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Acute kidney injury associated with cardiac surgery is a common and significant postoperative complication. With a frequency of 9 - 39% according to different studies, it is the second most common cause of acute kidney injury in intensive care units, and an independent predictor of mortality. This study aimed to investigate the importance of preoperative hemoglobin and uric acid levels as risk factors for acute kidney injury in the postoperative period in cardiac surgery patients. Material and Methods. The study includeda total of 118 patients who were divided into two groups. Each group included 59 patients; the fist group included patients who developed acute kidney injury and required renal replacement therapy, and the second included patients without acute kidney injury. Types of cardiac surgery included coronary, valvular, combined, aortic dissection, and others. All necessary data were collected from patient medical records and the electronic database. Results. A statisticallysignificant difference was found between the groups in preoperative hemoglobin levels (108.0 vs. 143.0 g/l, p = 0.0005); postoperative urea (26.4 vs. 5.8 mmol/l, p = 0.0005) and reatinine (371.0 vs. 95.0μmol/l, p = 0.0005), acute phase inflammatory reactants Creactive protein (119.4 vs. 78.9 mg/l, p = 0.002) and procalcitonin (7.0 vs. 0.2 ng/ml, p = 0.0005), creatine kinase myocardial band isoenzyme (1045.0 vs. 647.0 mg/l, p = 0.014); duration of extracorporeal circulation (103.5 vs. 76.0 min, p = 0.0005) and ascending aortic clamp during cardiac surgery (89.0 vs. 67.0 min, p = 0.0005). The exception was the preoperative uric acid level, where there was no statistically significant difference (382.0 vs. 364.0 μmol/l, p = 0.068). There was a statistically significant correlation between the use of inotropic agents and acute kidney injury development. Conclusion. There is a correlation between the preoperative low hemoglobin levels and postoperative acute kidney injury. There is no statistically significant correlation between the preoperative levels of uric acid and postoperative acute kidney injury. [ABSTRACT FROM AUTHOR]

In the northern Adriatic Sea and in most semienclosed coastal regions worldwide, hypoxia induced by eutrophication in the late 20th century caused major die-offs of coastal marine organisms. However, ecosystem responses to hypoxia over longer centennial scales are unclear because the duration of direct observations is limited to a few decades and/or the temporal resolution of sedimentary archives is compromised by slow sedimentation and bioturbation. To assess whether perturbations of ecosystems by hypoxia recurred over centuries in the northern Adriatic Sea, we evaluate the timing and forcing of past hypoxia events based on the production history of the opportunistic, hypoxia-tolerant bivalve Corbula gibba, using 210Pb data, radiocarbon dating, amino acid racemization, and distribution of foraminifers in sediment cores that capture the past 500 yr in the Gulf of Trieste. Unmixing the stratigraphic record on the basis of 311 shells of C. gibba, we show that the reconstructed fluctuations in abundance do not correlate with abundances in the raw stratigraphic record. We find that production of C. gibba has undergone major decadal-scale fluctuations since the 18th century, with outbreaks corresponding to density of more than 1000 individuals per square meter. These outbreaks represent long-term phenomena in the northern Adriatic ecosystem rather than novel states characteristic of the 20th century eutrophication. They positively correlate with centennial-scale fluctuations in sea-surface temperature, indicating that the hypoxia events were coupled with water-column stratification rather than with nutrient enrichment. [ABSTRACT FROM AUTHOR]