Abstract
BackgroundVascular calcification (VC) contributes to high mortality rates in chronic kidney disease (CKD). High serum phosphate and FGF23 levels and impaired phosphaturic response to FGF23 may affect VC. Therefore, their relative contribution to abdominal aortic calcification (AAC) was examined in patients CKD stages 3–4.MethodsPotential risk factors for AAC, measured by the Kauppila Index (KI), were studied in 178 patients.ResultsIn multivariate linear analysis, AAC associated positively with age, male gender, CKD-stage, presence of carotid plaques (CP) and also with FGF23, but negatively with fractional excretion of phosphate (FEP). Intriguingly, FEP increased with similar slopes with elevations in PTH, with reductions in GFR, and also with elevations in FGF23 but the latter only in patients with none (KI = 0) or mild (KI = 1-5) AAC. Lack of a FEP-FGF23 correlation in patients with severe AAC (KI > 5) suggested a role for an impaired phosphaturic response to FGF23 but not to PTH in AAC. Logistic and zero-inflated analysis confirmed the independent association of age, CKD stage, male gender and CP with AAC, and also identified a threshold FEP/FGF23 ratio of 1/3.9, below which the chances for a patient of presenting severe AAC increased by 3-fold. Accordingly, KI remained unchanged as FEP/FGF23 ratios decreased from 1/1 to 1/3.9 but markedly increased in parallel with further reductions in FEP/FGF23 < 1/3.9.ConclusionsIn CKD 3–4, an impaired phosphaturic response to FGF23 with FEP/FGF23 < 1/3.9 associates with severe AAC independently of age, gender or CP.
Highlights
Vascular calcification (VC) contributes to high mortality rates in chronic kidney disease (CKD)
The contradictory evidence on the role of high FGF23 on VC in CKD may result from the inability to discriminate between adaptive increases in serum FGF23 that translate into an adequate renal phosphaturic response from further elevations in FGF23 resulting from the failure of the damaged kidney to handle the phosphate load
Dominguez et al [19] have recently shown that in patients with cardiovascular disease but without CKD, the lower is the phosphaturic response of the kidney the higher is the association between serum FGF23 levels and adverse cardiovascular events
Summary
Vascular calcification (VC) contributes to high mortality rates in chronic kidney disease (CKD). High serum phosphate and FGF23 levels and impaired phosphaturic response to FGF23 may affect VC Their relative contribution to abdominal aortic calcification (AAC) was examined in patients CKD stages 3–4. Dominguez et al [19] have recently shown that in patients with cardiovascular disease but without CKD, the lower is the phosphaturic response of the kidney the higher is the association between serum FGF23 levels and adverse cardiovascular events. The high impact of VC on adverse cardiovascular events and mortality risk [20] led us to assess the influence of an abnormal renal handling of the phosphate/ FGF23 axis on abdominal aortic calcification (AAC) in CKD patients stages 3 and 4
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