Circulating concentration of FGF-23 increases as renal function declines in patients with chronic kidney disease, but does not change in response to variation in phosphate intake in healthy…

By T. Larsson, U. Nisbeth, O. Ljunggren, H. Jüppner, K. Jonsson. Kidney International, 2003

700 citations recorded by the source corpus.

How researchers see this paper

The researchers whose trusted networks rank it highest, strongest advocate first. Every researcher gets a different order.

Fibroblast growth factor-23 mitigates hyperphosphatemia but accentuates calcitriol deficiency in chronic kidney disease. (2005, methodology): “though accumulation of inactive fragments may have increased in advanced CKD, these assays have been used in previously published studies of CKD patients (17).”
Serum phosphate levels and mortality risk among people with chronic kidney disease. (2005, background): “Differences in the activity of this transporter or in the levels of phosphaturic factors that modulate this channel (27,28) might lead to different steady-state phosphate concentrations.”
Fibroblast growth factor 23 (FGF23) predicts progression of chronic kidney disease: the Mild to Moderate Kidney Disease (MMKD) Study. (2007, neutral): “001 FGF23 intact (pg/ml) 35 28 (18, 29, 45) 69 70 (31, 48, 80) 0.”
Diabetic Nephropathy: Challenges in Pathogenesis, Diagnosis, and Treatment (2021, background): “Another study also reported that 1,25(OH)2D3 can reduce hypercorrection levels of fibroblast growth factor 23 (FGF23) which is also a risk factor for DN development and can damage podocytes [179].”
Fibroblast growth factors: from molecular evolution to roles in development, metabolism and disease. (2011, background): “These results suggest that FGF23 has a compensatory role in the disease (101).”