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Year : 2009  |  Volume : 53  |  Issue : 4  |  Page : 401-407 Table of Contents     

Renal Dysfunction after Off-Pump Coronary Artery Bypass Surgery- Risk Factors and Preventive Strategies

1 .Consultant, Department of Anesthesiology, Perioperative Medicine And Pain, Apollo Gleneagles Hospitals,Kolkata, India
2 Resident, Department of Anesthesiology, Perioperative Medicine And Pain, Apollo Gleneagles Hospitals,Kolkata, India
3 Hony Consultant, Department of Anesthesiology, Perioperative Medicine And Pain, Apollo Gleneagles Hospitals,Kolkata, India

Date of Web Publication3-Mar-2010

Correspondence Address:
Ahsan Ahmed
C/O-S.M.Nasiruddin, 21, Chamru SinghLane,Kolkata, PIN-700011
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Source of Support: None, Conflict of Interest: None

PMID: 20640201

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Postoperative renal dysfunction is a relatively common and one of the serious complications of cardiac surgery. Though off-pump coronary artery bypass surgery technique avoids cardiopulmonary bypass circuit induced adverse effects on renal function, multiple other factors cause postoperative renal dysfunction in these groups of patients. Acute kidney injury is generally defined as an abrupt and sustained decrease in kidney function. There is no consen­sus on the amount of dysfunction that defines acute kidney injury, with more than 30 definitions in use in the literature today. Although serum creatinine is widely used as a marker for changes in glomerular filtration rate, the criteria used to define renal dysfunction and acute renal failure is highly variable. The variety of definitions used in clinical studies may be partly responsible for the large variations in the reported incidence. Indeed, the lack of a uniform definition for acute kidney injury is believed to be a major impediment to research in the field. To establish a uniform definition for acute kidney injury, the Acute Dialysis Quality Initiative formulated the Risk, Injury, Failure, Loss, and End-stage Kidney (RIFLE ) classification. RIFLE , defines three grades of increasing severity of acute kidney injury -risk (class R), injury (class I) and failure (class F) - and two outcome classes (loss and end-stage kidney disease). Various perioperative risk factors for postoperative renal dysfunction and failure have been identified. Among the important preoperative factors are advanced age, reduced left ventricular function, emergency surgery, preoperative use of intraaortic balloon pump, elevated preoperative serum glucose and creatinine. Most important intraoperative risk factor is the intraoperative haemodynamic instability and all the causes of postoperative low output syndrome com­prise the postoperative risk factors. The most important preventive strategies are the identification of the preoperative risk factors and therefore the high risk groups by developing clinical scoring systems. Preoperative treatment of congestive cardiac failure and volume depletion is mandatory. Avoidance of nephrotoxic drugs and prevention of significant hemodynamic events that may insult the kidney are essential. Perioperative hydration, aggressive control of serum glucose, haemodynamic monitoring and optimization of ventricular function are important strategies. Several drugs have been evaluated with inconsistent results. Dopamine and diuretics once thought to be renoprotective has not been shown to prevent renal failure. Mannitol is probably effective if given before the insult takes place. Some of the newer drugs like fenoldopam, atrial natriuretic peptide, N-acetylcysteine, clonidine and diltiazem have shown some promise in preventing renal dysfunction but more studies are needed to establish their role of renoprotection in cardiac surgery.

Keywords: Off-pump CABG, Renal dysfunction, Risk factors, Preventive strategies

How to cite this article:
Maitra G, Ahmed A, Rudra A, Wankhede R, Sengupta S, Das T. Renal Dysfunction after Off-Pump Coronary Artery Bypass Surgery- Risk Factors and Preventive Strategies. Indian J Anaesth 2009;53:401-7

How to cite this URL:
Maitra G, Ahmed A, Rudra A, Wankhede R, Sengupta S, Das T. Renal Dysfunction after Off-Pump Coronary Artery Bypass Surgery- Risk Factors and Preventive Strategies. Indian J Anaesth [serial online] 2009 [cited 2021 May 10];53:401-7. Available from: https://www.ijaweb.org/text.asp?2009/53/4/401/60310

   Introduction Top

Postoperative renal dysfunction is are latively com­monand one of the serious complications of cardiac surgery. Renal dysfunction orfailure occurs nearly in 8% of all patients undergoing myocardial revascularization [1] . It is multifactorial in origin [2] . Though off-pump coronary artery bypass surgery (OPCAB) technique avoids cardiopulmonary bypass (CPB) cir­cuit induced adverse effects on renal function, multiple otherfactors cause postoperative renal dysfunction in these group of patients [3],[4],[5] . Each year, 600,000 patients worldwide undergo coronary artery bypass surgery [1] . With an increasing numberof elderly populations com­ing for coronary artery bypass surgery, clinicians will continually be challenged to mitigate peioperative re­nalfailure. Compared with patients who do not have postoperative renal dysfunction, patients with renal dysfunction (who do not need dialysis) remain twice as long in both the intensive care unit and hospital wards and have significantly highermortality rate (1% com­pared with 19%) [1],[6],[7] . Furthermore, approximately 1 in 6 patients with renal dysfunction will need dialysis and two third of them will not survive their hospitalization [8],[9],[10],[11]. Many more patients suffer from occult, sub clinical, and transient renal injury without requiring hemodialy­sis. Despite advances in surgical technique and better understanding of the pathophysiology of acute renal failure (ARF), mortality and morbidity associated with ARF have not markedly changed in the last decade [8],[9],[10],[11],[12],[13],[14],[15],[16] . These data highlight the importance of identifying the risk factors associated with cardiac bypass surgery and implementing specific therapies that are based on the knowledge of well designed clinical trials. The lack of progress, though disappointing, offers an opportunity to as certain why we have not been successful.

Definitions and Incidence

Although serum creatinine (Cr) is widely used as amarker for changes in glomerular filtration rate (GFR), the criteria used to define renal dysfunction and acute renal failure (ARF) is highly variable- [1],[2],[3],[4],[12],[13],[14],[15] .Depend­ing upon the definition, the incidence varies across the studies. Some studies used the absolute serum Cr value alone and others used widely differing relative change criteria, this yielded incidence of renal dysfunction rang­ing from 3% to 29% [4],[6],[8],[12],[13],[14],[15] . To establish a uniform definition for acute kidney injury; the Acute Dialysis Quality Initiative formulated the Risk, Injury, Failure, Loss, and End-stage Kidney (RIFLE) classification. RIFLE defines three grades of increasing severity of acute kidney injury- risk(class R), injury (class I) and failure (class F)-and two outcome classes (loss and end-stage kidney disease). A unique feature of the RIFLE classification is that it provides three grades of severity for acute kidney injury based on changes in either serum creatinine or urine output from the baseline condition. This allows classification ofpatients with acute kidney injury into one of the three RIFLE sever­ity. Until recently; no consensus existed about how to best defile, characterize, and study acute renal failure. This lack of a standard definition has been a major im­pediment to the progress of clinical and basic research in this field.

When using RIFLE criteriafor assessment of re­nal dysfunction, two large retrospective studies indi­cate the incidence of acute kidney injury (AKI) after cardiac surgery is about 15% to 20% [17],[18] . Most of the authors define renal failure by the need for dialysis after surgery. Though serum Cr is used as a marker for GFR, it is seen that, GFR may be amore accurate parameter than serum Cr to predict long-term outcome [7],[19].

Perioperative risk factors associated with ARF

Several studies have examined the risk factors associated with the development of po stop erative re­nal failure. Most patients at increased risk forpostop - erative renal dysfunction can be identified before their surgical procedures. Certain preoperative risk factors have been repeatedly associated with an increased risk of ARF [1],[19],[20],[21],[22],[23] . These include female gender, advanced age, reduced left ventricular function or presence of congestive heart failure, diabetes mellitus, chronic ob­structive pulmonary disease, peripheral vascular dis­ease, need for emergent surgery, preoperative use of intraaortic balloon pump (IABP), elevated preopera­tive serum glucose, elevated preoperative serum crea­tinine or patients with preexisting renal disease. The in­cidence ofpostoperative ARF approximately doubles with one preoperative risk factor and quadruples with two risk factors [1] . Increased cardiopulmonary bypass or aortic cross-clamp time (>2hrs) have been consid­ered intraoperative riskfactors for postoperative renal dysfunction [1] . OPCAB (off-pump coronary artery by-­pass) obviously removes the intraoperative risk factors associated with cardiopulmonary bypass circuit. But the greater hemodynamic instability secondary to ven­tricular compression when the heart is manipulated in different positions to access the coronary arteries may be an important contributing factor m development of postoperative renal failure. Though one study [24] showed that the choice of operative techniques (OPCAB vs on-pump CABG) was not associated with reduced renalmorbidity, the bulk of data supported lower risk of ARF in patients who underwent OPCAB [25],[26],[27],[28] . Post­ operative risk factors that critically affect renal function are those that cause or are markers of low output syn­drome -myocardial infarction, hemorrhage, patients requiring IABP, patients with moderate to severe com­promise in ventricularfunction congestive cardiac fail­ure, or use of at least three inotropic drugs. [1] Low car­diac output syndrome in the postoperative period after OPCAB is a high risk for developing ARF as the vul­nerable kidney is subjectedto marginal perfusion pres­sures. Patients requiring an IABP had a nearly seven­fold increase for postoperative renal dysfunction. Use of at least three inotropic drugs is associated with an increased risk for postoperative renal failures [1] .


The pathologic changes in the kidney of patients with ARF following OPCAB are largely assumed to be due to acute tubular necrosis which is usually con­firmed by granular casts in the urine. Hypoxia-ischemia is the predominant cause of perioperative ARF and results from low renal blood flow due to a reduced cardiac output; from regional factors reducing renal blood flow; or from disturbances ofintrarenal blood flow related to inflammation, sepsis or toxin [29] . It was demonstrated that the transmembrane gradient for glomemlarultrafiltration was significantly diminished and there is a back-leak of glornerular ultrafiltrate across the injured epithelium. ARF begins with an early phase of vasomotornephropathy in which there is associated alterations in vasoreactivity and renal perfusion leading to prerenalazotaemia and eventually cellular ATP deple­tion. These ultimately lead to mitochondrial dysfunc­tion and accumulation of intracellular sodium, calcium and reactive oxygen species. Subsequently, multiple enzyme systems are activated and cause disruption of the cytoskeleton, membrane damage, nucleic acid degradation and cell death. Vascular endothelial cell injury induces vascular congestion, edema and infiltration of inflammatory cells. Furthermore, elaborations of inflam­matory mediators lead to additional cellular injury [30],[31],[32],[33],[34],[35] .

Preventive strategies

Perioperative optimization of renal function

Prevention ofp ostoperative renal dysfunction af­ter OPCAB needs knowledge of identifyingthe pre­operative risk factors. Several groups have developed clinical scoring systems that help to predict the risk [20],[21],[22],[23],[36] .The aim is to select patients who are at risk and then to adopt strategies that would offer renal protec­tion. Congestive cardiac failure and volume depletion should be treated preoperatively so as to increase car­diac output and therefore renal perfusion. Medications such as nonsteroidal antiinflammatory drugs (NSAIDs) and other nephrotoxic agents should be discontinued. Preventing significant hem odynarnic events which may insult the kidney and meticulous postoperative care in­cluding optimizing ventricular function, aggressive con­trol of serum glucose and close monitoring of fluid and renal status, perioperative hydration and use ofhemo­dynamic monitoring and inotrop is agents to optimize cardiac output are of important strategies [1] .

Pharmacologic Interventions

Several drugs have been tried in attempting to reduce postoperative renal dysfunction with inconsis­tent results. Loop diuretics increase renal cortical blood flow [37] .However, several studies have shown no ben­efit and possibly even harm from perioperative diuretic therapy in cardiac surgical patients [37],[38],[39],[40] . Therefore, there is insufficient evidence to support the routine use of loop diuretics as specific renoprotective agents. Mannitol, an osmotic diuretic, has been evaluated in several stud­ies of cardiac surgical patients [41],[42] . In addition to the lack of beneficial effect onthe kidney, studies have iden­tified a nephrotoxic potential of high dose ofmannitol especially in patients with preexisting renal insufficiency [43]. Nevertheless, it is probably effective in de­creasingthe severity of the decline in GFR if given before the insult takes place but once the damage is es­tablished there is no evidence of therapeutic benefit [44] . Dopamine at low doses certainly interacts with vascu­lar dopaminergic receptors and stimulates diuresis and natriuresis [45] . However, use in high risk patients has failed to show benefits [46] and it may have widespread adverse effects [47] . So, while dopamine and diuretics were once thought to be renoprotective, neither has demonstrated efficacy to prevent renal failure [48]. Fenoldopam, a selective Dl receptor antagonist, has shown some promise in the prevention of contrast-in­duced nephropathy [49],[50] though randomized controlled studies are very few evaluatingthe efficacy in postop­erative renal dysfunction after cardiac surgery. Few studies showed reduction of renal dysfunction in pa­tients after cardiac surgery [51],[52],[53] , while other studies [54],[55] failed to show any renoprotective effect of fenoldopam. Therefore, more studies are needed to establish its role forreno protection in cardiac surgery. Atria' Natriuretic Peptide (ANP) increases natriuresis by increasing GFR as well as by inhibiting sodium reabsorption by the medullary collecting duct [56] . In a multicentric trial, anaritide, a25- amino acid synthetic form ofANP was administered to critically ill patients to treat acute tubu­lar necrosis. Whether patients received anaritide or not, dialysis free survival was the same for both the groups [57] . In other study, recombinant human ANP (rh ANP) was used to treat ARF after cardiac surgery with a signifi­cant reduction in the incidence of dialysis at day 21 afterthe start of the treatment [58] . N-acetylcysteine (N­AC) has been shown to block oxidant stress on car­diac surgery patients [59] and may hold promise as apro­tective measure. Although it has been used in the pre­vention of contrast-induced nephropathy, two rmeta­analysis concluded that research on N-acetylcysteine andthe incidence of contrast-induced nephropathy are too inconsistent to warrant any definitive conclusion on its effrcacy [60],[61] . Studies of N-AC to prevent postop­erative dysfunction following cardiac surgery did not show any benefit [62],[63] . In a recent study of N-AC to prevent acute kidney injury in cardiac surgery patients with pre-existing moderate renal insufficiency, N-AC did not cause astatistically significant improvement in postoperative estimated GFR; nonetheless its treatment effect was consistent with a plausible smallto moder­ate benefit [64] . Therefore, N-AC should definitely be evaluated in large randomized trial. Activation of sym­pathetic system during and after cardiac surgery may lead to impairment of renal function. Two clinical trials using clonidine (an alpha2 agonist) has been used to attenuate these effects and have shown some promise in preventing deterioration ofrenal function after car­diac surgery [65],[66] . The calcium channelb locker diltiazem has been evaluated as a renoprotective agent in car­diac surgery due to its renal vasodialatory effects [67] . In one study, perioperative infusion of diltiazem for 36 hrs has been shown to increase GFR significantly though tubular function was not influenced [68] . Another studywith 24hrs diltiazem infusion has shown no differences in postoperative serum creatinine levels [69] . Hyperglycemia is common in cardiac surgery and increased serum glu­cose in pre orintraoperative period is independently known to cause ARF after cardiac surgery [1] . Though there is no study of insulin as renoprotective agent for human cardiac surgery, ischemia-reperfusion injury models in rats showed significant benefit ofinsulin if used before the renal insult occured [70] . Prophylactic hemodialysis has also been attempted in a study in pa­tients with highest risk for acute kidney injury which showed a reduction in postoperative ARF requiring dialysis than in the control group [71] . Stillmorerandom­ized trials are needed to support the invasive approach before it can be broadly recommended.

The development of renal dysfunction after car­diac surgery is an independent predictor of poor out­come. We must develop a standard definition of ARF that is sensitive and specific to determine the true inci­dence of this complication, permit an accurate assess­ment of ARE on outcomes, and allow comparison of patients across centers. Early preventive measures may be away of reducing postoperative ARE. Thus, sensi­tive markers of renal injury are desirable for early in­tervention to diminish and minimize the perioperative renal insults. Some recent studies demonstratethat sen­sitive markers of tubular injury may be altered much earlierthan arise in serum creatinine and may allow us to define the time points when injury occurs [72],[73] . However, the studies on kidney-specific proteins vary widely with regard to the marker used, the study period, and the kind of patients and because different `gold stan­dards' of kidney dysfunction were used, neither a sys­tematic review nor a meta-analysis is possible at present [74] . Therefore, future studies should be designed to identify high-risk individuals based on a score and provide timely interventions for prevention or amelio­ration of renal injury to obtain optimal outcomes.

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