Nephrogenic systemic fibrosis is associated with hypophosphataemia: a case-control study.
OBJECTIVE
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.


METHODS
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.


RESULTS
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.


CONCLUSIONS
Differences in phosphorus metabolism may exist between patients with stage 5 CKD and NSF compared with patients with stage 5 CKD without NSF.
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. ejb2153@columbia.edu.
Elana J
EJ
Bernstein
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.
Tamara
T
Isakova
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.
Mary E
ME
Sullivan
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.
Lori B
LB
Chibnik
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.
Myles
M
Wolf
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.
Jonathan
J
Kay
D000368:Aged; D016022:Case-Control Studies; D003287:Contrast Media / Q000009:adverse effects; D005260:Female; D000089703:Fibroblast Growth Factor-23; D005682:Gadolinium / Q000009:adverse effects; D006801:Humans; D017674:Hypophosphatemia / Q000150:complications*; D008297:Male; D008875:Middle Aged; D054989:Nephrogenic Fibrosing Dermopathy / Q000209:etiology*; D051436:Renal Insufficiency, Chronic / Q000150:complications; D012307:Risk Factors
D003287:Contrast Media; C000717427:FGF23 protein, human; D000089703:Fibroblast Growth Factor-23; D005682:Gadolinium
chronic kidney disease; dialysis; fibroblast growth factor 23; gadolinium; magnetic resonance imaging; nephrogenic systemic fibrosis; phosphorus