Abstract
Dysequilibrium in calcium and phosphate metabolism with development of secondary hyperparathyroidism (SHPT) is common in patients with chronic kidney disease (CKD) stage III and IV. Dietary phosphate restrictions and calcium based oral phosphate binders have not been effective in all subjects with SHPT, and soft tissue and vascular calcifications with an increased risk of cardiovascular death related are known consequences. Treatment with the calcimimetic Cinacalcet (Cc) has contributed to a better calcium and phosphate control in patients given hemodialysis treatment. In this retrospective study we present our experience with Cc given to ten (one year) or five (two years) patients with CKD stage III and IV and SHPT not suitable for surgery. With conventional therapy target levels of intact parathyroid hormon (iPTH) are seldomly reached the reason why an iPTH value < 300 ng/l was considered acceptable. Levels of iPTH decreased significantly after 3 months of Cc treatment and remained at the lower level. Plasma ionized-Ca (Ca) concentrations decreased initially but remained above 1.00 mmol/l in all but one patient. Phophate (P) levels increased to 1.41 ± 0.09 mmol/l (mean ± SE) leaving the Ca × P product unchanged. While patients with high iPTH needed high Cc doses up to 90 mg/day, some of the patients required very low doses 4.5-20 mg/day in order to achieve a decrease in iPTH levels. Only one patient reported gastric pain needing dose reduction and other adverse effects were not found. No changes in QT-time were observed. We experienced that Cc treatment was promising to control SHPT and stabilized the Ca-P balance in patients with CKD stage III and IV. Dosing may be challenging and laboratory values should be controlled often (monthly) as these patients may have variable response to Cc treatment. Due to the minimal knowledge about its effect on morbidity and mortality in the predialytic population further controlled studies are needed to confirm its efficacy and safety.
Highlights
Disturbances in calcium (Ca) and phosphate (P) metabolism is accompanied with significant secondary hyperparathyroidism (SHPT) in patients with chronic kidney disease (CKD) in the stage III to IV,[1] and have been linked to tissue and cardiovascular (CV) calcifications with increased mortality.[2,3]
Hypocalcemia and low intact parathyroid hormone (iPTH) levels ( 80 ng/l) was found temporarily in two patients which was corrected with an increased dose of calcium carbonate and vitamin-D analogue (AC)
In our cases we found that Cc was effective in lowering iPTH levels
Summary
Disturbances in calcium (Ca) and phosphate (P) metabolism is accompanied with significant secondary hyperparathyroidism (SHPT) in patients with chronic kidney disease (CKD) in the stage III to IV,[1] and have been linked to tissue and cardiovascular (CV) calcifications with increased mortality.[2,3] Increased levels of intact parathyroid hormone (iPTH) correlated significantly with CV death[4] and CV mortality proportionally with the elevation of iPTH levels.[5] In spite of restriction of dietary P intake and treatment with oral P-binders which may provide some help in the predialytic population many patients continue to present with elevated iPTH. In the presence of low serum Ca and acceptable P levels oral treatment with calcitriol, alphacalcidol, or paricalcitol could be used to lower iPTH levels and eventually prevent renal osteodystrophy. Treatment of SHPT with vitamin-D analogues may cause hyperphosphataemia and hypercalcaemia leading to soft-tissue and vascular calcifications
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