The FGF23 (Fibroblast growth factor 23) hormone originates in bone to communicate with the kidney whose duty it is to excrete excess phosphorus that the bone detects. Its main function is bone-kidney communication to eliminate phosphorus, but what happens when the person has renal failure and kidneys that do not work in addition to an impaired excretion ability? What happens is that the failing kidney is unable to abide by FGF23. Nevertheless, the bone keeps producing this hormone because it does not detect that the kidney has stopped working, resulting in a build-up of FGF23 in the blood.
The build-up of this hormone causes troublesome effects on other organs. For instance, the cardiovascular system is affected by high levels of this hormone; the heart enlarges (this is known as hypertrophy) and this increases risk of death. This led a research team made up of researchers from the University of Cordoba's Medical School, the GC13 and GC07 groups from the Maimonides Institute of Biomedical Research (the acronym is IMIBIC in Spanish) and the Nephrology Unit at the Queen Sofia University Hospital to focus on how to lower levels of FGF23.
After a clinical trial on 21 patients in dialysis treatment for forty weeks, they were able to prove that by following a diet with low phosphorus intake and taking medication based on phosphate binders, which prevent the body from absorbing it, the group of patients showed a correction of the high levels of phosphorus and produced a considerable decrease of the FGF23 hormone. Therefore, the effort of lowering phosphorus levels would also work to decrease the concentration of FGF23 and reduce the risks of circulation and heart problems.
Call it by its name
Another advance coming out of this research project, headed by researcher Cristian Rodelo Haad and including UCO Medicine Professors Mariano Rodriguez and Alejandro Martin-Malo, is differentiating two parts of the hormone: intact FGF23 (iFGF23) and FGF23 c-terminal (c-FGF23). In this research project, made up of 150 patients, the complete intact hormone was considered and conversely the resulting parts of fragmentation (c-terminal), since the final quantity of these depends on specific factors.
While phosphorus is responsible for more than 60% of the molecule values in both cases, for the intact hormone phosphorus and calcium in the blood are defining, and for the c-terminal the time that the patient has undergone dialysis and inflammation are factors that increase its concentration.
Once proven that with medication and a diet low in phosphorus people who suffer from kidney failure are able to lower the levels of FGF23 in their bodies, future research aims to study how this reduction increases life expectancy in the long term.
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Rodelo-Haad, C; Rodriguez-Ortiz, ME; Martin-Malo, A; de Mier, MVPR; Aguera, ML; Munoz-Castaneda, JR; Soriano, S; Caravaca, F; Alvarez-Lara, MA; Felsenfeld, A; Aljama, P; Rodriguez, M. Phosphate control in reducing FGF23 levels in hemodialysis patients. PLOS ONE https://doi.org/10.1371/journal.pone.0201537
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http://dx.doi.org/10.1371/journal.pone.0201537
