Hypokalemia | EPFL Graph Search

Hypokalemia is a low level of potassium (K+) in the blood serum. Mild low potassium does not typically cause symptoms. Symptoms may include feeling tired, leg cramps, weakness, and constipation. Low potassium also increases the risk of an abnormal heart rhythm, which is often too slow and can cause cardiac arrest. Causes of hypokalemia include vomiting, diarrhea, medications like furosemide and steroids, dialysis, diabetes insipidus, hyperaldosteronism, hypomagnesemia, and not enough intake in the diet. Normal potassium levels in humans are between 3.5 and 5.0 mmol/L (3.5 and 5.0 mEq/L) with levels below 3.5 mmol/L defined as hypokalemia. It is classified as severe when levels are less than 2.5 mmol/L. Low levels may also be suspected based on an electrocardiogram (ECG). Hyperkalemia is a high level of potassium in the blood serum. The speed at which potassium should be replaced depends on whether or not there are symptoms or abnormalities on an electrocardiogram. Potassium levels that are only slightly below the normal range can be managed with changes in the diet. Lower levels of potassium require replacement with supplements either taken by mouth or given intravenously. If given intravenously, potassium is generally replaced at rates of less than 20 mmol/hour. Solutions containing high concentrations of potassium (>40 mmol/L) should generally be given using a central venous catheter. Magnesium replacement may also be required. Hypokalemia is one of the most common water–electrolyte imbalances. It affects about 20% of people admitted to hospital. The word hypokalemia comes from hypo- 'under' + kalium 'potassium' + -emia 'blood condition'. Mild hypokalemia is often without symptoms, although it may cause elevation of blood pressure, and can provoke the development of an abnormal heart rhythm. Severe hypokalemia, with serum potassium concentrations of 2.5–3 meq/L (Nl: 3.5–5.0 meq/L), may cause muscle weakness, myalgia, tremor, and muscle cramps (owing to disturbed function of skeletal muscle), and constipation (from disturbed function of smooth muscle).

Kidney-Specific CAP1/Prss8-Deficient Mice Maintain ENaC-Mediated Sodium Balance through an Aldosterone Independent Pathway

Simona Frateschi, Thibaud Peyrollaz

The serine protease prostasin (CAP1/Prss8, channel-activating protease-1) is a confirmed in vitro and in vivo activator of the epithelial sodium channel ENaC. To test whether proteolytic activity or CAP1/Prss8 abundance itself are required for ENaC activat ...

MDPI2022