Physiology: outer membrane protein of Leptospira inhibits the Na/K/Cl cotransporter in the thick ascending limb of Henle, causing hypokalemia and renal sodium wasting
Potassium Replacement in the Setting of Hyponatremia
Potassium Replacement is Critical in This Setting, Due to the Role of Potassium in Increasing the Serum Sodium Back Toward Normal
See “Complications of Treatment of Hypokalemia” Section Below
While Potassium Replacement is a Critical Component of Correcting Hyponatremia, Care Must Be Taken to Correct the Serum Sodium <8 mEq/L Per Day to Avoid the Complication of Osmotic Demyelination Syndrome (ODS) (see Osmotic Demyelination Syndrome)
Potassium is as Osmotically Active as Potassium and Replacing Potassium in the Setting of Hypokalemia Will Increase Serum Osmolality (Am J Kidney Dis, 2010) [MEDLINE]
Potassium Movement Intracellularly Increases the Serum Sodium by the Following Mechanisms
Intracellular Movement of Potassium Will Result in an Exchange of Sodium into the Extracellular Fluid (to Maintain Intracellular Electroneutrality)
Intracellular Movement of Potassium Will Result in an Exchange of Hydrogen Ions into the Extracellular Fluid
Hydrogen Ions are Buffered by Extracellular Bicarbonate (and Plasma Proteins), Creating Carbon Dioxide and Water (Bicarbonate is Replaced by Chloride Which was Administered with the Potassium)
Intracellular Movement of Potassium Drags Drags Chloride into the Cells, Increasing the Intracellular Osmolality, Which Results in Free Water Movement into Cells
Intracellular Movement of Potassium Increases the Intracellular Osmolality, Which Results in Free Water Movement into Cells
References
A patient with severe hyponatremia and hypokalemia: osmotic demyelination following potassium repletion. Am J Kidney Dis. 2010 Apr;55(4):742-8 [MEDLINE]