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Open access

Laura Potasso, Julie Refardt, Irina Chifu, Martin Fassnacht, Wiebke Kristin Fenske, and Mirjam Christ-Crain

Objective: Hyperkalemia has been reported upon different hypertonic saline infusion protocols. Since hypertonic saline test has recently been validated for the differential diagnosis of diabetes insipidus (DI), we aimed to investigate the course of plasma potassium during the test.

Design: We analyzed data of 90 healthy volunteers and 141 patients with polyuria-polydipsia syndrome (PPS) from two prospective studies evaluating the hypertonic saline test. Our primary outcome was the incidence rate of hypertonic saline induced hyperkalemia >5mmol/L.

Methods: Participants received a 250 ml bolus of 3% NaCl solution, followed by 0.15ml/min/kg body weight continuously infused targeting a plasma sodium level of 150mmol/L. Blood samples and clinical data were collected every 30 minutes.

Results: Of the 231 participants, 16% (n=37/231) developed hyperkalemia. The incidence of hyperkalemia was higher in healthy volunteers and in patients with primary polydipsia (25.6% (n=23/90) and 9.9% (n=14/141) respectively), and only occurred in 3.4% (n=2/59) of patients with diabetes insipidus. Hyperkalemia developed mostly at or after 90-minute test duration (81.1%, n= 30/37). Predictors of hyperkalemia (OR (95% CI)) were male sex (2.9 (1.2-7.4), p=0.02), a plasma potassium at baseline >3.9mmol/L (5.2, (1.8-17.3), p=0.004), normonatremia at 30-minute test duration (3.2 (1.2-9.5), p=0.03), and an increase in potassium levels already at 30-minute test duration as compared to baseline (4.5 (1.7-12.3), p=0.003). Hyperkalemia was transient and resolved spontaneously in all cases.

Conclusion: The hypertonic saline test can lead to hyperkalemia, especially in patients with primary polydipsia who experience a longer test duration. Monitoring potassium levels in these patients is recommended.

Open access

Bettina Winzeler, Michelle Steinmetz, Julie Refardt, Nicole Cesana-Nigro, Milica Popovic, Wiebke Fenske, and Mirjam Christ-Crain

Objective

The syndrome of inappropriate antidiuresis (SIAD) is a common condition in hospitalized patients. It is crucial to establish the cause of SIAD, especially in order to exclude underlying malignancy. As malignant SIAD may be due to a paraneoplastic synthesis of arginine vasopressin, we hypothesized that its stable surrogate marker copeptin can be used as a diagnostic tool to differentiate between malignant and non-malignant SIAD.

Methods

Prospective observational study. We analyzed data from 146 SIAD patients of two different cohorts from Switzerland and Germany. Patients were included while presenting at the emergency department and underwent a standardized diagnostic assessment including the measurement of copeptin levels.

Results

Thirty-nine patients (median age: 63 years, 51% female) were diagnosed with cancer-related SIAD and 107 (median age: 73 years, 68% female) with non-malignant SIAD. Serum sodium levels were higher in cancer-related versus non-malignant SIAD: median (IQR) 124 mmol/l (120; 127) versus 120 mmol/l (117; 123) (P<0.001). Median (IQR) copeptin levels of patients with cancer-related SIAD were 11.1 pmol/l (5.2; 37.1) and 10.5 pmol/l (5.2; 25.2) with non-malignant SIAD (P = 0.38). Among different cancer entities, patients suffering from small-cell lung cancer showed the highest copeptin values, but overall no significant difference in copeptin levels between cancer types was observed (P = 0.46).

Conclusions

Copeptin levels are similar in cancer-related and non-malignant SIAD. Therefore, Copeptin does not seem to be suitable as a marker of malignant disease in SIAD.

Open access

Julie Refardt, Clara Odilia Sailer, Bettina Winzeler, Matthias Johannes Betz, Irina Chifu, Ingeborg Schnyder, Martin Fassnacht, Wiebke Fenske, Mirjam Christ-Crain, and for the CODDI-Investigators

The pathomechanism of primary polydipsia is poorly understood. Recent animal data reported a connection between fibroblast growth factor 21 (FGF-21) and elevated fluid intake independently of hormonal control by the hormone arginine-vasopressin (AVP) and osmotic stimulation. We therefore compared circulating FGF-21 levels in patients with primary polydipsia to patients with AVP deficiency (central diabetes insipidus) and healthy volunteers. In this prospective cohort study, we analyzed FGF-21 levels of 20 patients with primary polydipsia, 20 patients with central diabetes insipidus and 20 healthy volunteers before and after stimulation with hypertonic saline infusion targeting a plasma sodium level ≥150 mmol/L. The primary outcome was the difference in FGF-21 levels between the three groups. Baseline characteristics were similar between the groups except for patients with central diabetes insipidus being heavier. There was no difference in baseline FGF-21 levels between patients with primary polydipsia and healthy volunteers (122 pg/mL (52,277) vs 193 pg/mL (48,301), but higher levels in patients with central diabetes insipidus were observed (306 pg/mL (114,484); P = 0.037). However, this was not confirmed in a multivariate linear regression analysis after adjusting for age, sex, BMI and smoking status. Osmotic stimulation did not affect FGF-21 levels in either group (difference to baseline: primary polydipsia −23 pg/mL (−43, 22); central diabetes insipidus 17 pg/mL (−76, 88); healthy volunteers −6 pg/mL (−68, 22); P = 0.45). To conclude, FGF-21 levels are not increased in patients with primary polydipsia as compared to central diabetes insipidus or healthy volunteers. FGF-21 therefore does not seem to be causal of elevated fluid intake in these patients.