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Changes in serum cystatin C, creatinine, and C-reactive protein after cardiopulmonary bypass in patients with normal
Anders S Svensson1,2, John-Peder Escobar Kvitting1,2, Csaba P Kovesdy3,4
1Department of Cardiothoracic Surgery and Anaesthesia, Linköping University Hospital, Linköping, Sweden.
Insights
Serum creatinine and cystatin C levels change after cardiopulmonary bypass (CPB). Inflammation significantly impacts these kidney biomarkers, potentially mimicking acute kidney injury (AKI).
Area of Science:
- Cardiology
- Nephrology
- Biomarkers
Background:
- Cardiopulmonary bypass (CPB) can alter serum creatinine and cystatin C levels independently of glomerular filtration rate.
- Acute inflammation following CPB is a known factor influencing these biomarkers.
Purpose of the Study:
- To quantify temporal changes in serum creatinine, cystatin C, and C-reactive protein (CRP) after CPB.
- To investigate the impact of inflammation on these biomarker changes.
Main Methods:
- Prospective study of 38 patients undergoing cardiac surgery with CPB.
- Compared pre- and postoperative serum creatinine and cystatin C levels.
- Analyzed the association between CRP levels and biomarker changes using mixed-effects regression.
Main Results:
- Serum creatinine and cystatin C initially decreased post-CPB due to hemodilution.
- Serum creatinine returned to baseline, while cystatin C significantly increased at 72 hours post-CPB.
- Elevated CRP levels post-CPB correlated with increased serum creatinine and cystatin C.
Conclusions:
- Serum creatinine and cystatin C are not interchangeable after CPB.
- Inflammation significantly affects post-CPB biomarker levels, potentially leading to misinterpretation as acute kidney injury (AKI).
- Careful interpretation of cystatin C is needed in the context of CPB and inflammation.
Aim:
The use of cardiopulmonary bypass (CPB) can cause changes in serum creatinine and cystatin C independent of glomerular filtration rate. We aimed to quantify the temporal changes of these biomarkers and C-reactive protein (CRP) after CPB.
Methods:
This was a prospective study at an academic medical centre between April and October 2013. We compared postoperative changes in serum creatinine and cystatin C in 38 patients with normal preoperative kidney function who underwent cardiac surgery using CPB and did not develop perioperative acute kidney injury (AKI). The effect of inflammation on intra-individual changes was examined in mixed effects regressions, using measurements of pre- and postoperative CRP.
Results:
Both serum creatinine (79.9 ± 22.7 vs. 92.6 ± 21.4 µmol/L, P = 0.001) and cystatin C (1.16 ± 0.39 vs. 1.33 ± 0.37 mg/L, P = 0.012) decreased significantly in the first 8 h postoperatively compared to preoperatively, as a result of haemodilution. Thereafter serum creatinine returned to preoperative levels, whereas serum cystatin C continued to rise and was significantly elevated at 72 h post-CPB compared to preoperative levels (1.53 ± 0.48 vs. 1.33 ± 0.37 mg/L, P = 0.003). CRP levels increased significantly post-CPB and were significantly associated with increases in both serum creatinine and cystatin C.
Conclusion:
Serum creatinine and cystatin C appear not to be interchangeable biomarkers during and immediately after CPB. Processes unrelated to kidney function such as acute inflammation have a significant effect on post-CPB changes in these biomarkers, and may result in significant increases in serum cystatin C that could erroneously be interpreted as AKI.
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