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Original Abstract of the Article

Major Research Findings

Calcium acetate is an effective phosphate binder used in the treatment of hyperphosphatemia in patients with chronic kidney disease. 17 14 15 3 6 A study comparing calcium acetate to calcium carbonate showed that calcium acetate was more effective at controlling serum phosphorus levels. 17 Calcium acetate was also found to be more effective at lowering phosphorus levels than calcium carbonate and had a lower risk of hypercalcemia. 14 A study investigating the effectiveness of iron-based phosphate binders found calcium acetate to be effective and have fewer side effects than conventional phosphate binders. 15 A review of phosphate binders for chronic kidney disease found that calcium acetate was as effective as sevelamer in reducing serum phosphorus with a similar safety profile and lower pill burden. 3 Calcium acetate/magnesium carbonate was found to be equally effective and safe as sevelamer in controlling serum phosphorus and calcium levels and resulted in lower costs. 6

Reasons for Side Effects

Side effects of calcium acetate are often due to calcium overload, which can lead to hypercalcemia, vascular calcification, and constipation. 17 10 11 12 13 14 3 6 2

Common Side Effects

Hypercalcemia

Calcium acetate has a high calcium content and therefore poses a risk of hypercalcemia. 17 14 3 6 Hypercalcemia can increase the risk of vascular calcification, heart disease, and kidney stones. 12

Vascular Calcification

Overconsumption of calcium acetate can increase the risk of vascular calcification. 11 Vascular calcification can increase the risk of heart disease, stroke, and peripheral artery disease. 12

Constipation

Calcium acetate can cause constipation. 10 Constipation can cause abdominal pain, bloating, and nausea. 11

Gastrointestinal Discomfort

Calcium acetate can cause gastrointestinal discomfort. 16 Gastrointestinal discomfort can cause nausea, vomiting, abdominal pain, and diarrhea. 3 6

Other Side Effects

Other side effects of calcium acetate include headache, dizziness, rash, and shortness of breath. 17

Side Effects Management

Hypercalcemia Management

Managing hypercalcemia includes adjusting the dose of calcium acetate and consuming foods low in calcium. 14 7 It may also be helpful to use drugs that inhibit calcium absorption. 3

Vascular Calcification Management

Managing vascular calcification includes treating hyperphosphatemia, hypertension, and diabetes to control risk factors. 11 Using calcium-free phosphate binders instead of calcium acetate can also be effective. 13 3

Constipation Management

Managing constipation includes consuming foods high in fiber and drinking plenty of fluids. 10 Constipation medication may be taken as needed. 11

Gastrointestinal Discomfort Management

Managing gastrointestinal discomfort includes taking calcium acetate with food and in smaller doses. 16 Antacids and digestive aids may be taken as needed.

Comparison Between Studies

Commonalities

Multiple studies have shown that calcium acetate is effective in treating hyperphosphatemia in patients with chronic kidney disease. 17 14 15 3 6 Calcium acetate can also cause side effects like hypercalcemia, vascular calcification, and constipation. 17 10 11 12 13 14 3 6

Differences

Studies comparing calcium acetate and calcium carbonate found calcium acetate to be more effective at controlling serum phosphorus levels. 17 14 Calcium acetate also had a lower risk of hypercalcemia than calcium carbonate. 14 A study investigating the effectiveness of iron-based phosphate binders found calcium acetate to be effective and have fewer side effects than conventional phosphate binders. 15 Calcium acetate was as effective as sevelamer in reducing serum phosphorus with a similar safety profile and lower pill burden. 3 Calcium acetate/magnesium carbonate was equally effective and safe as sevelamer in controlling serum phosphorus and calcium levels and resulted in lower costs. 6

Real-Life Application Considerations

While calcium acetate is an effective treatment for hyperphosphatemia in chronic kidney disease, it is important to be aware of the potential for side effects. 17 10 11 12 13 14 3 6 It is important to follow your doctor's instructions and take the correct dosage. 17 16 Consult your doctor immediately if you suspect any side effects. 17

Limitations of Current Research

There is a lack of sufficient research on the long-term effects and safety of calcium acetate. 17 15 There is also a lack of sufficient data on the side effects of calcium acetate. 10

Future Research Directions

Further research on the long-term effects and safety of calcium acetate is necessary. 17 15 More research is also needed on the side effects of calcium acetate. 10 Specifically, more research is needed on how to reduce the risk of vascular calcification. 11 12

Conclusion

Calcium acetate is an effective drug for treating hyperphosphatemia in patients with chronic kidney disease, but it's essential to understand the potential for side effects. 17 10 11 12 13 14 3 6 It's crucial to follow your doctor's directions and take the correct dosage. 17 16 Consult your doctor immediately if you suspect any side effects. 17


Literature analysis of 18 papers
Positive Content
16
Neutral Content
1
Negative Content
1
Article Type
3
0
0
8
17

Language : English


Language : English


Author: BrandiLisbet


Chronic uremia is characterized by decreased plasma 1,25(OH)2D3 levels due to reduced renal 1-hydroxylase activity and decreased renal phosphate excretion. This leads to secondary hyperparathyroidism due to low plasma calcium and 1,25(OH)2D3 levels and high phosphate levels. Secondary hyperparathyroidism is linked to increased mortality and cardiovascular calcifications in chronic uremic patients. Treatment focuses on preventing hyperphosphatemia with oral phosphate binders and replacing the reduced renal hydroxylation with 1 alpha-hydroxylated vitamin D analogs. This thesis explores the effects of 1alpha(OH)D3 treatment in chronic dialysis patients, focusing on its ability to suppress plasma PTH levels without causing hypercalcemia. The study found that intravenous administration of 1alpha(OH)D3 effectively suppressed plasma PTH levels in patients on chronic hemodialysis without causing serious side effects, and hypercalcemia could be prevented by monitoring plasma Ca 2+ levels and adjusting 1alpha(OH)D3 doses accordingly. Long-term intermittent intravenous treatment with 1alpha(OH)D3 effectively suppressed plasma intact PTH levels. When plasma intact PTH was suppressed to a stable level with intravenous 1alpha(OH)D3, the suppression could be maintained by intermittent oral 1alpha(OH)D3 therapy. The study also investigated the effects of a treatment modality combining 1alpha(OH)D3 and CaCO3 as phosphate binders with reduced calcium concentration in dialysis fluid to prevent hypercalcemia. The combination prevented the development of secondary hyperparathyroidism in patients with normal PTH levels and suppressed PTH levels in patients with secondary hyperparathyroidism. No signs of adynamic bone disease were observed. Intravenous 1alpha(OH)D3 prevented bone mineral density (BMD) decrease in the lumbar spine and femoral neck of hemodialysis patients. The study also examined the pharmacokinetic differences between intravenous and oral administration of 1,25(OH)2D3 and 1alpha(OH)D3 and their acute effects on plasma PTH, Ca 2+, and phosphate levels.

Language : English


Language : English


Language : English


Language : Japanese


Language : English


Language : English


Language : English


Language : English


Language : English


Language : English


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