Abstract: PO1396
Dietary Potassium Restriction Induces Nephrogenic Diabetes Insipidus
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Basic
October 22, 2020 | Location: On-Demand
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolyte, and Acid-Base Disorders
- 901 Fluid, Electrolyte, and Acid-Base Disorders: Basic
Authors
- Al-Qusairi, Lama, Johns Hopkins University, Baltimore, Maryland, United States
- Grimm, Paul Richard, Johns Hopkins University, Baltimore, Maryland, United States
- Welling, Paul A., Johns Hopkins University, Baltimore, Maryland, United States
- Zapf, Ava, Johns Hopkins University, Baltimore, Maryland, United States
Background
Dietary potassium deficiency is well-appreciated to induce diabetes insipidus (DI) but the underlying mechanisms have not been established.
Methods
C57BL6J mice were randomized to control or diets with graded reductions in dietary K+ for 8 days. Kindey function tests were performed in metabolic cages, and tissues were harvested for western blotting and immunocytochemistry at the end of the experiment.
Results
We found that C57BL6J mice rapidly develop DI when potassium is eliminated from the diet, coincidence with the development of hypokalemia. Loss of free-water reabsorption, polyuria and polydipsia was observed within four days, despite increased plasma copeptin, a vasopressin surrogate. In contrast to control mice, desmopressin treatment failed to increase urine osmolality and urine volume after potassium deprivation. Altogether, these observations indicate dietary potassium restriction induces nephrogenic DI (NDI). Characterization of responses to graded reductions in dietary K+diet revealed NDI was dependent on the development of hypokalemia. Females were more prone to develop hypokalemia, even in response to modest changes in dietary potassium, and displayed more severe DI than males. Females also exhibited a much greater decrease in AQP2 and phosphorylated s256AQP2 in response to dietary potassium deprivation.
Conclusion
This data together indicate that i) hypokalemia-induced DI is nephrogenic, ii) a tight relationship links hypokalemia to renal concentrating ability, ii) females are more prone to develop hypokalemia and as a consequence, more prone to NDI.
Funding
- NIDDK Support