What is active vitamin CKD?

Chronic Kidney Disease (CKD), especially renal insufficiency patients often have disorders of mineral metabolism, which can cause systemic multisystemic damage including bone disease and cardiovascular disease. According to the recommendations of the K/DOQI guidelines, relevant testing and treatment should be initiated from CKD stage 3. Indicators monitored include corrected total serum calcium, blood phosphorus, and whole-segment parathyroid hormone (iPTH) levels. Secondary hyperparathyroidism (SHPT) is one of the most important types of mineral metabolism disorders, which can not only cause severe damage to the bones, but can also exacerbate abnormalities in calcium and phosphorus metabolism, causing phlegmatic skin, anemia, neurological damage, and cardiovascular disease. Active vitamin D is an important drug in the treatment of SHPT, which not only facilitates the treatment of bone disease associated with secondary hyperparathyroidism, but also facilitates the improvement of systemic damage to other organs caused by SHPT. However, the use of active vitamin D without monitoring can lead to a series of adverse consequences. Therefore, the use of active vitamin D must be rationalized and blood iPTH, calcium, phosphorus and calcium-phosphorus product (CaxP) must be strictly monitored. I. Target values for corrected serum total calcium, blood phosphorus and whole segment parathyroid hormone (iPTH) levels in patients with CKD Depending on the different stages of CKD, it is required that blood iPTH and calcium and phosphorus levels be maintained in the target value range. Treatment principles of secondary hyperparathyroidism (a) Reduce blood phosphorus 1. Limit the intake of dietary phosphorus to 800-1000 mg per day. 2. 2, the use of phosphorus binding agent: for dietary phosphorus restriction still can not control blood phosphorus in the target target range. (1) Calcium-containing phosphorus binding agents, such as calcium carbonate, calcium acetate, etc., and taken with meals to maximize the effect of lowering blood phosphorus. (To prevent hypercalcemia, the total calcium supplied by calcium-containing phosphorus-binding agents should not exceed 1500 mg/d, and the total calcium intake, including diet, should be less than 2000 mg/d.) (2) If there is high blood calcium, the use of calcium-containing phosphorus binding agents should be discontinued, and calcium-free phosphorus binding agents, such as Renagel ( Sevelamer HCL ), lanthanum carbonate, etc., can be selected if available. (3) If the above measures and full dialysis still have serious high blood phosphorus >2.26 mmol/L ( 7 mg/dl ), can be short-term ( 3 – 4 weeks ) to use aluminum-containing phosphorus binding agent, and then switch to other agents. 3. Adequate dialysis:Increasing the frequency and duration of dialysis helps phosphorus clearance. (ii) Adjustment of blood calcium Patients with all stages of CKD should maintain blood calcium in the target target range. For patients with low blood calcium with hypocalcemia symptoms or iPTH higher than the target range, calcium supplements or active vitamin D preparations can be used. Hypercalcemia must also be prevented. In dialysis patients with blood calcium concentrations >2.54 mmol/L (10.2 mg/dl), measures should be taken, such as reducing or discontinuing the use of calcium-containing preparations and active vitamin D, and using low-calcium dialysis solutions (1.25 mmol/L or lower). (iii) Application of active vitamin D The application of active vitamin D should be rationalized according to the level of PTH. iPTH, calcium and phosphorus levels should be closely monitored and drug dosage should be adjusted during the application process. (iv) For severe SHPT (iPTH persistently >> 800 pg/ml) that cannot be controlled by standardized drug therapy and with persistent hypercalcemia and/or hyperphosphatemia, those who are resistant to treatment, and those who have the presence of parathyroid adenomas or nodules confirmed by isotope or ultrasound examination, sub-total resection of the parathyroid glands or total resection of the parathyroid glands plus autotransplantation are recommended. Rational application of active vitamin D in secondary hyperparathyroidism (1) Mechanism of action 1. Direct action: act on parathyroid glands, reduce the transcription of PTH gene, reduce the proliferation of parathyroid cells, inhibit the synthesis and secretion of PTH. 2. Indirect effect: Promote the absorption of calcium in the small intestine, increase the blood calcium level, and inhibit the secretion of PTH. (II) Indications 1, plasma iPTH exceeds the corresponding target range (CKD3>70 pg/ml , CKD4>> 110 pg/ml , CKDS>300 pg/ml), need to give active vitamin D preparations. (2) Abnormal calcium and phosphorus levels must be corrected prior to active vitamin D therapy so that CaxP < 55 mg2/dl 2 3. Patients without rapid deterioration of renal function who are willing to undergo follow-up. (C) Use of active vitamin D The current domestic active vitamin D preparations are 1,25 (OH)=D, and 1-ct trans-vitamin D'. The following application methods for 1,25 (OH)}D, are recommended as follows: 1, small-dose continuous therapy: mainly for patients with mild SHPT or patients with moderate-to-severe SHPT in the maintenance phase of treatment. Dosage:0.25wg, 1 time per day, orally. Dosage Adjustment: (1)If the iPTH can be lowered to the target range, the original dose can be reduced by 25%}SO%, or even taken on alternate days. And according to the iPTH level, keep adjusting the dose gradually to avoid excessive decrease and rebound of the iPTH level, until the iPTH is maintained in the target range with the minimum dose. (2) If there is no significant decrease in iPTH level, increase the dose by 50% of the original dose. If there is still no decrease in iPTH or it reaches the target range after 4-8 weeks of treatment, High Dose Intermittent Therapy can be tried. 2.High dose intermittent therapy (shock therapy): mainly for patients with moderate to severe SHPT. Dose Adjustment: (1) If the iPTH level does not decrease significantly after 4-8 weeks of treatment, increase the dose of 1,25(0H)Yin per week by 25%-50%. (2) Once iPTH has fallen into the target range, the 1,25(OH)=D, dose is decreased by 25% - 50% and the 1,25(0H)Yin, dose is continuously adjusted according to the iPTH level. Ultimately, the smallest 1,25(OH)=D,dose was selected for intermittent or continuous administration. (D) Monitoring of blood iPTH, calcium and phosphorus levels during treatment with active vitamin D. 1, CKD3,4 patients: (1) blood calcium and phosphorus: at least once a month during the first 3 months of treatment, and may be changed to once every 3 months thereafter; (2) serum iPTH: at least once a month during the first 6 months of treatment, and may be changed to once every 3 months thereafter. 2, CKDS patients: (1) blood calcium and phosphorus: at least every 2 weeks during the first 1-3 months of treatment, and then every month; (2) serum iPTH: at least once a month during the first 3 months of treatment (preferably every 2 weeks), and then every 3 months when the target range is reached. See Table 20 3. When using low-calcium dialysate, phosphorus binding agent containing calcium, high-dose active vitamin D shock therapy or when there are large changes in blood calcium, phosphorus and iPTH in vivo, the frequency of blood calcium, phosphorus and iPTH monitoring should be increased accordingly to the condition, so as to adjust the treatment in time. (E) Application of active vitamin D common adverse reactions and their countermeasures 1, common adverse reactions: elevated blood calcium and blood phosphorus. In addition, improper application of active vitamin D may cause excessive inhibition of IPT'H, which may lead to power-deficient bone disease. Countermeasures: (1) Closely monitor blood Ca}P}iPTH and calcium and phosphorus product levels. (2) If there is elevated blood phosphorus, first actively reduce phosphorus. (3) If blood calcium >2.54 mmol/L (10.2 mg/ml) ① should reduce or stop using calcium-containing phosphorus binding agent; when possible, use calcium-free phosphorus binding agent; ② severe hypercalcemia should be reduced or discontinue the use of active vitamin D, and restart using it again when the blood calcium is back to normal; ③ dialysis patients, according to the level of calcium, low-calcium dialysate can be used (1.25 mmol/L or lower). The patient’s symptoms and blood pressure should be closely monitored during dialysis. ④ It is recommended that active vitamin D be administered at night before sleep when the intestinal calcium load is lowest.