In a multivariate Cox-proportional

regression analysis, the mortality risk was correlated with the severity of hyponatremia (hazard ratio [HR]: 1.65, 95% confidence interval [CI]: 1.38–1.96; HR: 2.24, 95% CI: 1.69–2.98; HR: 2.20, 95% CI: 1.25–3.90, for patients with mild, moderate, and severe hyponatremia compared with patients with normonatremia, KU 57788 respectively). An independent association between hyponatremia and long-term mortality was sustained among various subpopulations, and patients with persistent hyponatremia had a worse prognosis as compared those with hyponatremia that was resolved or acquired during hospitalization. Conclusion: In conclusion, a substantial proportion of patients developed hyponatremia SB203580 cell line during hospitalization, and the long-term mortality risk increased even in mild cases of hyponatremia. Hyponatremia should be considered as an important prognostic factor in patients with colorectal cancer. SUNG CHIH-CHIEN1, CHENG CHIH-JEN1,2, CHIANG WEN-FANG3, CHAU TOM4, HSU YU-JUEI1, YANG SUNG-SEN1,2, LIN SHIH-HUA1,2 1Division of Nephrology, Department of Medicine, Tri-Service General Hospital, National Defense Medical Center; 2Graduate Institute of Medical Science, National Defense Medical Center, Taipei, Taiwan; 3Department of Medicine, Armed Forces Taoyuan General Hospital, Taoyuan, Taiwan; 4Department

of Medicine, Providence St. Vincent Medical Center, Portland, Oregon, USA Background: Non-hypokalemic periodic paralysis (non-HypoPP) represents a group of diverse causes SDHB of a large potassium (K+) deficit. To rapidly diagnose its underlying causes with appropriate management is still challenging. Purpose: This study was to analyze the etiologies and characterize therapeutic course in non-HypoPP patients. Methods: Fifty-eight patients (44 male and 14 female) with non-HypoPP and the exclusion of HypoPP were consecutively

enrolled over an eight-year period. Blood and spot urine samples were collected for electrolytes, acid-base and biochemistry measurement on admission and during therapy. Intravenous potassium chloride (KCl) at a rate of 10–20 mmol/hour was administered until muscle strength recovered. Urine K+ to creatinine ratio < 2 mmol/mmol was categorized as low and ≥2 mmol/mmol as high urinary K+ excretion. Results: The average K+ concentration was 1.8 ± 0.2 mmol/L. Their etiology could be simplified by the urinary K+ excretion rate. For patients with a low urinary K+ excretion (n = 17), chronic alcoholism, anorexia/bulimia nervosa, and remote diuretics use were the most common causes. For patients with a high urinary K+ excretion (n = 41), renal tubular acidosis and chronic toluene abuse with metabolic acidosis as well as primary aldosteronism, Gitelman’s syndrome and use of diuretics with metabolic alkalosis were common. Muscle strength was restored after administering 3.8 ± 0.8 mmol/kg KCl.