Key result
Serum PIIINP, a marker of collagen synthesis, was significantly associated with arterial stiffness (pulse wave velocity) independent of eGFR (β = 0.45, P=0.0017), but not with left ventricular mass.
Observational (n=242)
Effect estimate: β = 0.45
p-value: p=0.0017
In patients with CKD, the collagen synthesis biomarker PIIINP is independently associated with arterial stiffness (pulse wave velocity), suggesting a role for altered collagen turnover in its pathogenesis.
May signal arterial stiffness risk in CKD; hypothesis-generating for collagen turnover as target, pending causal confirmation.
BACKGROUND: Markers of collagen turnover have not been well studied in the context of cardiovascular disease in patients with chronic kidney disease (CKD). We investigated the associations between serum markers of collagen turnover [N-terminal procollagen type 3 propeptide (PIIINP) and carboxy-terminal telopeptide (C1TP)] and both pulse wave velocity (PWV) and left ventricular mass index (LVMI) in a CKD cohort. METHODS: The study included 242 patients (mean age 60 ± 15 years, 53% males, 80% Caucasian, CKD Stages 3-5) from the Renal Research Institute (RRI)-CKD Study. Serum PIIINP and C1TP levels were analyzed by radioimmunoassay. PWV was obtained by applanation tonometry from carotid and femoral pressure wave contours. LVMI was measured by echocardiography. Statistical analyses included Pearson's correlations and multiple linear regression. RESULTS: Both PIIINP and C1TP values were significantly higher in more advanced stages of CKD (P < 0.05). A positive correlation was demonstrated between PWV and LVMI (r = 0.25, P = 0.0018), persisting after adjustment for potential confounders (partial r = 0.27, P = 0.0009). PIIINP correlated with PWV (r = 0.16, p = 0.029) and LVMI (r = 0.16, P = 0.0018), while C1TP correlated with LVMI (r = 0.18, P = 0.013) but not with PWV (r = 0.12, P = 0.09). In multivariable analysis adjusting for race, diabetes, estimated glomerular filtration rate (eGFR) and renin-angiotensin-aldosterone system inhibitors, only PWV (β = 0.45, P = 0.0017) but not LVMI (P = 0.09) remained significantly associated with serum PIIINP. CONCLUSIONS: Our results demonstrate the association of PIIINP (but not C1TP), a circulating biomarker of collagen synthesis with arterial stiffness (but not with LVMI) in a CKD cohort, independent of eGFR. This suggests that altered collagen turnover may play a role in the pathogenesis of arterial stiffness in CKD.
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Dellegrottaglie et al. (2011) conducted an observational in Chronic kidney disease (CKD) (n=242). Serum markers of collagen turnover (PIIINP and C1TP) was evaluated on Pulse wave velocity (PWV) and left ventricular mass index (LVMI) (β = 0.45, p=0.0017). Serum PIIINP, a marker of collagen synthesis, was significantly associated with arterial stiffness (pulse wave velocity) independent of eGFR (β = 0.45, P=0.0017), but not with left ventricular mass.
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