OP2026 Poster Presentations Clinical Audits and Service Improvements (40 abstracts)
Robert Jones & Agnes Hunt Orthopaedic Hospital NHS Foundation Trust, Oswestry, United Kingdom
Background: Bone Alkaline Phosphatase (BAP) is the gold standard for measuring bone turnover in patients with impaired renal function. PINP has been recommended as the bone formation marker of choice by the IOF/IFCC. Intact PINP is thought to be unaffected by renal function, making it a potential biomarker for assessing treatment response in patients with reduced renal function. The aim of this work was to examine the clinical utility of these markers in untreated and denosumab treated patients with CKD2-3b.
Methods: In this retrospective study, data from 67 untreated patients and 107 patients on denosumab treatment attending a hospital metabolic bone unit were analysed. PINP and BAP were measured using an i-SYS autoanalyzer (IDS Ltd) following the standard protocol. Routine biochemistry data was also collected. Subjects were sub-divided according to CKD status, CKD3b (n36), CKD3a (n42) and CKD2 (n96). Treatment response was defined as having a bone marker level in the lower half of the premenopausal reference range.
Results: Denosumab patients were significantly older than untreated subjects (83.1 ±6.0 vs. 76.4±17.1; P 0.001) but there were no differences in eGFR or PTH levels between the 2 groups. PINP levels were positively correlated with BAP in both the untreated (spearman rank 0.514; P 0.002) and treated groups (spearman rank 0.524; P 0.001). Neither marker correlated with eGFR in either group. 4.5% of untreated subjects had a PINP level in the lower half of the premenopausal reference range compared to none with BAP. There was no difference in PINP or BAP values or number of responders between the different CKD groups. More denosumab subjects showed a response to treatment with PINP compared to BAP (75% vs 51%; chi-squared P 0.001). A similar response was seen in the CKD2 group (84% vs 53%, P 0.01).
Conclusion: PINP and BAP correlate well with each other in both untreated and treated groups. Neither PINP or BAP correlated with eGFR and there were no differences in PINP or BAP levels between the CKD groups. Further work needs to be done to determine if this is true for those with the poorest renal function.