Platelet count and volume indices in patients with contrast-induced acute kidney injury and acute myocardial infarction treated invasively

The aetiology of contrast-induced acute kidney injury (CI-AKI) is not well understood. We hypothesised that the pathophysiology of CI-AKI and impaired coronary reperfusion (IR), observed after invasive treatment of acute myocardial infarction (AMI), could be similar and might be related to platelet count (PC) and platelet volume indices (PVI). To evaluate the relation between PC, PVI, IR, and CI-AKI in patients with AMI treated invasively. A single-centre study evaluated 607 consecutive AMI-patients treated invasively. Comparative analyses were performed between patients with CI-AKI and without CI-AKI for the total study population (CI-AKI, n = 156; 25.7% vs. nCI-AKI, n = 451; 74.3%), for patients with diabetes mellitus (CI-AKI-DM, n = 56; 9.2% vs. nCI-AKI-DM, n = 123; 20.3%), and for patients with baseline kidney dysfunction (CI-AKI-BKD, n = 31; 5.1% vs. nCI-AKI-BKD, n = 67; 11.0%). Subjects with IR, who developed CI-AKI, were compared to the remaining patients with respect to platelet parameters (CI-AKI-IR, n = 47; 7.7% vs. controls, n = 560; 92.3%). For total population, as well as studied subgroups, multivariate logistic regression analyses were performed to reveal independent factors associated with CI-AKI. The results of the models were reported as odds ratios (OR) and 95% confidence intervals (95% CI). PC was higher in CI-AKI-DM-patients (224.8 ± 62.8 × 10(9)/L vs. 197.9 ± 63.3 × 10(9)/L; p = 0.014) and in CI-AKI-BKD-patients (248.9 ± 86.5 × 10(9)/L vs. 202.5 ± 59.3 × 10(9)/L; p = 0.004) than in appropriate controls. Within the studied groups, there were no differences between CI-AKI and nCI-AKI patients with respect to PVI. Comparing CI-AKI-IR-patients with controls, no differences in PC or PVI were found. IR was observed more often in CI-AKI-patients than in nCI-AKI-patients only among diabetics (48.2% vs. 27.6%; p = 0.008). Increase in admission PC was independently associated with CI-AKI in patients with diabetes (per one unit increase OR 1.006; CI 1.0-1.01; p = 0.04) as well as with baseline kidney dysfunction (per one unit increase OR 1.01; CI 1,0-1,02; p = 0.02). Any similarities in the pathophysiology of CI-AKI and IR were not reflected in platelet parameters. CI-AKI development was not related to PVI; however, higher PC was an independent risk factor for CI-AKI in patients with diabetes or baseline kidney dysfunction.