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Objective: To determine whether pre-hospital statin use is associated with lower renal replacement therapy requirement and/or death during intensive care unit stay. Methods: Prospective cohort analysis. We analyzed 670 patients consecutively admitted to the intensive care unit of an academic tertiary-care hospital. Patients with ages ranging from 18 to 80 years admitted to the intensive care unit within the last 48 hours were included in the study. Results: Mean age was 66±16.1 years old, mean body mass index 26.6±4/9kg/m2 and mean abdominal circumference was of 97±22cm. The statin group comprised 18.2% of patients and had lower renal replacement therapy requirement and/or mortality (OR: 0.41; 95%CI: 0.18-0.93; p=0.03). The statin group also had lower risk of developing sepsis during intensive care unit stay (OR: 0.42; 95%CI: 0.22-0.77; p=0.006) and had a reduction in hospital length-of-stay (14.7±17.5 days versus 22.3±48 days; p=0.006). Statin therapy was associated with a protective role in critical care setting independently of confounding variables, such as gender, age, C-reactive protein, need of mechanical ventilation, use of pressor agents and presence of diabetes and/or coronary disease. Conclusion: Statin therapy prior to hospital admission was associated with lower mortality, lower renal replacement therapy requirement and sepsis rates.

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Genetic variations in TGF-beta and IFN-gamma may interfere with proinflammatory cytokine production and, consequently, may be involved with inflammatory diseases, as acute kidney injury (AKI). We considered that genetic polymorphisms of these cytokines may have a crucial role in the outcome of critically ill patients. To investigate whether the genetic polymorphisms of rs1800470 (codon 10 T/C), rs1800471 (codon 25 C/G) from the TGF-beta, and rs2430561 (+874 T/A) from IFN-gamma may be a risk factor for ICU patients to the development of AKI and/or death. in a prospective nested case-control study, were included 139 ICU patients who developed AKI, 164 ICU patients without AKI, and 244 healthy individuals. We observed a higher frequency to T/A genotype for IFN-gamma (intermediate producer phenotype) and higher frequency of TT GG and TC GG genotype (high producer) for TGF-beta polymorphism in overall population. However, these polymorphisms have not been shown as a predictor of risk for AKI and death. We found an increased prevalence of high and intermediate producer phenotypes from TGF-beta and IFN-gamma, respectively, in patients in ICU setting. However, the studied genetic polymorphism of the TGF-beta and IFN-gamma was not associated as a risk factor for AKI or death in our population. Universidade Federal de São Paulo, UNIFESP, Div Nephrol, São Paulo, Brazil Hosp Israelita Albert Einstein, São Paulo, Brazil Tufts Univ New England Med Ctr, Boston, MA USA Univ Nove Julho, UNINOVE, São Paulo, Brazil Universidade Federal de São Paulo, UNIFESP, Div Nephrol, São Paulo, Brazil FAPESP: 07/58363-0 Web of Science

Fundação de Amparo à Pesquisa do Estado de São Paulo (FAPESP) Genetic polymorphism studies of cytokines may provide an insight into the understanding of acute kidney injury (AKI) and death in intensive care unit (ICU) patients. the aim of this study was to investigate whether the genetic polymorphisms of -308 G < A tumour necrosis factor (TNF)-alpha, - 174 G > C interleukin (IL)- 6 and - 1082 G > A IL- 10 may predispose ICU patients to the development of AKI and/or death. in a prospective nested case-control study, 303 ICU patients and 244 healthy individuals were evaluated. the study group included ICU patients who developed AKI (n = 139) and 164 ICU patients without AKI. the GG genotype of TNF-alpha (low producer phenotype) was significantly lower in the with AKI than without AKI groups and healthy individuals (55 versus 62 versus 73%, respectively; P = 0.01). When genotypes were stratified into four categories of TNF-alpha/IL-10 combinations, it was observed that low TNF-a plus low IL- 10 producer phenotypes were more prevalent in patients with AKI, renal replacement therapy and death (P < 0.05). in logistic regression analysis, low TNF-alpha producer plus low IL-10 producer phenotypes remained as independent risk factors for AKI and/or death [ odds ratio (OR) = 2.37, 95% confidence interval (CI): 1.16- 4.84; P = 0.02] and for renal replacement therapy (RRT) and/or death (OR = 3.82, 95% CI: 1.19- 12.23; P = 0.02). in this study, the combination of low TNF-alpha plus low IL- 10 producer phenotypes was an independent risk factor to AKI and/or death and RRT and/or death in critically ill patients. Our results should be validated in a larger prospective study with long- term follow- up to emphasize the combination of these genotypes as potential risk factors to AKI in critically ill patients. Universidade Federal de São Paulo, Hosp Israelita Albert Einstein, BR-04039032 São Paulo, Brazil Universidade Federal de São Paulo, Div Nephrol, BR-04039032 São Paulo, Brazil Tufts Univ New England Med Ctr, Boston, MA USA Universidade Federal de São Paulo, Hosp Israelita Albert Einstein, BR-04039032 São Paulo, Brazil Universidade Federal de São Paulo, Div Nephrol, BR-04039032 São Paulo, Brazil FAPESP: 07/58363-0 FAPESP: 05/59242-7 Web of Science

Introduction. Cystatin C has been used in the critical care setting to evaluate renal function. Nevertheless, it has also been found to correlate with mortality, but it is not clear whether this association is due to acute kidney injury (AKI) or to other mechanism. Objective. To evaluate whether serum cystatin C at intensive care unit (ICU) entry predicts AKI and mortality in elderly patients. Materials and Methods. It was a prospective study of ICU elderly patients without AKI at admission. We evaluated 400 patients based on normality for serum cystatin C at ICU entry, of whom 234 (58%) were selected and 45 (19%) developed AKI. Results. We observed that higher serum levels of cystatin C did not predict AKI ( versus mg/L; ). However, it was an independent predictor of mortality, H.R. = 6.16 (95% CI 1.46–26.00; ), in contrast with AKI, which was not associated with death. In the ROC curves, cystatin C also provided a moderate and significant area (0.67; ) compared to AKI (0.47; ) to detect death. Conclusion. We demonstrated that higher cystatin C levels are an independent predictor of mortality in ICU elderly patients and may be used as a marker of poor prognosis.

Background: Patients undergoing orthotropic liver transplant (LTx) often present with chronic kidney disease (CKD). Identification of patients who will progress to end-stage renal disease (ESRD) might allow not only the implementation of kidney protective measures but also simultaneous kidney transplant.Study Design: Retrospective cohort study in adults who underwent LTx at a single center. ESRD, death, and composite of ESRD or death were studied outcomes.Results: 331 patients, who underwent LTx, were followed up for 2.6 +/- 1.4 years; 31(10%) developed ESRD, 6 (2%) underwent kidney transplant after LTx and 25 (8%) remained on chronic hemodialysis. Patients with preoperative eGFR lesser than 60 ml/min per 1.73 m(2) had a 4-fold increased risk of developing ESRD after adjustment for sex, diabetes mellitus, APACHE II score, use of nephrotoxic drugs, and severe liver graft failure (HR = 3.95, 95% CI 1,73, 9.01; p = 0.001). Other independent risk factors for ESRD were preoperative diabetes mellitus and post-operative severe liver graft dysfunction.Conclusion: These findings emphasize low eGFR prior to LTx as a predictor for ESRD or death. the consideration for kidney after liver transplant as a treatment modality should be taken into account for those who develop chronic kidney failure after LTx. Albert Einstein Israelita Hosp HIAE, Learning & Res Inst, Transplantat Program, São Paulo, Brazil Universidade Federal de São Paulo, Div Nephrol, São Paulo, Brazil Euryclides Jesus Zerbini Transplant Hosp Sao Paul, Liver Unit, São Paulo, Brazil Tufts Univ, Sch Med, St Elizabeths Med Ctr, Brighton, MA USA Universidade Federal de São Paulo, Div Nephrol, São Paulo, Brazil Web of Science

Background Acute kidney injury is a common complication of liver transplantation. In this single-centre retrospective observational study, we investigated the impact of acute kidney disease on liver recipient survival. Methods The study population consisted of patients who underwent a liver engraftment between January 2002 and November 2006, at a single transplantation centre in São Paulo, Brazil. Acute kidney injury diagnosis and staging were according to the recommendations of the Acute Kidney Injury Network and consisted of scanning the daily serum creatinine levels throughout the hospital stay. Patients requiring renal replacement therapy prior to transplantation, those who developed acute kidney injury before the procedure or those receiving their second liver graft were excluded from the study. Results A total of 444 liver transplantations were performed during the study period, and 129 procedures (29%) were excluded. The remaining 315 patients constituted the study population. In 207 procedures, the recipient was male (65%). The mean age of the population was 51 years. Cumulative incidence of acute kidney injury within 48 h, during the first week after transplantation, and throughout the hospital stay was 32, 81 and 93%, respectively. Renal replacement therapy was required within a week after the transplantation in 31 procedures (10%), and another 17 (5%) required replacement therapy after that period. Mean follow-up period was 2.3 years. Time in days from acute kidney injury diagnosis to initiation of replacement therapy or reaching serum creatinine peak was associated with lower overall survival even when adjusted for significant potential confounders (HR 1.03; 95% CI 1.01, 1.05; p=0.002). Overall, patients experiencing acute kidney injury lasting for a week or more before initiation of replacement therapy experienced a threefold increase in risk of death (HR 3.02; 95% CI 2.04, 4.46; p Conclusions Acute kidney injury after liver transplantation is remarkably frequent and has a substantial impact on patient survival. Delaying the initiation of renal replacement therapy in such population may increase mortality by more than 20% per day.