Renal magnesium loss

　　First, the causes of disease

　　1. Primary renal magnesium loss:Caused by autosomal recessive inheritance leading to tubular dysfunction, one type is simple renal tubular magnesium reabsorption dysfunction, associated with aminoaciduria. Another type is renal tubular magnesium reabsorption dysfunction accompanied by potassium transport abnormalities, also known as potassium transport disorder type.

　　2. Secondary renal magnesium loss:It is caused by kidney diseases itself, common causes include renal tubular acidosis, Bartter syndrome, renal failure, and post-transplantation. In addition, diseases outside the kidneys, such as primary hyperaldosteronism, hypercalcemia, hyperthyroidism, chronic alcoholism, and certain drugs such as calcitonin, growth hormone, diuretics, cardiotonics, aminoglycoside antibiotics, etc., can all increase urinary magnesium levels.

　　2. Pathogenesis

　　The disease is caused by multiple causes, so the pathogenesis has not been elucidated. It is generally believed that renal magnesium loss related to heredity is caused by polygenic defects leading to tubular dysfunction, while the pathogenesis of renal magnesium loss caused by secondary reasons can vary due to the underlying disease. For example, the pathogenesis of renal magnesium loss caused by hyperaldosteronism may be that aldosterone inhibits reabsorption or increases urinary filtration of sodium and magnesium through volume expansion, increasing the amount of sodium and magnesium reaching the distal tubules. In the distal tubules, aldosterone promotes the reabsorption of sodium but has no effect on the reabsorption of magnesium, resulting in increased urinary magnesium levels.

　　It can lead to multiple systemic symptoms, such as confusion of consciousness, disorientation, hallucinations, neuromuscular irritability, numbness of the limbs, tremors, hypotension, arrhythmias, and sudden cardiac arrest. Muscle tremors, tremors, cramps of the hands and feet, wrist-hand spasms, convulsions, positive facial nerve tapping test and arm-press test, unsteady gait, mental abnormalities. Nausea, vomiting, anorexia, weakness, dizziness, etc. can also occur. Blood phosphorus levels decrease, and the electrocardiogram shows flat or inverted T waves.

　　The main clinical manifestations of this disease are hypomagnesemia, increased urinary magnesium excretion, which may be accompanied by aminoaciduria, diabetes, renal magnesium and calcium loss, and neuromuscular symptoms caused by hypomagnesemia. Patients may present with muscle tremors, tremors, cramps of the hands and feet, wrist-hand spasms, convulsions, positive facial nerve tapping test and arm-press test, unsteady gait, mental abnormalities, and may also have nausea, vomiting, anorexia, weakness, dizziness, etc. Blood phosphorus levels decrease, and the electrocardiogram shows flat or inverted T waves. Secondary cases often have the manifestations of the primary disease. Since magnesium is the second most important cation in the cell, it is involved in the activation of enzyme systems and plays a key role in the intermediate metabolism and phosphorylation of the body. Its deficiency can cause systemic dysfunction. When blood magnesium levels drop to 10mg/L or below, central nervous system manifestations may occur, such as confusion of consciousness, disorientation, hallucinations, neuromuscular irritability, numbness of the limbs, tremors, etc. Gastrointestinal manifestations include anorexia, diarrhea, and abdominal pain; the cardiovascular system may present with ventricular arrhythmias, hypotension, and even cardiac arrest and death.

　　1. Prognosis

　　The prognosis of this disease varies due to different causes. If blood magnesium levels can be measured in time before the patient shows symptoms such as electrolyte imbalance (low K+, Na+, Ca+), early detection of hypomagnesemia and timely supplementation of magnesium salts can be expected to alleviate symptoms and improve prognosis.

　　2. Prevention

　　The hereditary factors do not have effective preventive measures; secondary renal magnesium loss is mainly to actively treat the primary disease and regularly detect blood magnesium levels to provide timely symptomatic treatment when the condition is found. To prevent the occurrence of severe complications.

　　1. Urine test:Significantly increased urinary magnesium >4mmol/L (urinary magnesium less than 12mg/24h is a sign of magnesium deficiency) accompanied by hypokalemia, there may be increased urinary potassium, and aminoaciduria and diabetes.

　　2. Blood tests:Reduced blood magnesium, reduced blood calcium (due to impaired secretion and action of PTH), reduced blood potassium, tubular concentrating dysfunction, mild metabolic alkalosis, increased plasma renin activity, but normal aldosterone content, normal glomerular filtration rate.

　　3. Routine imaging and B-ultrasound, electrocardiogram examination.

　　4. Renal biopsy examination:Can help with the diagnosis of the primary disease.

　　What foods are good for kidney magnesium loss

　　Kidney disease is recommended to eat chicken, peach, scallion, soybean, pork, chestnut, agastache, kidney, broussonetia papyrifera, oyster yellow, deer meat, deer fetus, deer tail, deer penis, deer horn glue, sea dog kidney, cow kidney, sheep kidney, bull penis, black bean, prepared rehmannia, salt, wuling shen, chicken kidney, duck kidney, quail, pheasant, chicken kidney grass, deer衔珠草.

　　(The above information is for reference only, please consult a doctor for details)

　　1. Treatment

　　It is mainly the supplementation of magnesium salts. Commonly used drugs are potassium magnesium aspartate solution (with 3mmol of potassium and 1.5-2.5mmol of magnesium per 10ml), which has a strong affinity for cells due to aspartate, facilitating the entry of magnesium and potassium into cells. It not only supplements magnesium but also potassium. In addition, there are magnesium sulfate, magnesium acetate, magnesium chloride, etc. 50% magnesium sulfate can be injected intramuscularly, 2.0g every 2 hours on the first day, 3 times, then 1 time every 6 hours, and the dose can be reduced according to the condition on the third day; severe cases can be administered intravenously with magnesium sulfate, which has adverse reactions such as lowering blood pressure and inhibiting respiration, and should be carefully monitored when used in high doses. Potassium and calcium deficiency should be corrected at the same time if hypokalemia and hypocalcemia are present.

　　2. Prognosis

　　The prognosis varies due to different causes. For example, if hypomagnesemia can be detected in time before the patient shows symptoms such as electrolyte disorder (low K, Na, Ca), and magnesium salts are supplemented early to improve hypomagnesemia, it is expected to alleviate symptoms and improve prognosis.