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Acute kidney injury in major abdominal surgery: incidence, risk factors, pathogenesis and outcomes
Annals of Intensive Care volume 8, Article number: 22 (2018)
Acute kidney injury (AKI) is a common complication in patients undergoing major abdominal surgery. Various recent studies using modern standardized classifications for AKI reported a variable incidence of AKI after major abdominal surgery ranging from 3 to 35%. Several patient-related, procedure-related factors and postoperative complications were identified as risk factors for AKI in this setting. AKI following major abdominal surgery has been shown to be associated with poor short- and long-term outcomes. Herein, we provide a contemporary and critical review of AKI after major abdominal surgery focusing on its incidence, risk factors, pathogeny and outcomes.
Acute kidney injury (AKI) is a common occurrence in hospitalized patients and it has a detrimental effect on patient outcome. Indeed, AKI is associated with increased costs, length of hospital stay and in-hospital mortality [1,2,3]. Postoperative AKI has been associated with higher risk of developing chronic kidney disease (CKD) [4, 5] and increased early [6,7,8,9,10,11,12,13,14,15,16,17] and long-term mortality [10,11,12,13,14,15,16,17,18,19,20,21,22], comparable to the consequences of AKI facing critically ill patients. Postoperative AKI is hence of particular interest, serving as a measurable indicator of perioperative harm and an important potential target for intervention .
The clinical characteristics and the impact of AKI in cardiac surgery have been extensively studied [24, 25], and most of the published data regarding AKI in the noncardiac surgery population are limited to high-risk aortic procedures [26,27,28,29,30,31]. Abdominal surgery is frequently associated with AKI. Recently, a number of studies have addressed AKI following major abdominal surgery [11, 19, 32, 33], especially since it shows a pathophysiology that is distinct from that of cardiac and vascular surgery. Therefore, it is unsuitable to assume that the risk factors for AKI after abdominal surgery are the same as those after cardiac and vascular surgery. The purpose of this review is therefore to perform a critical and contemporary review of the incidence, risk factors, pathogenesis and outcome of AKI in patients undergoing major nonvascular abdominal surgery.
Incidence, risk factors and pathogenesis
Over the last decade, the definition of AKI has evolved from the former term acute renal failure to a set of uniform criteria combining small changes in creatinine and urine output ultimately defining AKI . The first definition of AKI, the Risk, Injury, Failure, Loss of kidney function and End-stage kidney disease (RIFLE) classification, was published in 2004 . In 2007, the Acute Kidney Injury Network (AKIN) classification, also known as ‘modified RIFLE’, was published . In recent times, the RIFLE and AKIN classifications have been merged into the Kidney Disease: Improving Global Outcomes (KDIGO) classification in order to provide simpler and more integrated criteria applicable in clinical activity, research, and public health surveillance. (Table 1)  AKI is thus defined as an increase in serum creatinine (SCr) by ≥ 0.3 mg/dl (≥ 26.5 μmol/l) within 48 h; or an increase in SCr to ≥ 1.5 times the baseline value, which is known or presumed to have occurred within the prior 7 days; or urine volume < 0.5 ml/kg/h for 6 h . These classifications also categorize patients according to the severity of AKI .
In the past decades, the incidence of AKI has suffered an increase and has been related to multiple factors such as an increasingly aging population, increasing number of comorbidities of the hospitalized population, increased prevalence of chronic kidney disease and diabetes, and the liberal use of intravenous contrast agents for imaging and cardiovascular intervention procedures .
Additionally, mortality has been trending downwards despite the reported modifications in the clinical profile and characteristics of patients with AKI [40, 41]. Nonetheless, it is not clear if this fact can be credited to an improvement in patient care or to specific interventions or therapies directed at those with AKI [42, 43].
Depending on the classification system employed in the studies, the reported incidence of AKI varies from 5.0 to 7.5% in hospitalized patients, reaching up to 50–60% in critically ill patients [2, 44,45,46].
Surgery remains a leading cause of AKI in hospitalized patients, accounting for up to 40% of in-hospital AKI cases. The incidence of AKI in this group of patients is variable, depending on the surgical setting and the AKI definition used, with the highest rates found after cardiac (18.7%), general (13.2%), and thoracic (12.0%) surgeries [47, 48].
A considerable heterogeneity regarding the rate of AKI reported has been shown in recent studies of AKI following major abdominal surgery. (Table 2) The incidence varied between 3.1 and 35.3%, with the majority of patients in all studies placing in the less severe stage of AKI (Risk or Stage 1). One of the major limitations of these studies is that, only three evaluated simultaneously serum creatinine and urine output to define and categorize AKI, as recommended .
Urine output (UO) is a sensitive and early marker for AKI, independent of serum creatinine, thereby included as a criterion to diagnose AKI [49, 50]. However, recent literature reports that there is a physiologic reduction in UO as a result from hypovolemia, anesthesia and release of aldosterone and vasopressin in response to stress, which raises the hypothesis that UO may not be a reliable criterion for postoperative AKI, or that the threshold for AKI diagnosis with UO should be lower [51,52,53].
Research has focused on serum and urine biomarkers that could predict AKI before functional damage occurs . This has been investigated mainly in cardiac procedures, with the most promising marker being plasma and urinary neutrophil gelatinase-associated lipocalin (NGAL) . Also, the combination of urinary Kidney Injury Molecule-1 (KIM-1), N-acetyl-beta-d-glucosaminidase, and NGAL improved the sensitivity of early recognition of postoperative AKI when compared with individual biomarkers . Recently, tissue inhibitor of metalloproteinases-2 (TIMP-2) and insulin-like growth factor binding protein 7 (IGFBP7) have been validated as risk predictors for AKI .
According to a recently published meta-analysis of 19 studies representing 82,514 patients undergoing abdominal surgery, the pooled incidence of AKI was 13.4% . However, the incidence did not significantly vary by AKI definition, surgical category or inclusion or exclusion of preexisting CKD, demonstrating that other factors are probably also implied, such as the different surgical settings and baseline patient characteristics between individual studies .
A number of studies have investigated and identified patient- and procedure-related risk factors associated with the development of AKI, namely older age, African American race, hypertension, diabetes mellitus and CKD [20, 48]. Patient-related factors are often more strongly associated with postoperative mortality than surgical factors .
Focusing on major abdominal surgery, demographic patient characteristics such as male gender, older age, and higher body mass index, as well as preexisting CKD, hypertension, cardiovascular disease, diabetes, chronic obstructive pulmonary disease, metastatic cancer, hypoalbuminemia, use of angiotensin-converting enzyme inhibitors (ACEI) or angiotensin-receptor blockers have been implicated as predisposing to AKI [8, 9, 58,59,60,61,62,63,64,65].
Additionally, several risk assessment scores have been associated with higher incidence of AKI. A higher MELD score, which predicts liver failure progression; a higher Revised Cardiac Index score, developed to predict cardiac complications and mortality after major noncardiac surgery; and higher SAPS II score, used to evaluate disease severity, have all been independently associated with AKI [8, 63, 65, 66].
Numerous studies have established the negative bearing of surgery or procedure-related factors in AKI in major abdominal surgery, specifically the use of intravenous contrast for vascular imaging and intervention, the use of diuretics and vasopressors, more invasive procedures, episodes of intraoperative hemodynamic instability, need for intraoperative blood transfusions, large colloid infusion during surgery, epidural anesthesia in liver resections and cases of emergent surgery [8, 9, 58, 60,61,62,63, 65, 67,68,69].
Nevertheless, the impact of the urgency of surgery has not been consensual in all studies. For instance, urgent surgery was not associated with an increased risk of postoperative AKI in a recent study by Teixeira et al. , despite the higher incidence of risk factors for AKI in these patients.
The role of laparoscopy has also been studied as the creation of a pneumoperitoneum is concomitant to increased intraabdominal pressure and the associated hormonal modifications that have been associated with decreased renal blood flow and could be linked to AKI . Nevertheless, Teixeira et al.  demonstrated no difference in AKI between patients undergoing laparoscopy versus laparotomy.
O’Connor et al.  essayed to determine AKI incidence in different surgical settings, namely gastrointestinal, upper gastrointestinal, hepato-biliary, colorectal and major gynecological surgeries, however they were not able to demonstrate a significant difference in pooled AKI between these subgroups due to substantial heterogeneity between the studies. Similarly, in the study by Teixeira et al., colorectal surgery had an increased rate of AKI, which was not evidenced in other surgery types such as gastric, hepato-biliary and pancreatic, small bowel and esophageal. However, this finding was not independently associated with a higher risk of postoperative AKI . These studies did not analyze the incidence of AKI after liver transplant surgery which can reach up to 70%, as it includes several specific risk factors in its pathogenesis, namely those related to the recipient and graft [70, 71]. Also important to consider, with the increasing prevalence of obesity in the global population, the prevalence of bariatric surgery has risen in the past decades and AKI has also been reported in 5–10% of these patients [72, 73].
Growing evidence has demonstrated that the need for intraoperative blood transfusions may contribute to organ injury in susceptible patients by promoting a pro-inflammatory state, exacerbating tissue oxidative stress, and activating leukocytes and the coagulation cascade, thus impairing oxygen delivery paradoxically [74,75,76].
Colloids have been used for acute fluid resuscitation in trauma, perioperatively and in critically ill patients, due to their longer intravascular persistence. Recent studies have shown no evidence of a significant mortality benefit from resuscitation with colloids [77,78,79,80,81]. In critically ill patients, the use of hydroxyethyl starch has been associated with AKI [77, 82]. However, this association has not been demonstrated in the surgical setting, namely after living donor hepatectomy, cardiac surgery, or gastroenterological surgery [83,84,85].
Furthermore, patients who developed significant postoperative complications, such as leak, respiratory failure and sepsis, also have an increased rate of AKI [58, 59, 61, 62] (Fig. 1).
The pathogenesis of postoperative AKI is complex and multifactorial. In this setting, we must consider not only the effects of fluid depletion, but also the neuroendocrine response to anesthesia and surgery itself [86, 87].
Fluid depletion includes the preoperative period as a result of the routine nil-by mouth regimens and the loss of fluid through concomitant pathology, and the perioperative period resulting from blood and intravascular fluid losses, insensible losses, and the so-called third space effect, through extravasation of fluid out of the vascular compartment. Mechanical ventilation of the intubated patient constitutes an additional mechanism for increased fluid loss during general anesthesia. The perioperative fluid requirements vary according to the extent of the surgical insult .
The renal response to hypoperfusion is afferent arteriole dilation and efferent arteriole vasoconstriction to maintain glomerular filtration in addition to neurohormonal responses as a means to expand the intravascular volume [57, 86, 87]. The increases in sympathomimetic hormones lead to renal cortical vasoconstriction, which is a compensatory attempt to redistribute blood flow to the renal medulla, but in fact causes ischemia of the medulla which is particularly vulnerable due to its elevated metabolic demand [57, 86, 87].
Most anesthetics cause peripheral vasodilatation and myocardial depression, also impairing kidney perfusion [86, 87]. The effect of the surgery results in both an increase in catabolic hormones and cytokines, leading to increased secretion of antidiuretic hormone, which will result in water retention. Increases in aldosterone, through activation of the renin–angiotensin system, associated with increased glucocorticoids cause sodium and water retention and potassium loss. Plasma renin activity is also elevated as a result of a decrease in circulating blood volume. Thus, adjustments in overall fluid and electrolyte homeostasis occur on account of impaired water excretion, impaired sodium excretion, and increased excretion of potassium .
Patients with long-term ACEI therapy have higher risk of postoperative renal dysfunction as a result of a loss of ability of the renin–angiotensin system to compensate for decreases in renal perfusion [86, 87].
Ischemic kidneys are more susceptible to continuing detrimental insults, such as, nephrotoxins and sepsis . Nephrotoxins such as contrast media increase intrarenal vasoconstriction, decrease medullary blood supply and present the medullary nephrons with an increased osmotic load leading to an increased oxygen requirement in the presence of an already low tissue oxygen tension .
Nevertheless, in most cases, hemodynamic or toxic actions seem to be insufficient in the pathogenesis of AKI . The role of nonhemodynamic factors, such as dysfunctional inflammatory cascades, oxidative stress, activation of proapoptotic pathways, differential molecular expression, and leukocyte trafficking, in AKI has been increasingly recognized [89, 90]. During abdominal surgery, a pro-inflammatory response is activated by the released endotoxin load from gut ischemia, impaired visceral perfusion, and portal endotoxaemia . Furthermore, in the postischemic or reperfusion period there is further tubular injury caused by reactive oxygen species and tissue inflammation [90, 92]. The immune activation following AKI appears to negatively impact other organs .
Various studies have verified the deleterious impact of AKI on the early outcomes of patients, namely longer lengths of hospital stay, increased healthcare costs, increased mortality and an increased likelihood of discharge to an extended care facility [46, 93,94,95,96,97]. Granting that AKI patients may have more comorbidities than non-AKI patients, these do not appear to account for all of the increased early mortality associated with AKI [3, 46, 97, 98]. Other factors should perhaps be regarded since even increases in SCr considered as minor lead to worse outcomes [88, 97, 98]. Accordingly, AKI has been progressively more thought of as part of a systemic disease with underlying mechanisms that cause multiorgan dysfunction including the kidney, which could help explain the decreased survival observed in AKI patients [87, 99].
An observational study by Grams et al. demonstrated an association between postoperative AKI after major surgery and longer lengths of stay (15.8 vs 8.6 days) and higher rates of 30-day hospital readmission (21 vs 13%) .
The association between a higher incidence of other postoperative complications, increased length of stay, higher healthcare costs and increased hospital readmissions and postoperative AKI related to major abdominal surgery has also been widely described. Lee et al. performed a retrospective analysis of 595 esophageal cancer surgery patients and established that the extent of hospital stay was significantly longer in patients with AKI . In a retrospective review of 339 colectomies by Causey et al., AKI development was associated with a 5-day increase in hospital length of stay and nearly doubled the rate of other infectious complications (56 vs 30%) . Tomozawa et al. reported that AKI after liver resection surgery was correlated with prolonged length of stay, and increased rates of artificial ventilation, need for reintubation, and requirement for renal replacement therapy . In a retrospective study by Kim et al. gastric surgery patients with AKI had significantly longer hospital stay and higher prevalence of intensive care unit (ICU) admission after the operation (mean 18.7 vs 12.0 days, P < 0.001; 9.1 vs 1.2%, P < 0.001, respectively) .
The influence of postoperative AKI on higher in-hospital and 30-day mortality has also been demonstrated after major abdominal surgery. Kim et al. conducted a retrospective study of 4718 gastric surgery patients and reported that the in-hospital and 3-month mortality for patients with AKI were significantly higher than those for patients without AKI (3.5 vs 0.2%, P < 0.001; 3.8 vs 0.3%, P < 0.001, respectively), and moreover that the rate of in-hospital and 3-month mortality increased with the advancement in the stage of AKI, in a stepwise manner . In a retrospective analysis of 642 liver resection patients by Tomozawa et al., AKI was associated with increased mortality (14.1 vs 2.3%, P < 0.0001) . In a study by Teixeira, et al., 450 major abdominal surgery patients were retrospectively studied and postoperative AKI was independently associated with increased in-hospital mortality (20.8 vs 2.3%, P < .0001; unadjusted OR 11.2, 95% CI 4.8–26.2, P < .0001; adjusted OR 3.7, 95% CI 1.2–11.7, P = 0.024), furthermore there was a direct relationship between more severe AKI and increased in-hospital mortality . O’Connor has also recently reported a 12.6-fold relative mortality risk in patients with postoperative AKI after major abdominal surgery .
Additionally, it is known that the detrimental effects of AKI persist after hospitalization, with greater risk of developing CKD and increased long-term mortality in AKI patients [20, 100, 101]. Progression to CKD results from an inadequate resolution of the acute insult following AKI, with persistent inflammation, increased transformation of pericytes into myofibroblasts in response to tubular injury, and consequent build-up of extracellular matrix and vascular rarefaction, leading to permanent scarring in renal structure and changes in renal function . The risk of development or progression of CKD occurs in proportion to the severity of AKI . The increased risk of proteinuria and hypertension and GFR decline described after AKI are known risk factors for cardiovascular disease, and may contribute to the decrement in survival observed among AKI survivors [104,105,106,107].
The long-term effect of AKI in postoperative patients has also been described. In a retrospective cohort study of 10,518 patients with AKI discharged after a major surgery, Bihorac et al.  reported that even small changes in creatinine level during hospitalization were associated with an independent long-term risk of death. Also, Grams et al.  performed an observational study of 3.6 million veterans submitted to major surgery and described an association between postoperative AKI and 1-year end-stage renal disease (0.94 vs 0.05%), and mortality (19 vs 8%), with more severe stage of AKI relating to poorer outcomes.
In a retrospective cohort of 390 major abdominal surgery patients, Gameiro et al.  demonstrated that AKI was independently associated with worse renal outcomes, comprising renal function decline and/or long-term need for dialysis (47.2 vs 22.0%, P < 0.0001), as well as with mortality after hospital discharge (47.2 vs 20.5%, P < 0.0001).
AKI is a frequent occurrence following major abdominal surgery and is independently associated with both in-hospital and long-term mortality, as well as with a higher risk of progressing to CKD. Preventive strategies such as hemodynamics stabilization, fluid balance control, evasion of nephrotoxins, improved preoperative patient management (body weight reduction, hypertension, diabetes, cardiovascular and pulmonary disease control) and prevention/treatment of any postoperative complications encountered could potentially reduce postoperative AKI and thereby improve patient outcomes.
acute kidney injury
chronic kidney disease
Risk, Injury, Failure, Loss of kidney function and End-stage kidney disease
Acute Kidney Injury Network
Kidney Disease: Improving Global Outcomes
angiotensin-converting enzyme inhibitors
Model for end-stage liver disease
- SAPS II:
Simplified Acute Physiology Score
intensive care unit
kidney injury molecule-1
neutrophil gelatinase-associated lipocalin
Chertow G, Burdick E, Honour M, Bonventre J, Bates D. Acute kidney injury, mortality, length of stay, and costs in hospitalized patients. J Am Soc Nephrol. 2005;16(11):3365–70.
Uchino S, Kellum JA, Bellomo R, et al. Beginning and Ending Supportive Therapy for the Kidney (BEST Kidney) Investigators. Acute renal failure in critically ill patients: a multinational, multicenter study. JAMA. 2005;294(7):813–8.
Barrantes F, Tian J, Vazquez R, Amoateng-Adjepong Y, Manthous CA. Acute kidney injury criteria predict outcomes of critically ill patients. Crit Care Med. 2008;36:1397–403.
Cho E, Kim SC, Kim MG, Jo S-K, Cho W-Y, Kim H-K. The incidence and risk factors of acute kidney injury after hepatobiliary surgery: a prospective observational study. BMC Nephrol. 2014;15:169.
Ryden L, Sartipy U, Evans M, Holzmann MJ. Acute kidney injury after coronary artery bypass grafting and long-term risk of end-stage renal disease. Circulation. 2014;130:2005–11.
Elmistekawy E, McDonald B, Hudson C, et al. Clinical impact of mild acute kidney injury after cardiac surgery. Ann Thorac Surg. 2014;98:815–22.
Hobson C, Ozrazgat-Baslanti T, Kuxhausen A, et al. Cost and mortality associated with postoperative acute kidney injury. Ann Surg. 2015;261:1207–14.
Teixeira C, Rosa R, Rodrigues N, et al. Acute kidney injury after major abdominal surgery: a retrospective cohort analysis. Crit Care Res Pract. 2014;2014:132175.
Vaught A, Ozrazgat-Baslanti T, Javed A, et al. Acute kidney injury in major gynaecological surgery: an observational study. BJOG. 2015;122:1340–8.
Harris DG, Koo G, McCrone MP, et al. Acute kidney injury in critically ill vascular surgery patients is common and associated with increased mortality. Front Surg. 2015;2:8.
Abelha FJ, Botelho M, Fernandes V, et al. Determinants of post-operative acute kidney injury. Crit Care. 2009;13:R79.
Biteker M, Dayan A, Tekkesin AI, et al. Incidence, risk factors, and outcomes of perioperative acute kidney injury in noncardiac and nonvascular surgery. Am J Surg. 2014;207:53–9.
Drews JD, Patel HJ, Williams DM, et al. The impact of acute renal failure on early and late outcomes after thoracic aortic endovascular repair. Ann Thorac Surg. 2014;97:2027–33 (discussion 2033).
Kandler K, Jensen ME, Nilsson JC, et al. Acute kidney injury is independently associated with higher mortality after cardiac surgery. J Cardiothorac Vasc Anesth. 2014;28:1448–52.
Munoz-Garcia AJ, Munoz-Garcia E, Jimenez-Navarro MF, et al. Clinical impact of acute kidney injury on short- and long-term outcomes after transcatheter aortic valve implantation with the CoreValve prosthesis. J Cardiol. 2015;66:46–9.
Zhu JC, Chen SL, Jin GZ, et al. Acute renal injury after thoracic endovascular aortic repair of Stanford type B aortic dissection: incidence, risk factors, and prognosis. J Formos Med Assoc. 2014;113:612–9.
Pickering JW, James MT, Palmer SC. Acute kidney injury and prognosis after cardiopulmonary bypass: a meta-analysis of cohort studies. Am J Kidney Dis. 2015;65:283–93.
Adalbert S, Adelina M, Romulus T, et al. Acute kidney injury in peripheral arterial surgery patients: a cohort study. Ren Fail. 2013;35:1236–9.
Kheterpal S, Tremper KK, Englesbe MJ, et al. Predictors of post-operative acute renal failure after noncardiac surgery in patients with previously normal renal function. Anesthesiology. 2007;107:892–902.
Bihorac A, Yavas S, Subbiah S, et al. Long-term risk of mortality and acute kidney injury during hospitalization after major surgery. Ann Surg. 2009;249:851–8.
Hobson CE, Yavas S, Segal MS, et al. Acute kidney injury is associated with increased long-term mortality after cardiothoracic surgery. Circulation. 2009;119:2444–53.
Hansen MK, Gammelager H, Mikkelsen MM, et al. Postoperative acute kidney injury and five-year risk of death, myocardial infarction, and stroke among elective cardiac surgical patients: a cohort study. Crit Care. 2013;17:R292.
O’Connor M, Kirwan C, Pearse R, Prowle JR. Incidence and associations of acute kidney injury after major abdominal surgery. Intensive Care Med. 2016;42(4):521–30.
Sirvinskas E, Andrejaitiene J, Raliene L, et al. Cardiopulmonary bypass management and acute renal failure: risk factors and prognosis. Perfusion. 2008;23(6):323–7.
De Santo LS, Romano G, Galdieri N, et al. RIFLE criteria for acute kidney injury in valvular surgery. J Heart Valve Dis. 2010;19(1):139–47 (discussion 148).
Svensson L, Crawford E, Hess K, Coselli J, Safi H. Experience with 1509 patients undergoing thoracoabdominal aortic operations. J Vasc Surg. 1993;17(2):357–68 (discussion 368–70).
Svensson L, Coselli J, Safi H, Hess K, Crawford E. Appraisal of adjuncts to prevent acute renal failure after surgery on the thoracic or thoracoabdominal aorta. J Vasc Surg. 1989;10(3):230–9.
Wald R, Waikar S, Liangos O, Pereira B, Chertow G, Jaber B. Acute renal failure after endovascular vs open repair of abdominal aortic aneurysm. J Vasc Surg. 2006;43(3):460–6 (discussion 466).
Tallgren M, Niemi T, Pöyhiä R, et al. Acute renal injury and dysfunction following elective abdominal aortic surgery. Eur J Vasc Endovasc Surg. 2007;33(5):550–5.
Arnaoutakis G, Bihorac A, Martin T, et al. RIFLE criteria for acute kidney injury in aortic arch surgery. J Thorac Cardiovasc Surg. 2007;134(6):1554–60 (discussion 1560–1).
Mori Y, Sato N, Kobayashi Y, Ochiai R. Acute kidney injury during aortic arch surgery under deep hypothermic circulatory arrest. J Anesth. 2011;25(6):799–804.
Causey M, Maykel J, Hatch Q, Miller S, Steele S. Identifying risk factors for renal failure and myocardial infarction following colorectal surgery. J Surg Res. 2011;170(1):32–7.
Cho A, Lee J, Kwon G, et al. Post-operative acute kidney injury in patients with renal cell carcinoma is a potent risk factor for new-onset chronic kidney disease after radical nephrectomy. Nephrol Dial Transplant. 2011;26(11):3496–501.
Sawhney S, Fraser SD. Epidemiology of AKI: utilizing large databases to determine the burden of AKI. Adv Chronic Kidney Dis. 2017;24(4):194–204.
Bellomo R, Ronco C, Kellum JA, et al. Acute renal failure—definition, outcome measures, animal models, fluid therapy and information technology needs: the Second International Consensus Conference of the Acute Dialysis Quality Initiative (ADQI) Group. Crit Care. 2004;8:R204–12.
Mehta RL, Kellum JA, Shah SV, et al. Acute Kidney Injury Network: report of an initiative to improve outcomes in acute kidney injury. Crit Care. 2007;11(2):R31.
Kidney Disease: Improving Global Outcomes (KDIGO) Acute Kidney Injury Work Group. KDIGO clinical practice guideline for acute kidney injury. Kidney Int Suppl. 2012;2:S1–138.
Kellum JA, Lameire N, KDIGO AKI Guideline Work Group. Diagnosis, evaluation, and management of acute kidney injury: a KDIGO summary (Part 1). Crit Care. 2013;17(1):204.
Lameire N, Van Biesen W, Vanholder R. The changing epidemiology of acute renal failure. Nat Clin Nephrol. 2006;2:364–77.
Brown J, Rezaee M, Marshall E, Matheny M. Hospital mortality in the United States following acute kidney injury. Biomed Res Int. 2016;2016:4278579.
Ympa YP, Sakr Y, Reinhart K, Vincent JL. Has mortality from acute renal failure decreased? A systematic review of the literature. Am J Med. 2005;118:827–32.
Liaño F, Junco E, Pascual J, Madero R, Verde E. The spectrum of acute renal failure in the intensive care unit compared with that seen in other settings. The Madrid Acute Renal Failure Study Group. Kidney Int Suppl. 1998;66:S16–24.
Bellomo R. The epidemiology of acute renal failure: 1975 versus 2005. Curr Opin Crit Care. 2006;12:557–60.
Thakar CV, Christianson A, Freyberg R, Almenoff P, Render ML. Incidence and outcomes of acute kidney injury in intensive care units: a Veterans Administration study. Crit Care Med. 2009;37(9):2552–8.
Case J, Khan S, Khalid R, Khan A. Epidemiology of acute kidney injury in the intensive care unit. Crit Care Res Pract. 2013;2013:479730.
Hoste EA, Clermont G, Kersten A, et al. RIFLE criteria for acute kidney injury are associated with hospital mortality in critically ill patients: a cohort analysis. Crit Care. 2006;10(3):R73.
Thakar CV. Perioperative acute kidney injury. Adv Chronic Kidney Dis. 2013;20:67–75.
Grams ME, Sang Y, Coresh J, et al. Acute kidney injury after major surgery: a retrospective analysis of veteran’s health administration data. Am J Kidney Dis. 2016;67(6):872–80.
Macedo E. Urine output assessment as a clinical quality measure. Nephron. 2015;131:252–4.
Macedo E, Malhotra R, Bouchard J, Wynn S, Mehta R. Oliguria is an early predictor of higher mortality in critically ill patients. Kidney Int. 2011;80(7):760–7.
Alpert RA, Roizen MF, Hamilton WK, et al. Intraoperative urinary output does not predict postoperative renal function in patients undergoing abdominal aortic revascularization. Surgery. 1984;95:707–11.
Hahn RG. Volume kinetics for infusion fluids. Anesthesiology. 2010;113(2):470–81.
Goren O, Matot I. Perioperative acute kidney injury. Br J Anaesth. 2015;115(Suppl 2):ii3–14.
Koyner JL, Parikh CR. Clinical utility of biomarkers of AKI in cardiac surgery and critical illness. Clin J Am Soc Nephrol. 2013;8(6):1034–42.
Han WK, Wagener G, Zhu Y, Wang S, Lee HT. Urinary biomarkers in the early detection of acute kidney injury after cardiac surgery. Clin J Am Soc Nephrol. 2009;4(5):873–82.
Meersch M, Schmidt C, Van Aken H, et al. Urinary TIMP-2 and IGFBP7 as early biomarkers of acute kidney injury and renal recovery following cardiac surgery. PLoS ONE. 2014;9(3):e93460.
Calvert S, Shaw A. Perioperative acute kidney injury. Perioper Med. 2012;4(1):6.
Bell S, Davey P, Nathwani D, et al. Risk of AKI with gentamicin as surgical prophylaxis. J Am Soc Nephrol. 2014;25(11):2625–32.
Armstrong T, Welsh FK, Wells J, Chandrakumaran K, John TG, Rees M. The impact of pre-operative serum creatinine on short-term outcomes after liver resection. HPB (Oxford). 2009;11:622–8.
Correa-Gallego C, Berman A, Denis SC, et al. Renal function after low central venous pressure-assisted liver resection: assessment of 2116 cases. HPB (Oxford). 2015;17:258–64.
Causey MW, Maykel JA, Hatch Q, Miller S, Steele SR. Identifying risk factors for renal failure and myocardial infarction following colorectal surgery. J Surg Res. 2011;170:32–7.
Lee EH, Kim HR, Baek SH, et al. Risk factors of postoperative acute kidney injury in patients undergoing esophageal cancer surgery. J Cardiothorac Vasc Anesth. 2014;28:948–54.
Bredt L, Peres L. Risk factors for acute kidney injury after partial hepatectomy. World J Hepatol. 2017;9(18):815–22.
Slankamenac K, Breitenstein S, Held U, Beck-Schimmer B, Puhan MA, Clavien PA. Development and validation of a prediction score for postoperative acute renal failure following liver resection. Ann Surg. 2009;250:720–8.
Tomozawa A, Ishikawa S, Shiota N, Cholvisudhi P, Makita K. Perioperative risk factors for acute kidney injury after liver resection surgery: an historical cohort study. Can J Anaesth. 2015;62:753–61.
Ford MK, Beattie SW, Wijeysundera DN. systematic review: prediction of perioperative cardiac complications and mortality by the revised cardiac risk index. Ann Intern Med. 2010;152:26–35.
Kambakamba P, Slankamenac K, Tschuor C, et al. Epidural analgesia and perioperative kidney function after major liver resection. Br J Surg. 2015;102:805–12.
Kim CS, Oak CY, Kim HY, et al. Incidence, predictive factors, and clinical outcomes of acute kidney injury after gastric surgery for gastric cancer. PLoS ONE. 2013;8:e82289.
Sun LY, Wijeysundera DN, Tait GA, Beattie WS. Association of intraoperative hypotension with acute kidney injury after elective noncardiac surgery. Anesthesiology. 2015;123:515–23.
de Haan JE, Hoorn EJ, de Geus HRH. Acute kidney injury after liver transplantation: recent insights and future perspectives. Best Pract Res Clin Gastroenterol. 2017;31(2):161–9.
Chen J, Singhapricha T, Hu K-Q, et al. Postliver transplant acute renal injury and failure by the RIFLE criteria in patients with normal pretransplant serum creatinine concentrations: a matched study. Transplantation. 2011;91:348–53.
Thakar CV, Kharat V, Blanck S, Leonard AC. Acute kidney injury after gastric bypass surgery. Clin J Am Soc Nephrol. 2007;2(3):426–30.
Weingarten TN, Gurrieri C, McCaffrey JM, et al. Acute kidney injury following bariatric surgery. Obes Surg. 2013;23(1):64–70.
Almac E, Ince C. The impact of storage on red cell function in blood transfusion. Best Pract Res Clin Anaesthesiol. 2007;21(2):195–208.
Koch C, Li L, Sessler D, et al. Duration of red-cell storage and complications after cardiac surgery. N Engl J Med. 2008;358(12):1229–39.
Karkouti K, Wijeysundera D, Yau TM, et al. Acute kidney injury after cardiac surgery. Focus on modifiable risk factors. Circulation. 2009;119(4):495–502.
Ricci Z, Romagnoli S, Ronco C. Perioperative intravascular volume replacement and kidney insufficiency. Best Pract Res Clin Anaesthesiol. 2012;26(4):463–74.
Myburgh JA, Finfer S, Bellomo R, et al. Hydroxyethyl starch or saline for fluid resuscitation in intensive care. N Engl J Med. 2012;367:1901–11.
Perel P, Roberts I, Ker K. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev. 2013;2:CD000567.
Raiman M, Mitchell C, Biccard B, Rodseth R. Comparison of hydroxyethyl starch colloids with crystalloids for surgical patients: a systematic review and meta-analysis. Eur J Anaesthesiol. 2016;33(1):42–8.
Zazzeron L, Gattinoni L, Caironi P, et al. Role of albumin, starches and gelatins versus crystalloids in volume resuscitation of critically ill patients. Curr Opin Crit Care. 2016;22(5):428–36.
Shaw AD, Kellum JA. The risk of AKI in patients treated with intravenous solutions containing hydroxyethyl starch. Clin J Am Soc Nephrol. 2013;8(3):497–503.
Kim SK, Choi SS, Sim JH, et al. Effect of hydroxyethyl starch on acute kidney injury after living donor hepatectomy. Transplant Proc. 2016;48(1):102–6.
Vives M, Callejas R, Duque P, et al. Modern hydroxyethyl starch and acute kidney injury after cardiac surgery: a prospective multicentre cohort. Br J Anaesth. 2016;117(4):458–63.
Umegaki T, Uba T, Sumi C, et al. Impact of hydroxyethyl starch 70/0.5 on acute kidney injury after gastroenterological surgery. Korean J Anesthesiol. 2016;69(5):460–7.
Sear J. Kidney dysfunction in the postoperative period. Br J Anaesth. 2005;95(1):20–32.
Carmichael P, Carmichael AR. Acute renal failure in the surgical setting. ANZ J Surg. 2003;73:144–53.
Levy EM, Viscoli CM, Horwitz RI. The effect of acute renal failure on mortality. A cohort analysis. JAMA. 1996;275:1489–94.
Grams ME, Rabb H. The distant organ effects of acute kidney injury. Kidney Int. 2012;81:942–8.
Kerrigan CL, Stotland MA. Ischemia reperfusion injury: a review. Microsurgery. 1993;14:165–75.
Welborn MB, Oldenburg HS, Hess PJ, et al. The relationship between visceral ischemia, proinflammatory cytokines, and organ injury in patients undergoing thoracoabdominal aortic aneurysm repair. Crit Care Med. 2000;28:3191–7.
Gobe G, Willgoss D, Hogg N, Schoch E, Endre Z. Cell survival or death in renal tubular epithelium after ischemia- reperfusion injury. Kidney Int. 1999;56:1299–304.
Neves JB, Jorge S, Lopes JA. Acute kidney injury: epidemiology, diagnosis, prognosis, and future directions. EMJ Nephrol. 2015;3(1):90–6.
Chertow GM, Burdick E, Honour M, Bonventre JV, Bates DW. Acute kidney injury, mortality, length of stay, and costs in hospitalized patients. J Am Soc Nephrol. 2005;16:3365–70.
Lopes JA, Fernandes P, Jorge S, et al. Acute kidney injury in intensive care unit patients: a comparison between the RIFLE and the Acute Kidney Injury Network classifications. Crit Care. 2008;12(R110):16–31.
Ostermann M, Chang RW. Acute kidney injury in the intensive care unit according to RIFLE. Crit Care Med. 2007;35:1837–43.
Lai CF, Wu VC, Huang TM, et al. Kidney function decline after a non-dialysis-requiring acute kidney injury is associated with higher long-term mortality in critically ill survivors. Crit Care. 2012;16:R123.
Coca SG, Peixoto AJ, Garg AX, Krumholz HM, Parikh CR. The prognostic importance of a small acute decrement in kidney function in hospitalized patients: a systematic review and meta-analysis. Am J Kidney Dis. 2007;50(5):712–20.
Li X, Hassoun HT, Santora R, Rabb H. Organ crosstalk: the role of the kidney. Curr Opin Crit Care. 2009;15:481–7.
Coca SG, Yusuf B, Shlipak MG, Garg AX, Parikh CR. Long-term risk of mortality and other adverse outcomes after acute kidney injury: a systematic review and meta-analysis. Am J Kidney Dis. 2009;53:961–73.
Linder A, Fjell C, Levin A, Walley KR, Russell JA, Boyd JH. Small acute increases in serum creatinine are associated with decreased long-term survival in the critically ill. Am J Respir Crit Care Med. 2014;189(9):1075–81.
Ferenbach DA, Bonventre JV. Mechanisms of maladaptive repair after AKI leading to accelerated kidney ageing and CKD. Nat Rev Nephrol. 2015;11(5):264–76.
Coca SG, Singanamala S, Parikh CR. Chronic kidney disease after acute kidney injury: a systematic review and meta-analysis. Kidney Int. 2012;81:442–8.
Spurgeon-Pechman KR, Donohoe DL, Mattson DL, Lund H, James L, Basile DP. Recovery from acute renal failure predisposes hypertension and secondary renal disease in response to elevated sodium. Am J Physiol Renal Physiol. 2007;293:F269–78.
Basile DP. The endothelial cell in ischemic acute kidney injury: implications for acute and chronic function. Kidney Int. 2007;72:151–6.
Sarafidis PA, Bakris GL. Microalbuminuria and chronic kidney disease as risk factors for cardiovascular disease. Nephrol Dial Transplant. 2006;21:2366–74.
Go AS, Chertow GM, Fan D, McCulloch CE, Hsu CY. Chronic kidney disease and the risks of death, cardiovascular events, and hospitalization. N Engl J Med. 2004;351:1296–305.
Gameiro J, Neves JB, Rodrigues N, et al. Acute kidney injury, long-term renal function and mortality in patients undergoing major abdominal surgery: a cohort analysis. Clin Kidney J. 2016;9(2):192–200.
The authors participated as follows: JG and JAF drafted the article, SJ and MN revised the article, JAL revised the article and approved the final version to be submitted for publication. All authors read and approved the final manuscript.
The authors declare that they have no competing interests.
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Gameiro, J., Fonseca, J.A., Neves, M. et al. Acute kidney injury in major abdominal surgery: incidence, risk factors, pathogenesis and outcomes. Ann. Intensive Care 8, 22 (2018). https://doi.org/10.1186/s13613-018-0369-7
- Acute kidney injury
- Risk factors