponatremia in a Patient with ADPKD on Tolvaptan
Session Information
Category: Genetic Diseases of the Kidneys
- 1201 Genetic Diseases of the Kidneys: Cystic (Monogenic)
Authors
- Gopireddy, Naga Sumanth Reddy, University of Iowa Health Care, Iowa City, Iowa, United States
- Fravel, Michelle A., University of Iowa Health Care, Iowa City, Iowa, United States
- Noureddine, Lama A., University of Iowa Health Care, Iowa City, Iowa, United States
Introduction
Tolvaptan, a selective vasopressin V2 receptor antagonist approved for rapidly progressive ADPKD, characteristically causes aquaresis and typically increases serum sodium in states of total body water excess,. Hyponatremia occurring during tolvaptan therapy is therefore paradoxical and underrecognized and forms the basis of this report.
Case Description
A 56-year-old male with ADPKD (Mayo Class 1C, htTKV 1192.3 mL/m), CKD G3A1 (cystatin C eGFR ~34 mL/min), type 2 diabetes mellitus, and hypertension was initiated on tolvaptan 45/15 mg daily in February 2025 following MRI-confirmed rapid progression. Per standard guidelines, he was simultaneously counseled on dietary sodium restriction (<3 g/day) and high fluid intake (≥3 L/day). Routine monitoring in early 2026 revealed progressive hyponatremia with serum sodium declining from 130 mEq/L to a nadir of 119 mEq/L, with the patient remaining entirely asymptomatic throughout. Contributing factors included strict dietary sodium restriction and markedly reduced overall caloric intake. Tolvaptan was held on March 2026. Following dietary liberalization with increased sodium and protein intake, serum sodium recovered to 134 mEq/L by April 2026. Renal function and liver enzymes remained stable throughout. Urine studies were not consistent with inappropriate ADH activity, and there was no evidence of heart failure, liver disease, hypothyroidism, or adrenal insufficiency.
Discussion
This case illustrates a paradoxical drug–diet interaction unique to ADPKD management. While tolvaptan’s aquaretic mechanism typically raises serum sodium, concurrent aggressive sodium restriction reduced solute intake can produce net sodium depletion, overriding the aquaretic effect and precipitating hyponatremia. Underlying CKD further impairs urinary diluting capacity, amplifying this risk. Notably, the patient remained asymptomatic at a sodium of 119 mEq/L, highlighting the inadequacy of symptom-driven detection and the necessity of proactive electrolyte surveillance.
Conclusion: Clinicians should avoid universal sodium restriction in ADPKD patients receiving tolvaptan and instead individualize dietary counseling based on volume status, solute intake, and kidney function, with frequent electrolyte monitoring—particularly during periods of reduced oral intake.