BP lowering increased fibroblast growth factor 23 despite eGFR changes for patients with CKD
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Patients with chronic kidney disease and hypertension who underwent intensive blood pressure lowering had increases in fibroblast growth factor 23 levels regardless of changes in eGFR, according to a published study.
“Serum concentrations of fibroblast growth factor 23 (FGF23) and parathyroid hormone (PTH) are elevated in patients with [chronic kidney disease] CKD, and higher concentrations are well established as risk factors for cardiovascular disease and death,” Charles Ginsberg, MD, of the University of California, San Diego, and colleagues wrote. “In the Systolic Blood Pressure Intervention Trial (SPRINT), intensive systolic BP lowering led to lower rates of cardiovascular events and mortality despite a more rapid decline in eGFR. Given that FGF23 and PTH would be expected to increase in the setting of declining eGFR, the effects of intensive systolic BP control on these key potential intermediates are of considerable interest.”
To investigate the impact of intensive systolic BP lowering (defined as BP <120 mm/Hg vs. standard BP target of 140 mm/Hg) on patients with CKD and hypertension, researchers included 987 participants from the SPRINT study (mean age, 72 years; mean eGFR, 46 mL/min/1.73m2).
Participants in the standard BP lowering group had baseline FGF23 concentrations of 65 pg/m vs. 66 pg/m for those who underwent intensive BP lowering. Mean changes in eGFR were +1.58 mL/min/1.73m2 and -2.12 mL/min/1.73m2 for each of these groups, respectively.
Although they hypothesized that reductions in eGFR due to intensive BP lowering would lead to increases in FGF23 and PTH, researchers observed that the increases in FGF23 “persisted despite accounting for concurrent changes in eGFR,” with a mean increase of 11.5% for those in the intensive BP lowering group vs. the standard group.
They added that the relative difference in FGF23 was not only unchanged after adjusting for eGFR, but also after adjusting for albuminuria, and that PTH did not change.
According to researchers, the clinical implications of these findings are “uncertain.”
“Although longitudinal increases in FGF23 levels have been associated with greater cardiovascular risk in patients with CKD,” they wrote, “the intensive arm of the SPRINT experienced lower cardiovascular events and mortality risk despite the concurrent rise in FGF23. Thus, mechanisms leading from intensive BP lowering to cardiovascular protection are likely via pathways distinct from FGF23.”
In addition, they suggested the findings point to mechanisms distinct from changes in eGFR as drivers of the observed FGF23 increases.
The researchers concluded that although more study is needed in this area, they do not discourage clinicians from “pursuing aggressive systolic BP lowering in patients with CKD.” – by Melissa J. Webb
Disclosures: Ginsberg reports no relevant financial disclosures. Please see the study for all other authors’ relevant financial disclosures.
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