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Abstract: FR-PO558

Hyponatremia in the Outpatient: Does Low GFR Contribute to Hyponatremia?

Session Information

Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders

  • 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical


  • Nagahama, Masahiko, St. Luke's International Hospital, Tokyo, Japan
  • Kawaguchi, Takehiko, St. Luke's International Hospital, Tokyo, Japan
  • Fujimaru, Takuya, St. Luke's International Hospital, Tokyo, Japan
  • Ito, Yugo, St. Luke's International Hospital, Tokyo, Japan
  • Taki, Fumika, St. Luke's International Hospital, Tokyo, Japan
  • Nakayama, Masaaki, St. Luke's International Hospital, Tokyo, Japan

The essential mechanism of developing hyponatremia is decreased urinary dilution in response to vasopressin (AVP). Because urinary dilution is affected as kidney function deteriorates, it is plausible that the risk of developing hyponatremia is related to decreased GFR. However, the results of previous studies on the prevalence of hyponatremia in CKD populations are contradictory. On the other hand, AVP secretion by various comorbid conditions, such as CHF and malignancy was identified. We hypothesized that comorbidity induced AVP secretion rather than decreased GFR contribute to hyponatremia.


We performed an observational cross-sectional investigation in a single hospital (35 specialties in outpatient clinic) in Tokyo, Japan. Among 351,662 patients who visited the outpatient clinic from January 2010 to December 2020, we analyzed clinical and biochemical parameters of 131,184 patients. Using the Diagnosis Procedure Combination database, we collected 10 most common comorbidities in clinic: diabetes, malignancy, hypertension, COPD, CVA, dementia, depression, arthritis, anxiety and CHF. Comorbidity in our study is defined by presence of either 1 of those 10 diseases. Dialysis and transplant patients were excluded. Risk factors for hyponatremia were sought using multivariate logistic regression.


Prevalence of hyponatremia (serum Na<135mEq/L) was 2.9% in all patients. Multivariate logistic regression analysis identified higher eGFR (OR;1.01 95% CI 1.01-1.01) and positive dipstick proteinuria (OR;2.09 95% CI 1.87-2.33), but not comorbidity (OR;1.0 95% CI 0.79-1.27) as independent risk factors for hyponatremia. However, stratifying the analyses by eGFR of 60ml/min, the association of eGFR, comorbidity and proteinuria with hyponatremia was pronounced in eGFR>60 patients (OR;1.01 95% CI 1.00-1.01 for eGFR, OR;1.42 95% CI 1.02-1.9 for comorbidity, OR;2.46 95% CI 2.09-2.89 for proteinuria), but diminished in eGFR≦60 patients (OR;1.00 95% CI 0.98-1.02 for eGFR, OR;0.49 95% CI 0.09-2.54 for comorbidity, OR;0.67 95% CI 0.36-1.25 for proteinuria).


The present study shows that development of hyponatremia is correlated with not a lower but a higher GFR. Comorbidity becomes more prominent risk factor as GFR increases. These results suggest that the concomitant comorbidities combined with a higher GFR affect hyponatremia.