Palmer Suetonia C, McGregor David O, Craig Jonathan C, Elder Grahame, Macaskill Petra, Strippoli Giovanni Fm
Renal Division, Brigham and Women's Hospital, Harvard Medical School, Harvard Institute of Medicine, Room 550, 4 Blackfan Street, Boston, MA, USA, 02115.
Cochrane Database Syst Rev. 2009 Oct 7(4):CD008175. doi: 10.1002/14651858.CD008175.
Vitamin D compounds are used to suppress elevated serum parathyroid hormone (PTH) in people with chronic kidney disease (CKD).
To assess the efficacy of vitamin D therapy on biochemical, bone, cardiovascular, and mortality outcomes in people with CKD and not requiring dialysis.
We searched The Cochrane Renal Group's specialised register, Cochrane's Central Register of Controlled Trials (CENTRAL), MEDLINE, EMBASE, and reference lists of retrieved articles.
Randomised controlled trials (RCTs) comparing different forms, schedules, or routes of administration of vitamin D compounds for people with CKD not requiring dialysis were included. Vitamin D compounds were defined as established (calcitriol, alfacalcidol, 24,25(OH)(2)vitamin D(3)) or newer (doxercalciferol, maxacalcitol, paricalcitol, falecalcitriol) vitamin D compounds.
Data were extracted by two authors. Statistical analyses were performed using the random effects model. Results were summarized as risk ratio (RR) for dichotomous outcomes or mean differences (MD) for continuous outcomes with 95% confidence intervals (CI).
Sixteen studies (894 patients) were included. No formulation, route, or schedule of vitamin D compound was found to alter the mortality risk or need for dialysis. Vitamin D compounds significantly lowered serum PTH (4 studies, 153 patients: MD -49.34 pg/mL, 95% CI -85.70 to -12.97 (-5.6 pmol/L, 95% CI -9.77 to -1.48)) and were more likely to reduce serum PTH > 30% from baseline value (264 patients: RR 7.87, 95% CI 4.87 to 12.73). Vitamin D treatment was associated with increased end of treatment serum phosphorus (3 studies, 140 patients: MD 0.37 mg/dL, 95% CI 0.09, 0.66 (0.12 mmol/L, 95% CI 0.03, 0.21)) and serum calcium (5 studies, 184 patients: MD 0.20 mg/dL, 95% CI 0.17 to 0.23 (0.05 mmol/L, 95% CI 0.04 to 0.06)). Few data were available comparing intermittent with daily vitamin D administration, or other schedules of dosing.
AUTHORS' CONCLUSIONS: There are not sufficient data to determine the effect of vitamin D compounds on mortality and cardiovascular outcomes in people with CKD not requiring dialysis. While vitamin D compounds reduce serum PTH (49.3 pg/mL (5.6 pmol/L)) compared with placebo, the relative clinical benefits of PTH lowering versus treatment-related increases in serum phosphorus and calcium remain to be understood.
维生素D化合物用于抑制慢性肾脏病（CKD）患者升高的血清甲状旁腺激素（PTH）。
评估维生素D治疗对非透析CKD患者生化指标、骨骼、心血管及死亡率结局的疗效。
我们检索了Cochrane肾脏组专业注册库、Cochrane对照试验中心注册库（CENTRAL）、MEDLINE、EMBASE以及检索到文章的参考文献列表。
纳入比较不同剂型、给药方案或给药途径的维生素D化合物用于非透析CKD患者的随机对照试验（RCT）。维生素D化合物定义为已确立的（骨化三醇、阿法骨化醇、24,25 - 二羟维生素D3）或新型的（度骨化醇、马沙骨化醇、帕立骨化醇、法骨化三醇）维生素D化合物。
由两位作者提取数据。采用随机效应模型进行统计分析。结果以二分类结局的风险比（RR）或连续性结局的均值差（MD）及95%置信区间（CI）进行总结。
纳入16项研究（894例患者）。未发现维生素D化合物的任何剂型、给药途径或给药方案能改变死亡风险或透析需求。维生素D化合物显著降低血清PTH（4项研究，153例患者：MD - 49.34 pg/mL，95%CI - 85.70至 - 12.97（- 5.6 pmol/L，95%CI - 9.77至 - 1.48）），且更有可能使血清PTH较基线值降低>30%（264例患者：RR 7.87，95%CI 4.87至12.73）。维生素D治疗与治疗结束时血清磷升高相关（3项研究，140例患者：MD 0.37 mg/dL，95%CI 0.09，0.66（0.12 mmol/L，95%CI 0.03，0.21））以及血清钙升高相关（5项研究，184例患者：MD 0.20 mg/dL，95%CI 0.17至0.23（0.05 mmol/L，95%CI 0.04至0.06））。关于间歇性与每日服用维生素D或其他给药方案比较的数据较少。
尚无足够数据确定维生素D化合物对非透析CKD患者死亡率和心血管结局的影响。虽然与安慰剂相比，维生素D化合物可降低血清PTH（49.3 pg/mL（5.6 pmol/L）），但降低PTH相对于治疗相关的血清磷和钙升高的相对临床益处仍有待明确。
