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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

Clara Odilia Sailer, Sophia Julia Wiedemann, Konrad Strauss, Ingeborg Schnyder, Wiebke Kristin Fenske, and Mirjam Christ-Crain

Osmotic stimulus or stress results in vasopressin release. Animal and human in vitro studies have shown that inflammatory parameters, such as interleukin-8 (IL-8) and tumor necrosis factor-α (TNF-α), increase in parallel in the central nervous system and bronchial, corneal or intestinal epithelial cell lines in response to osmotic stimulus. Whether osmotic stimulus directly causes a systemic inflammatory response in humans is unknown. We therefore investigated the influence of osmotic stimulus on circulatory markers of systemic inflammation in healthy volunteers. In this prospective cohort study, 44 healthy volunteers underwent a standardized test protocol with an osmotic stimulus leading into the hyperosmotic/hypernatremic range (serum sodium ≥150 mmol/L) by hypertonic saline infusion. Copeptin – a marker indicating vasopressin activity – serum sodium and osmolality, plasma IL-8 and TNF-α were measured at baseline and directly after osmotic stimulus. Median (range) serum sodium increased from 141 mmol/L (136, 147) to 151 mmol/L (145, 154) (P < 0.01), serum osmolality increased from 295 mmol/L (281, 306) to 315 mmol/L (304, 325) (P < 0.01). Median (range) copeptin increased from 4.3 pg/L (1.1, 21.4) to 28.8 pg/L (19.9, 43.4) (P < 0.01). Median (range) IL-8 levels showed a trend to decrease from 0.79 pg/mL (0.37, 1.6) to 0.7 pg/mL (0.4, 1.9) (P < 0.09) and TNF-α levels decreased from 0.53 pg/mL (0.11, 1.1) to 0.45 pg/mL (0.12, 0.97) (P < 0.036). Contrary to data obtained in vitro, circulating proinflammatory cytokines tend to or decrease in human plasma after osmotic stimulus. In this study, osmotic stimulus does not increase circulating markers of systemic inflammation.