Acute kidney injury (AKI) is a widely held concern related to a substantial burden of morbidity, mortality and expenditure in the healthcare system. AKI is not a simple illness but a complex conglomeration of syndromes that often occurs as part of other syndromes in its wide clinical spectrum of the disease. Genetic factors have been suggested as potentially responsible for its susceptibility and severity. As there is no current cure nor an effective treatment other than generally accepted supportive measures and renal replacement therapy, updated knowledge of the genetic implications may serve as a strategic tactic to counteract its dire consequences. Further understanding of the genetics that predispose AKI may shed light on novel approaches for the prevention and treatment of this condition. This review attempts to address the role of key genes in the appearance and development of AKI, providing not only a comprehensive update of the intertwined process involved but also identifying specific markers that could serve as precise targets for further AKI therapies.

Nowadays, mortality rates in intensive care units are the highest of all hospital units. However, there is not a reliable prognostic system to predict the likelihood of death in patients with postsurgical shock. Thus, the aim of the present work is to obtain a gene expression signature to distinguish the low and high risk of death in postsurgical shock patients. In this sense, mRNA levels were evaluated by microarray on a discovery cohort to select the most differentially expressed genes between surviving and non-surviving groups 30 days after the operation. Selected genes were evaluated by quantitative real-time polymerase chain reaction (qPCR) in a validation cohort to validate the reliability of data. A receiver-operating characteristic analysis with the area under the curve was performed to quantify the sensitivity and specificity for gene expression levels, which were compared with predictions by established risk scales, such as acute physiology and chronic health evaluation (APACHE) and sequential organ failure assessment (SOFA). IL1R2, CD177, RETN, and OLFM4 genes were upregulated in the non-surviving group of the discovery cohort, and their predictive power was confirmed in the validation cohort. This work offers new biomarkers based on transcriptional patterns to classify the postsurgical shock patients according to low and high risk of death. The results present more accuracy than other mortality risk scores.

Aims To determine the effectiveness of the implantable cardioverter defibrillator (ICD) in preventing recurrence of syncope in patients with structural heart disease, previously unexplained syncope and inducible ventricular arrhythmias. Methods Thirty-eight patients with syncope, structural heart disease and inducible arrhythmias had an ICD implanted. All ICDs delivered antitachycardia pacing and shocks of adjusted energy. Detection and therapy were programmed according to uniform criteria. Results The mean age of the patients was 63±11 years and most of them were male (36/38). After a mean follow-up of 28±15 (4–61) months, six patients died and one underwent heart transplantation. Syncope recurred in three patients, but in none of them was it caused by an arrhythmic event. In 18 patients, 113 episodes of ventricular tachycardia/ventricular fibrillation were detected and appropriately treated by the ICD. The mean time from implant until first appropriate therapy was 18±14 months. The actuarial probability of receiving appropriate therapy was 20% and 42% at 12 and 24 months, respectively. Conclusions In patients with unexplained syncope, structural heart disease and inducible arrhythmias, ICD prevents syncope associated with arrhythmic events. Frequent effective use of antitachycardia pacing and shocks of adjusted energy seem essential to this aim. Copyright 2002 The European Society of Cardiology. Published by Elsevier Science Ltd. All rights reserved.