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Introduction: Although the effects of relatively high concentrations of endotoxin on endothelial activation/dysfunction and kidney markers has been described in literature, detailed insight in the LPS concentration-effect relationship, the magnitude, variability and timing of the response, and potential effects of endotoxemia on the kidneys is lacking. A study was performed to assess the effects of low-to moderate dose (0.5, 1 or 2 ng/kg) endotoxemia on the endothelium and kidneys as measured by a panel of novel highly sensitive kidney injury markers. Methods: This was a randomized, double-blind, placebo-controlled study with single ascending doses of LPS (0.5, 1 or 2 ng/kg) administered to healthy male volunteers (3 cohorts of 8 subjects, LPS: placebo 6: 2). Endothelial measures included selectins, cell adhesion molecules, and thrombomodulin. Renal measures included novel, sensitive and specific biomarkers of acute kidney injury. Results: Endotoxin exposure resulted in consistent LPS dose-dependent responses in inflammatory markers, E- and P-Selectin, VCAM1, ICAM1, and thrombomodulin. The observed biological responses were transient, reaching a level of significance of at least

Acute kidney injury (AKI) after hepatectomy occurs in around 10% of cases. AKI is often defined based only on postoperative serum creatinine increase. This study aimed to assess if postoperative urine output (UO) correlated with serum creatinine after hepatectomy. All consecutive hepatectomy patients (2010-2016) were assessed. AKI was defined according to KDIGO criteria: serum creatinine increase ≥26.5 μmol/l, creatinine increase ≥1.5x baseline creatinine, or postoperative oliguria. Oliguria was defined as daily mean UO 360 minutes was the only predictor of creatinine increase (HR = 3.6, 95%CI: 1.1-11.4, p = 0.032). Postoperative UO showed poor correlation with postoperative serum creatinine both in all patients and AKI patients. Surgery duration >360 minutes appeared as the only independent predictor of postoperative serum creatinine increase.

Acute kidney injury (AKI), mostly defined as a rise in serum creatinine concentration of more than 0.5 mg/dl, is a common, serious, and potentially preventable complication of percutaneous coronary intervention and is associated with adverse outcomes including an increased risk of inhospital mortality. Recent data from the National Cardiovascular Data Registry/Cath-PCI registry including 985,737 consecutive patients undergoing percutaneous coronary intervention suggest that approximately 7% experienced AKI with a reported incidence of 3–19%. In patients undergoing primary percutaneous coronary intervention for acute myocardial infarction (AMI), AKI occurs more frequently with rates up to 20% depending on patient and procedural characteristics. However, varying definitions of AKI limit comparisons of AKI rates across different studies. Recently, most studies have adopted the Acute Kidney Injury Network (AKIN) criteria for definition and classification of AKI. Beyond the AKIN criteria for AKI, other classifications such as the risk, injury, failure, loss and end-stage kidney disease (RIFLE) and kidney disease: improving global outcomes (KDIGO) criteria are used to define AKI. Notably, even small increases in serum creatinine beyond AKI may be associated with adverse outcomes including increased hospital length of stay and excess. Acute kidney injury (AKI) is a serious and potentially preventable complication of percutaneous coronary intervention (PCI). Worsening renal function is associated with adverse outcomes including a higher rate of in-hospital mortality. In patients undergoing primary PCI for acute myocardial infarction (AMI), AKI occurs up to 20% of such individuals. Varying definitions of AKI limit comparisons of AKI rates across different studies. Additionally, even small increases in serum creatinine beyond lavels meeting AKI definitions may be associated with adverse outcomes including increased hospital length of stay.

The knowledge on PK behavior of steroid drugs such as prednisolone or prednisone has indeed been expanding but at a rather slow pace. First, convenient, rapid, and specific determination of plasma levels of these steroids was largely indebted to the breakthrough of high performance liquid chromatography (HPLC). Second, prednisolone is non-linearly protein-bound. Since unbound prednisolone is the biologically active compound, only the measurement of this free fraction in plasma is relevant. Third, the short half-life of prednisolone precludes to reach steady-state levels and requires determination of the area under the concentration-time curve. Fourth, prednisolone and prednisone are mutually convertible. Intravenous prednisolone, however, is administered as a pro-drug ester, which renders comparison and interpretation of reported PK data of both agents unreliable. A poignant lack of awareness and knowledge regarding catabolism, clearance mechanisms, and elimination route of steroids fuels the ongoing controversy that surrounds adjunctive corticosteroid therapy in patients with chronic or acute inflammatory disease. This particular patient population is also more prone to develop early and significant kidney dysfunction, necessitating extra-renal support. A better understanding of steroid PK/PD, preferentially guided by HPLC measurement of plasma steroid concentrations, likely will have direct clinical implications, for instance by adapting steroid doses in IHD or implementing higher dose regimens during CRRT.