Preoperative ACEi/ARB usage was associated with functional but not structural acute kidney injury. As AKI from ACEi/ARB in this setting is unclear, interventional studies testing different strategies of perioperative ACEi/ARB use are warranted.
In many clinical settings, an increased beta-2-microglobulin (beta(2)M) excretion rate indicates renal tubular injury. In this cardiopulmonary bypass (CPB) study, a dopamine infusion (alone or with mannitol) resulted in an increased beta(2)M excretion rate. It is unclear whether this dopamine-related increase implies renal injury after CPB, and further investigations are required to examine the mechanism/clinical relevance of this observation.
Objective
Cardiac surgery is a major cause of acute kidney injury. In this setting receipt of blood transfusions appears to associate with a higher risk of AKI, as measured using serum creatinine values. We examined this association further, using urinary biomarkers of kidney injury.
Methods
1210 adults underwent cardiac surgery and were divided into three groups based on the receipt of intraoperative packed red blood cell units (PRBC): no blood (n=894), ≤ 2 PRBC (n=206) and > 2 PRBC (n=110). AKI was defined as: i) Doubling of serum creatinine from the pre-operative value; ii) first post-operative urinary interleukin-18 in the 5th quintile; iii) first postoperative urinary neutrophil gelatinase-associated lipocalin in the 5th quintile. We determined the relative risk for AKI outcome according to PRBC group after adjusting for 12 pre-operative and surgical variables. Using the Sobel test for mediation analysis, we also evaluated the role of biomarkers in causing AKI through alternative pathways.
Results
AKI was more common in those who received >2 PRBC. In patients receiving > 2 PRBC, the adjusted RRs were 2.3 (95% CI 1.2-4.4, p 0.01), 1.36 (95% CI 1.0-1.9, p 0.05), and 1.34 (95% CI 1.0-1.8, p 0.06) for doubling of serum creatinine, urinary IL-18 in the 5th quintile (>60 pg/ml), and urinary NGAL in the 5th quintile (>102 ng/ml), respectively. Furthermore, the effect of PRBC transfusion on AKI was partially mediated by IL-18.
Conclusions
Receipt of two or more PRBC during cardiac surgery is associated with a greater risk of AKI defined by serum creatinine and kidney injury biomarkers.
We identified the preoperative and intraoperative predictors associated with an increased incidence of postoperative gastrointestinal complications after cardiac surgery using cardiopulmonary bypass. Because these complications are associated with frequent morbidity and mortality, these predictors may be helpful in identifying patients at increased risk so that risk stratification can be modified and perioperative management can be appropriately adjusted.
Background: Acute kidney injury (AKI) is common in patients undergoing cardiac surgery and is associated with a high rate of death, long-term sequelae and healthcare costs. We conducted a systematic review of randomized controlled trials for strategies to prevent or treat AKI in cardiac surgery. Methods: We screened Medline, Scopus, Cochrane Renal Library, and Google Scholar for randomized controlled trails in cardiac surgery for prevention or treatment of AKI in adults. Results: We identified 70 studies that contained a total of 5,554 participants published until November 2008. Most studies were small in sample size, were single-center, focused on preventive strategies, and displayed wide variation in AKI definitions. Only 26% were assessed to be of high quality according to the Jadad criteria. The types of strategies with possible protective efficacy were dopaminergic agents, vasodilators, anti-inflammatory agents, and pump/perfusion strategies. When analyzed separately, dopamine and N-acetylcysteine did not reduce the risk for AKI. Conclusions: This summary of all the literature on prevention and treatment strategies for AKI in cardiac surgery highlights the need for better information. The results advocate large, good-quality, multicenter studies to determine whether promising interventions reliably reduce rates of acute renal replacement therapy and mortality in the cardiac surgery setting.
The new millennium ushered in a number of changes in cardiac surgery. Off-pump coronary artery bypass surgery became technically easier so that multivessel surgery became less of a challenge and cardiologists were supplied with new catheters that accessed lesions that were previously thought of as being unapproachable. New drugs were introduced that made the management of heart failure patients feasible on an outpatient basis, and new devices extend the bridging period to transplantation. However, these advances have not necessarily been attended by significant improvements in outcome, possibly because the less challenging a procedure becomes, the sicker the patients that can be managed. This observation is particularly true with the incidence and outcome of renal failure after cardiac surgery. Bypass factors have been manipulated without much effect, and the traditional drugs that were found to increase renal blood flow in animal experiments did not translate into clinical improvement in renal outcome. Recent research has given us insight into the pathophysiology of ischemic acute renal failure, and it has been found that the paradigm was not as simple as previously thought, possibly accounting for the failure of the more traditional renal drugs (dopamine, mannitol and diuretics). However, these new insights open up the possibility of novel targets for renal protection and repair.
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