Division of Rheumatology, Department of Medicine, Columbia University College of Physicians and Surgeons, New York, NY, Division of Nephrology, Feinberg School of Medicine, Northwestern University, Chicago, IL, MGH Clinical Research Center, Massachusetts General Hospital, Boston, MA, Department of Neurology, Program for Neuropsychiatric Genomics, Brigham & Women's Hospital, Harvard Medical School, Boston, MA and Division of Rheumatology, Department of Medicine, University of Massachusetts Medical School and UMass Memorial Medical Center, Worcester, MA, USA.
Rheumatology (Oxford). 2014 Sep;53(9):1613-7. doi: 10.1093/rheumatology/keu151. Epub 2014 Apr 4.
Nephrogenic systemic fibrosis (NSF) is an iatrogenic fibrosing disorder that primarily affects individuals with chronic kidney disease (CKD) following exposure to gadolinium-based contrast agents (GBCAs). Derangements of calcium and phosphorus have been reported in patients with NSF. The aim of this study was to investigate potential factors in addition to GBCA exposure that may be involved in the pathogenesis of NSF. We hypothesized that patients with stage 5 CKD and NSF would manifest greater alterations in calcium, phosphorus and fibroblast growth factor 23 (FGF23) levels than those who do not have NSF.
Levels of phosphorus, calcium, FGF23 and 25-hydroxy-vitamin D were measured in 10 patients with stage 5 CKD and biopsy-proven NSF and in 19 patients with stage 5 CKD without NSF. Statistical analyses were performed using Fisher's exact test for categorical variables and the Kruskal-Wallis test for continuous variables.
Patients with NSF had significantly lower phosphorus levels compared with controls (P = 0.01). There were no significant differences between NSF patients and controls in calcium, 25-hydroxy-vitamin D, intact parathyroid hormone or FGF23 levels.
Differences in phosphorus metabolism may exist between patients with stage 5 CKD and NSF compared with patients with stage 5 CKD without NSF.
肾源性系统性纤维化(NSF)是一种医源性纤维性疾病,主要影响慢性肾脏病(CKD)患者在接触钆基造影剂(GBCA)后。NSF 患者存在钙和磷的紊乱。本研究旨在探讨除 GBCA 暴露外,可能参与 NSF 发病机制的潜在因素。我们假设,与没有 NSF 的患者相比,5 期 CKD 和 NSF 患者的钙、磷和成纤维细胞生长因子 23(FGF23)水平会发生更大的变化。
测量了 10 例 5 期 CKD 伴活检证实的 NSF 患者和 19 例 5 期 CKD 无 NSF 患者的磷、钙、FGF23 和 25-羟维生素 D 水平。使用 Fisher 确切检验进行分类变量的统计分析,使用 Kruskal-Wallis 检验进行连续变量的统计分析。
与对照组相比,NSF 患者的磷水平显著降低(P = 0.01)。NSF 患者与对照组在钙、25-羟维生素 D、完整甲状旁腺激素或 FGF23 水平方面无显著差异。
与 5 期 CKD 无 NSF 的患者相比,5 期 CKD 和 NSF 患者的磷代谢可能存在差异。