Pulse versus daily oral Alfacalcidol treatment of secondary hyperparathyroidism in hemodialysis patients: a randomized controlled trial

Abstract

Background: Secondary hyperparathyroidism is a common complication of chronic kidney disease and is managed using vitamin D replacement therapy. Very few studies have examined the effectiveness of pulse alfacalcidol therapy in comparison to daily oral alfacalcidol therapy in suppressing serum parathyroid hormone (PTH) levels in hemodialysis patients. The aim of this randomized controlled trial was to replicate the findings of prior studies comparing effectiveness of pulse oral alfacalcidol therapy versus daily oral alfacalcidol therapy in suppressing PTH after 13 weeks of therapy using a Palestinian sample of hemodialysis patients, and to identify demographic and biomedical characteristics of patients that are independently associated with PTH levels. Methods: One hundred and sixty-seven patients completed the study, 88 in the daily group and 79 in the pulse group. The pulse group had more clinically significant reduction in mean PTH level by 75 pg/dL at 13 weeks than the daily group, but this was not statistically significant. Results:The effect of alfacalcidol therapy on metabolism of phosphate and corrected calcium levels was comparable in both groups, and pulse therapy was not associated with increased risk of hypercalcemia and hyperphosphatemia. Serum PTH levels were independently and inversely associated with older age and diabetes. Conclusion: Switching daily alfacalcidol therapy to thrice-weekly alfacalcidol pulse therapy seems safe and convenient, especially for hemodialysis patients with poor compliance with treatment. This study also highlights the importance of monitoring and preventing malnutrition in hemodialysis patients and maintaining optimal glycemic control in diabetic hemodialysis patients.

Bone mineral density in Palestinian patients with end-stage renal disease and the related clinical and biochemical factors: Cross-sectional study

“…These findings correlate with a previous study conducted in Japan that suggested a strong association with the hyperparathyroidism because of long duration on dialysis therapy and generalized bone loss [ 27 ]. This is attributed to a combination of factors, including reduction in vitamin D synthesis, hyperphosphatemia, hypocalcemia, and PTH skeletal resistance which will eventually increase the risk of mortality and morbidity as a result of bone disease and fractures [ 11 ]. The hyper activated PTH is considered to deteriorate bone mechanical properties, to rescue the state of hypocalcemia among ESRD patients, on the expense of changing bone structure and reducing bone mass [ 28 ].…”

“…Secondary hyperparathyroidism is a common complication of CKD and it is attributed to hyperphosphatemia, hypocalcemia, reduced vitamin D synthesis as well as PTH skeletal resistance [ 5 , 10 , 11 ]. The excessive secretion of PTH among renal failure patients results in increased bone turnover [ 11 – 13 ].…”

“…Secondary hyperparathyroidism is a common complication of CKD and it is attributed to hyperphosphatemia, hypocalcemia, reduced vitamin D synthesis as well as PTH skeletal resistance [ 5 , 10 , 11 ]. The excessive secretion of PTH among renal failure patients results in increased bone turnover [ 11 – 13 ]. In addition to high PTH levels, other risk factors are linked to low bone density such as advanced age, low serum albumin level as well as high serum alkaline phosphatase levels [ 9 , 10 ].…”

Osteoporosis, an Inevitable Circumstance of Chronic Kidney Disease: A Systematic Review

“…Causes of SHPT include phosphate retention, calcium and vitamin D reduction, and FGF-23 elevation, as well as decreased expression of CaSR, vitamin D receptor, FGF-23 receptor, and klotho in the parathyroid gland. Moreover, the expression of the parathyroid receptor is reduced by uremic toxins, for example, p-cresyl sulfate and indoxyl which increases cyclic adenosine 3', 5' monophosphate (cAMP) synthesis in the osteoblast [9,13,26]. This cAMP influences skeletal resistance to PTH and eventually osteoporotic fracture [9].…”