Paricalcitol for Secondary Hyperparathyroidism in Renal Transplantation

被引:51
作者
Trillini, Matias [1 ]
Cortinovis, Monica [1 ]
Ruggenenti, Piero [1 ,2 ]
Loaeza, Jorge Reyes [1 ]
Courville, Karen [1 ]
Ferrer-Siles, Claudia [1 ]
Prandini, Silvia [1 ]
Gaspari, Flavio [1 ]
Cannata, Antonio [1 ]
Villa, Alessandro [1 ]
Perna, Annalisa [1 ]
Gotti, Eliana [2 ]
Caruso, Maria Rosa [2 ]
Martinetti, Davide [1 ]
Remuzzi, Giuseppe [1 ,2 ]
Perico, Norberto [1 ]
机构
[1] IRCCS Ist Ric Farmacol Mario Negri, Clin Res Ctr Rare Dis Aldo & Cele Dacco, Bergamo, Italy
[2] Azienda Osped Papa Giovanni XXIII, Unit Nephrol, Bergamo, Italy
来源
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY | 2015年 / 26卷 / 05期
关键词
VITAMIN-D-RECEPTOR; GLOMERULAR-FILTRATION-RATE; CHRONIC KIDNEY-DISEASE; ORAL PARICALCITOL; 1,25-DIHYDROXYVITAMIN D-3; PARATHYROID-HORMONE; CARDIOVASCULAR EVENTS; DIABETIC-NEPHROPATHY; CALCITRIOL THERAPY; BONE-DISEASE;
D O I
10.1681/ASN.2013111185
中图分类号
R5 [内科学]; R69 [泌尿科学(泌尿生殖系疾病)];
学科分类号
1002 ; 100201 ;
摘要
Secondary hyperparathyroidism contributes to post-transplant CKD mineral and bone disorder. Paricalcitol, a selective vitamin D receptor activator, decreased serum parathyroid hormone levels and proteinuria in patients with secondary hyperparathyroidism. This single-center, prospective, randomized, crossover, open-label study compared the effect of 6-month treatment with paricalcitol (1 mu g/d for 3 months and then uptitrated to 2 mu g/d if tolerated) or nonparicalcitol therapy on serum parathyroid hormone levels (primary outcome), mineral metabolism, and proteinuria in 43 consenting recipients of renal transplants with secondary hyperparathyroidism. Participants were randomized 1:1 according to a computer-generated sequence. Compared with baseline, median (interquartile range) serum parathyroid hormone levels significantly declined on paricalcitol from 115.6 (94.8-152.0) to 63.3 (52.0-79.7) pg/ml (P<0.001) but not on nonparicalcitol therapy. At 6 months, levels significantly differed between treatments (P<0.001 by analysis of covariance). Serum bone-specific alkaline phosphatase and osteocalcin decreased on paricalcitol therapy only and significantly differed between treatments at 6 months (P<0.001 for all comparisons). At 6 months, urinary deoxypyridinoline-to-creatinine ratio and 24-hour proteinuria level decreased only on paricalcitol (P<0.05). L3 and L4 vertebral mineral bone density, assessed by dual-energy x-ray absorption, significantly improved with paricalcitol at 6 months (P<0.05 for both densities). Paricalcitol was well tolerated. Overall, 6-month paricalcitol supplementation reduced parathyroid hormone levels and proteinuria, attenuated bone remodeling and mineral loss, and reduced eGFR in renal transplant recipients with secondary hyperparathyroidism. Longterm studies are needed to monitor directly measured GFR, ensure that the bone remodeling and mineral effects are sustained, and determine if the reduction in proteinuria improves renal and cardiovascular outcomes.
引用
收藏
页码:1205 / 1214
页数:10
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