02091nas a2200193 4500000000100000008004100001260001700042100001600059700002200075700001100097700001600108700001800124700002100142245006500163300001200228490000700240520163600247022001401883 2018 d c-242712097221 aKumar Vinod1 aRamachandran Raja1 aJha V.1 aYadav Ashok1 aGupta Krishan1 aAggarwal Abhinav00aFibroblast growth factor 23 in untreated nephrotic syndrome. a362-3650 v233 a
AIM: Despite its importance in bone and cardiovascular disease in subjects with kidney disease, there are no data on fibroblast growth factor 23 (FGF23) perturbations in nephrotic syndrome. We evaluated FGF23 and markers of mineral bone metabolism in subjects with untreated NS.
METHODS: In this cross-sectional study, we measured circulating levels of FGF23, 25-hydroxy vitamin D [25(OH)D], 1,25 di-hydroxy vitamin D [1,25(OH)D], serum albumin, serum calcium, phosphorus, creatinine and intact parathyroid hormone (iPTH) in 101 patients with adults onset NS and 40 healthy controls. We examined the correlation between FGF23 and markers of mineral bone metabolism.
RESULTS: Compared to healthy controls, subjects with NS showed reduced levels of 25(OH)D (21.76 ± 10.18 vs 35.74 ± 40.27 nmol/L, P = 0.001), 1,25(OH)D (median; 37.80 vs 73.13 pmol/L, P = 0.0001) and FGF23 (37.81 ± 20.42 vs 48.20 ± 11.60 pg/mL, P = 0.004) levels. Serum phosphorus levels were marginally, but significantly higher in subjects with nephrotic syndrome compared to healthy controls (P = 0.004). Serum iPTH levels were significantly higher in subjects with NS compared to healthy controls (52.24 ± 39.58 vs 37.90 ± 14.60 pg/mL, P = 0.028).
CONCLUSIONS: We conclude that FGF23 is reduced in subjects with NS compared to healthy controls. The reduced levels of Vitamin D, and urinary losses may contribute to lower levels of FGF23 in NS.
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