Boudville Neil C, Hodsman Anthony B
School of Medicine and Pharmacology, University of Western Australia, Sir Charles Gairdner Hospital, Perth, WA, Australia.
Nephrol Dial Transplant. 2006 Sep;21(9):2621-4. doi: 10.1093/ndt/gfl201. Epub 2006 Apr 27.
Recent guidelines suggest supplementation with ergocalciferol (vitamin D(2)) in chronic kidney disease stages 3 and 4 patients with elevated parathyroid hormone (PTH) levels and 25-hydroxyvitamin D (25OHD) levels <75 nmol/l. These guidelines are also applied to renal transplant patients. However, the prevalence rates of 25OHD deficiency and its association with PTH levels in renal transplant populations have not been extensively examined. We aimed to document the prevalence rates of 25OHD deficiency [defined by serum levels <40 nmol/l (<16 ng/ml)] and insufficiency [<75 nmol/l (<30 ng/ml)] in a single renal transplant centre, and examine its relationship with PTH levels.
Serum 25OHD and PTH concentrations were measured in 419 transplant patients attending a single renal transplant clinic over a 4-month period. Demographic and biochemical data were also collected, including serum creatinine, calcium, phosphate and albumin. Simple and multiple linear regression analysis were performed.
In 27.3% of the patients, 25OHD deficiency was present, and 75.5% had insufficiency. On univariate analysis, 25OHD, serum albumin and estimated glomerular filtration rate (eGFR) were significantly associated with PTH levels (P < 0.0001, P = 0.004 and P < 0.0001, respectively). Multiple linear regression demonstrated that only 25OHD, eGFR and serum phosphate were significantly predictive of PTH levels (R(2) = 0.19, P < 0.0001). In this model, a 75 nmol/l increase in 25OHD will only result in a maximal reduction in PTH of 2.0 pmol/l.
We conclude that 25OHD deficiency and insufficiency are common in renal transplant patients and may exacerbate secondary hyperparathyroidism. However, 25OHD, eGFR and phosphate only account for 19% of the variability in PTH levels. In addition, even a large increase in serum 25OHD levels is likely to result in only a small reduction in PTH. Therefore, alternative approaches to managing hyperparathyroidism in renal transplant recipients rather than supplementation with ergocalciferol are warranted.
近期指南建议,对于慢性肾脏病3期和4期且甲状旁腺激素(PTH)水平升高、25-羟维生素D(25OHD)水平<75 nmol/l的患者,补充麦角钙化醇(维生素D2)。这些指南也适用于肾移植患者。然而,肾移植人群中25OHD缺乏的患病率及其与PTH水平的关联尚未得到广泛研究。我们旨在记录单一肾移植中心25OHD缺乏[定义为血清水平<40 nmol/l(<16 ng/ml)]和不足[<75 nmol/l(<30 ng/ml)]的患病率,并研究其与PTH水平的关系。
在4个月内,对一家单一肾移植诊所的419例移植患者测定血清25OHD和PTH浓度。还收集了人口统计学和生化数据,包括血清肌酐、钙、磷和白蛋白。进行了简单和多元线性回归分析。
27.3%的患者存在25OHD缺乏,75.5%的患者存在不足。单因素分析显示,25OHD、血清白蛋白和估计肾小球滤过率(eGFR)与PTH水平显著相关(分别为P<0.0001、P = 0.004和P<0.0001)。多元线性回归表明,只有25OHD、eGFR和血清磷是PTH水平的显著预测因素(R2 = 0.19,P<0.0001)。在该模型中,25OHD每增加75 nmol/l,PTH最多只会降低2.0 pmol/l。
我们得出结论,25OHD缺乏和不足在肾移植患者中很常见,可能会加重继发性甲状旁腺功能亢进。然而,25OHD、eGFR和磷仅占PTH水平变异性的19%。此外,即使血清25OHD水平大幅升高,PTH可能也只会有小幅降低。因此,肾移植受者甲状旁腺功能亢进的管理需要采用替代方法,而非补充麦角钙化醇。