Chronic kidney disease (CKD) is in the compensatory adaptation stage in the early stage. When blood calcium begins to decrease due to various reasons, it will stimulate the parathyroid gland to synthesize and release parathyroid hormone (PTH). The increase in PTH increases bone calcium outflow and renal calcium reabsorption [1], and also promotes the synthesis of 1,25-(OH)2-D3 to increase intestinal calcium absorption, thereby increasing blood calcium. Therefore, CKD patients do not have hypocalcemia in the early stage. When CKD enters the middle and late stages, the kidneys fail further and renal function is severely impaired, which causes the body's metabolic phosphorus to continue to decrease, forming hyperphosphatemia and leading to secondary hyperparathyroidism [2]. The resistance of bones to PTH hinders the mobilization of calcium in the bones, resulting in hypocalcemia. In addition, due to kidney disease, insufficient secretion of vitamin D leads to reduced gastrointestinal absorption of calcium, which can also cause hypocalcemia. Therefore, CKD patients only need calcium supplementation in the middle and late stages. What is hypocalcemia? Under normal circumstances, calcium is in a steady-state balance. The total calcium content in an adult is about 1000-1300 g, most of which exists in bones and teeth in the form of bone salts. Extracellular fluid calcium accounts for only 0.1% of the total calcium, about 1 g, and the blood calcium level is 2.2-2.6 mmol/L. When the plasma protein concentration is normal, when the blood calcium is lower than 2.2 mmol/L, it is called hypocalcemia. What are the dangers of hypocalcemia in CKD patients? 1. Due to the loss of calcium in the bones, hypocalcemia can lead to renal osteodystrophy, osteoporosis and pathological fractures. 2. Hypocalcemia can lead to cardiovascular diseases, including arrhythmias, heart failure, etc. 3. The most serious is hypocalcemic crisis. When blood calcium drops to an extremely low level, below 0.88 mmol/L, severe spasm of smooth muscles may occur, leading to epilepsy and asthma. In severe cases, laryngeal muscle spasms may lead to suffocation, and even worse, cardiac arrest[2]. How to treat hypocalcemia in the middle and late stages of CKD? Treatment goals Patients with CKD stages 3 to 4 should maintain blood calcium within the normal range. The blood calcium level of patients with CKD stage 5 is maintained in the normal range of 2.1 to 2.3 mmol/L. 1. In the diet, limit the intake of phosphorus and increase the intake of calcium-containing foods, such as milk and other dairy products, tofu and other soy products, and eggs. 2. Use phosphate binders to correct hyperphosphatemia. Phosphate binders are mainly divided into aluminum, calcium-containing phosphate binders, and calcium-free phosphate binders. Calcium-free phosphate binders have no systemic absorption, are highly safe, and can significantly reduce blood phosphorus levels. They are widely used, such as lanthanum carbonate and sevelamer. It should be noted that when the patient's blood calcium is >2.54 mmol/L, calcium-free phosphate binders should be used. 3. Supplement calcium to increase blood calcium levels, such as calcium lactate, calcium carbonate, etc. Calcium gluconate can also be selected, combined with calcitriol soft capsules or alfacalcidol. 4. Give 1,25-(OH)2-D3 treatment. 1,25-(OH)2-D3 can promote intestinal calcium absorption, reduce urinary calcium excretion, regulate bone metabolism, and increase blood calcium [3]. 5. Exercise is beneficial to the body's absorption of calcium from the diet and can also reduce calcium loss. It is recommended to perform moderate-intensity aerobic exercise 3 to 5 times a week, each time for 30 to 60 minutes, including walking, jogging, swimming, etc. 6. Sunbathing can promote the synthesis of active vitamin D in the body and is beneficial to calcium absorption. 6-12 noon and 4-5 pm are suitable times for sunbathing. summary Hypocalcemia is a common symptom in the middle and late stages of CKD. It is often accompanied by hyperphosphatemia, which can cause secondary hyperparathyroidism. Therefore, it is crucial to properly supplement calcium and reduce phosphorus in patients with middle and late stages of CKD to achieve a positive calcium balance in the body. In addition, care should be taken to avoid excessive calcium supplementation, which can lead to hypercalcemia or vascular calcification. During medication, blood calcium, phosphorus and intact PTH levels should be closely monitored, and the calcium supplementation regimen should be adjusted in a timely manner. References: [1]Felsenfeld AJ, Levine BS, Rodriguez M. Pathophysiology of Calcium, Phosphorus, and Magnesium Dysregulation in Chronic Kidney Disease. Semin Dial. 2015 Nov-Dec;28(6):564-77. doi: 10.1111/sdi.12411. Epub 2015 Aug 25. PMID: 26303319. [2]Ritter CS, Slatopolsky E. Phosphate toxicity in CKD: the killer among Us. Clin J Am Soc Nephrol. 2016;11:1088-100. [3] Lin Shan, Jia Junya. Rational application of calcium tablets and active vitamin D in chronic kidney disease[J]. Chinese Journal of Nephrology Research, 2014, 3(05): 241-245. |
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