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Abstract: SA-OR50

Detection of Low Osmolar Excretion Rate for the Etiology of Hyponatremia

Session Information

Category: Fluid, Electrolytes, and Acid-Base Disorders

  • 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

  • Da Silva, William, Ochsner Medical Center, New Orleans, Louisiana, United States
  • Smith, Alexander M., Ochsner Medical Center, New Orleans, Louisiana, United States
  • Kovvuru, Karthik, Ochsner Medical Center, New Orleans, Louisiana, United States
  • Velez, Juan Carlos Q., Ochsner Medical Center, New Orleans, Louisiana, United States
Background

Low solute intake and resulting low osmolar excretion rate (OER), colloquially known as “tea/toast” diet, is a known precipitant of hyponatremia (hypoNa). However, diagnostic evaluation of hypoNa does not routinely include assessment of OER. We hypothesized that identification of low OER by a 24-hr urine collection may help unmasking low solute intake as a cause or aggravating factor of hypoNa.

Methods

A retrospective review of medical records was conducted searching for cases of hypoNa seen in our nephrology clinic who completed a 24-hr urine collection to measure volume (V), urea nitrogen (UN), sodium (Na) and potassium (K) over a 6-year period. HypoNa was defined as a serum Na < 135 mmol/L. We defined low OER as < 6 mOsm/kg/day and was calculated as: [2 (Na + K) + UN/2.8]*V. Low protein intake (< 8 g UN/day), low Na intake (< 100 mmol/day) and low K intake (< 60 mmol/day) were also estimated. In a subset of patients with low OER, we assessed the impact of increasing solute intake on correction of hypoNa (serum Na rise ≥ 4 mmol/L). SIADH was diagnosed by spot urine Na, spot urine osmolality and standard criteria.

Results

We identified 24 patients who met the criteria. Median age was 71 years, median BMI was 25 kg/m2, median weight was 74 kg, 58% women, 96% white. Median serum Na was 130 mmol/L (range 121 – 132). By 24-hr urine, UN was assessed in all 24 patients, Na in 22 (92%) and K in 19 (79%). Full OER was completed in 17 patients: 11 (65%) had low OER. Moreover, low Na intake, low K intake, and low protein intake were found in 64%, 52% and 73%, respectively. SIADH was the cause of hyponatremia in 13/19 patients with available spot urine osmolality (68%), and among them, 9/11 (82%) had low OER. Following implementation of higher dietary solute intake, OER increased by ≥ 25% (by 69% on average) in 4/5 (80%) and hypoNa improved by ≥ 4 mEq/L (by 6 mEq on average) in all of those who increased solute intake.

Conclusion

Our findings revealed evidence of low solute intake in an ambulatory cohort of patients with chronic hypoNa. Thus, assessment of OER via 24 hour urine collection may be a useful test to identify individuals in whom low solute intake may drive or contribute to the etiology of chronic hypoNa, particularly in cases of SIADH, and to track responses to dietary therapeutic interventions.