Patients with hypokalemia can have what kind of urine?

Written by Gan Jun
Endocrinology
Updated on December 10, 2024
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When patients have hypokalemia, they often exhibit paradoxical aciduria, which is a typical manifestation of hypokalemia. In hyperkalemia, however, there is paradoxical alkaline urine. When serum potassium ions decrease, the renal tubular epithelium reduces its potassium excretion function and instead increases hydrogen excretion, leading to increased reabsorption of sodium and bicarbonate. This results in metabolic alkalosis, causing an increase in plasma bicarbonate, unlike typical alkalosis where alkaline urine is excreted. However, in the case of hypokalemia, acidic urine is excreted, hence it is called paradoxical aciduria.

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Intensive Care Unit
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Hypokalemia can cause

Hypokalemia can manifest as weakness, a bitter taste in the mouth, lack of appetite, irritability, or mood swings. In severe cases, symptoms like nausea, vomiting, drowsiness, reduced orientation ability, and confusion may occur. In terms of muscle and nerve effects, hypokalemia leads to decreased neuromuscular excitability, and when blood potassium levels fall below 2.5mmol/L, clinical symptoms of muscle weakness appear. If blood potassium levels drop below 2.0mmol/L, flaccid paralysis and disappearance or weakening of tendon reflexes may occur. In severe cases, paralysis of the respiratory muscles and even respiratory failure might develop. For the gastrointestinal tract, common symptoms include lack of appetite, nausea, and vomiting, with severe cases leading to intestinal paralysis. Hypokalemia can cause an increase in heart rate and even ventricular fibrillation, which can be fatal. Additionally, it can result in metabolic alkalosis. Hypokalemia can cause metabolic alkalosis, and vice versa, with each condition potentially leading to the other, often coexisting simultaneously.

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Causes of Hypokalemia

Common causes of hypokalemia include insufficient intake or prolonged inability to eat without intravenous supplementation. In such cases, while intake of potassium decreases, the kidneys continue to excrete potassium, leading to a loss of potassium in the blood. Additionally, increased excretion can cause hypokalemia, including losses from the gastrointestinal tract such as vomiting, diarrhea, and continuous gastrointestinal decompression, which results in a loss of digestive fluids rich in potassium. Potassium loss through the kidneys from prolonged use of potassium-wasting diuretics or during the polyuric phase of acute renal failure can also lead to hypokalemia. Furthermore, the shift of potassium from outside to inside the cells can cause hypokalemia.

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Hypokalemia is formed in what way?

Hypokalemia refers to a condition where the serum potassium level is below 3.5 millimoles per liter. The primary cause of hypokalemia is the loss of potassium in the body. Hypokalemia can be classified into three types based on its cause: potassium deficiency hypokalemia, redistributive hypokalemia, and dilutional hypokalemia. Potassium deficiency hypokalemia is mainly characterized by insufficient intake or excessive excretion. Insufficient intake is typically seen in patients who are fasting, have selective eating habits, or suffer from anorexia, while excessive excretion is mainly through gastrointestinal or renal loss of potassium. Redistributive hypokalemia usually occurs due to metabolic or respiratory alkalosis, the recovery phase of acidosis, heavy usage of glucose, instances of periodic paralysis, acute emergency situations, and the use of folic acid and vitamin B12 in treating anemia or repeat transfusions of cold stored washed red blood cells. Dilutional hypokalemia, on the other hand, is mainly caused by the retention of extracellular fluid, leading to excessive water or water intoxication-induced hypokalemia.

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What medicine should be taken for hypokalemia?

The treatment of hypokalemia primarily involves addressing the underlying disease. Symptomatic treatment should avoid excessive potassium supplementation, which can lead to hyperkalemia. The principle of potassium supplementation is as follows: for mild hypokalemia, such as in patients showing clinical signs, oral potassium can be administered at 40-80 millimoles per day. For patients with severe hypokalemia, or those whose gastrointestinal tract cannot utilize potassium, with potassium levels less than 2.0 millimoles per liter, intravenous potassium can be provided. An initial supplementation rate of 10-20 millimoles per hour is relatively safe. In cases of severe hypokalemia with life-threatening clinical signs, a rapid increase to 40-80 millimoles can be achieved in a short period, but close monitoring is necessary.

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When supplementing potassium for hypokalemia, what should be paid attention to?

When supplementing potassium for hypokalemia, the following should be noted: 1. Closely monitor the blood potassium levels. Supplement 60-80 mmol/L of potassium, or recheck the blood potassium level within 1-4 hours after supplementation. 2. If the rate of potassium supplementation exceeds 10 moles per hour, continuous ECG monitoring should be maintained, closely observe the changes in the ECG, and prevent the occurrence of life-threatening hyperkalemia. 3. The rate of potassium supplementation for patients with regenerative dysfunction should be 50% of that for patients with normal kidney function. 4. The daily amount of potassium supplementation should not exceed 100-200 millimoles. 5. Try not to use peripheral veins for high-concentration potassium supplementation. 6. Use sodium chloride solution to dilute potassium-containing solutions, and it is not recommended to use glucose or low molecular weight dextrorotatory sugar as the carrier.