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Ann Thorac Surg 2010;89:689-694. doi:10.1016/j.athoracsur.2009.11.018
© 2010 The Society of Thoracic Surgeons
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Original Articles: Adult Cardiac

Serum Cystatin C in Elderly Cardiac Surgery Patients

Anne Ristikankare, MDa,*, Reino Pöyhiä, MD, PhDa, Anne Kuitunen, MD, PhDa, Markus Skrifvars, MD, PhDa, Pekka Hämmäinen, MD, PhDb, Markku Salmenperä, MD, PhDa, Raili Suojaranta-Ylinen, MD, PhDa

a Department of Anesthesia and Intensive Care Medicine, Helsinki University Central Hospital, Helsinki, Finland
b Department of Cardiothoracic Surgery, Helsinki University Central Hospital, Helsinki, Finland

Accepted for publication November 4, 2009.

* Address correspondence to Dr Ristikankare, Department of Anesthesiology and Intensive Care Medicine, Helsinki University Hospital, PO Box 340, Helsinki FI - 00029 HUS, Finland (Email: anne.ristikankare{at}hus.fi).


CARDIOTHORACIC ANESTHESIOLOGY: The Annals of Thoracic Surgery CME Program is located online at http://cme.ctsnetjournals.org. To take the CME activity related to this article, you must have either an STS member or an individual non-member subscription to the journal.

 

   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Comment
 References
 
Background: Elderly cardiac surgery patients are more prone to develop postoperative acute kidney injury (AKI). The common clinical glomerular filtration marker, plasma creatinine, is considered to be inadequate to discover AKI in its early stage. The aim of this study was to determine if serum cystatin C can detect mild renal failure earlier than plasma creatinine.

Methods: From 110 cardiac surgery patients aged 70 or greater years, serum cystatin C and plasma creatinine samples were collected preoperatively and on postoperative days 1 to 5. Their urine output, creatinine, and estimated glomerular filtration rate were calculated and AKI was determined by the risk-injury-failure-loss-end-stage kidney disease criteria (RIFLE). The correlation of plasma creatinine and serum cystatin C to AKI was calculated.

Results: After cardiac surgery, 62 of the 110 patients (56.4%) developed AKI according to the RIFLE classification. In this group, both serum cystatin C and plasma creatinine peaked on postoperative day 3. Cystatin C and creatinine correlated equally with AKI at different time points calculated with receiver operating characteristic curves. On postoperative day 1 the area under the curve (AUC) for creatinine was 0.66 (0.55 to 0.76) and for cystatin C 0.71 (0.61 to 0.81); {Delta} AUC 0.05 (0.01 to 0.12), p = 0.11. On postoperative day 2 the AUC for creatinine was 0.74 (0.64 to 0.83) and for cystatin was C 0.77 (0.68 to 0.86); {Delta} AUC –0.03 (–0.09 to 0.03), p = 0.32.

Conclusions: Elderly cardiac surgery patients have a high incidence of AKI, as defined by the RIFLE criteria. After cardiac surgery serum cystatin C and plasma creatinine detected AKI similarly.

Acute kidney injury (AKI) is a serious complication which is associated with morbidity and mortality after cardiac surgery [1, 2]. Because glomerular filtration rate (GFR) decreases with age, and preoperative renal dysfunction has been identified as an important risk factor for postoperative renal failure, older cardiac surgical patients may have a greater risk of postoperative AKI [3, 4]. Even with normal renal function, elderly cardiac surgery patients have more subclinical alterations in renal function, measured by sensitive kidney specific proteins, than do younger patients [5]. The incidence of postoperative AKI has not decreased in recent years despite ongoing research. One of the considered reasons for this is the absence of biomarkers for early detection of AKI [6]. Even though there is no evidence-based method for the prevention of AKI, the adequate monitoring of hemodynamics, avoidance of hypovolemia, hypotension, and nephrotoxic drugs, and the early onset of renal replacement therapy (RRT) might improve the patient's outcome [7, 8]. Serum creatinine, which is most commonly used in clinical practice to measure GFR, is well known to be an insensitive indicator of renal dysfunction in its early stages [9]. The serum concentration of creatinine is affected by age, gender, muscle mass, medication, and hydration status, which all need to be carefully assessed in elderly cardiac surgical patients. Moreover, serum creatinine concentration may not change until 50% of kidney function has already been lost [9]. It has been proposed that serum cystatin C would be a reliable early indicator of renal dysfunction and more accurate than creatinine [10, 11].

Cystatin C is a nonglycosylated low molecular weight plasma protein (13.3 kDa) produced at a constant rate by all nucleated cells. It is freely filtered by the glomerulus, reabsorbed, and catabolized in the proximal tubule. Because cystatin C is eliminated almost solely by filtration in the renal glomerulus, its serum concentration provides a highly sensitive estimate of GFR [12, 13]. Serum cystatin C concentrations have demonstrated good inverse correlation with radionuclide-derived measurements of GFR [10]. It is less influenced by age and muscle mass than serum creatinine, and it may be more sensitive to early and mild changes in kidney function compared with creatinine [14–16].

So far, only a few studies have been published about serum cystatin C in cardiac surgery. In these studies it has performed as a promising indicator for renal dysfunction [17–19]. As none of these studies included patients in advanced age, we conducted this study to evaluate whether cystatin C is a valid indicator of AKI in elderly cardiac surgery patients.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Comment
 References
 
The Ethics Committee for Surgery in the Hospital District of Helsinki and Uusimaa approved this prospective study. Between January 2004 and December 2006, 110 patients aged 70 years or older undergoing cardiac surgery at the Helsinki University Hospital were included in the study after they provided written informed consent. Patients undergoing an operation without cardiopulmonary bypass (CPB) or requiring renal replacement therapy prior to surgery were excluded. All procedures were morning starts.

Anesthesia and CPB
On the morning of the surgery patients received their routine cardiac medication, excluding angiotensin-converting enzyme inhibitors and angiotensin II receptor antagonists. Patients who were treated with cortisone or thyroid hormone substitutes before the surgery continued to receive their medication up to and including the morning of the surgery. A glucocorticoid substitute was given during and after surgery; a thyroxin substitute was administered when patients normally took their medication orally.

An attending anesthesiologist decided whether to administer aprotinin or tranexamic acid during the surgery, otherwise anesthesia and CPB management were standardized. Anesthesia was induced with intravenous propofol or etomidate and sufentanil and maintained with inhaled sevoflurane and continuous infusion of sufentanil. Muscle relaxation was provided by rocuronium. Cardiopulmonary bypass was performed using a roller pump with a nonpulsatile flow of 2.4 L · minute–1 · m–2, hollow-fiber membrane oxygenator, and arterial filter. The perfusion circuit was primed with Ringer's acetate, and 10% mannitol (100 mL) was added to the priming solution. During CPB the patients were allowed to cool passively to 30°C to 32°C, and were rewarmed to 36°C before withdrawing CPB. During CPB mean arterial pressure was maintained between 50 and 90 mm Hg and the hematocrit above 20%. Myocardial protection was achieved with intermittent cold antegrade or retrograde crystalloid cardioplegia with blood in a ratio of 4:1 or 8:1. During surgery mediastinal suction blood was returned to the venous reservoir, and after the patient was weaned from CPB the content of the circuit was collected and returned to the patient. If the cardiac index after CPB decreased below 2.0 L · minute–1 · m–2, pulmonary capillary wedge pressure was maintained at least at 10 mm Hg, and an epinephrine infusion (0.02 to 0.2 µg · kg–1 · minute–1) was started. Norepinephrine was administrated when the mean systematic arterial pressure was below 70 mm Hg despite adequate pulmonary capillary wedge pressure. Milrinone and an intraaortic balloon pump were available for further cardiac support. Hemodynamic measurements, medication given, fluid balance, and laboratory results were recorded intraoperatively and postoperatively in the intensive care unit (ICU) with routine computerized data collection.

Laboratory Measurements
Blood samples for plasma creatinine and serum cystatin C were obtained before surgery in the operation room as a baseline and in the morning of 1 to 5 postoperative days. Thus, the first postoperative samples were collected from 15 to18 hours after operation and the follow-ups in 24-hour intervals. The samples were analyzed at the Helsinki University Hospital Laboratory. Serum cystatin C concentrations were analyzed with the Dako Cytomation Denmark A/S (Glostrup, Denmark) particle-enhanced immunoturbidimetric cystatin C assay adapted for the Hitachi 917 analyzer (Tokyo, Japan). Plasma creatinine was analyzed with the enzymatic CREA plus assay method of Roche Diagnostics GmbH (Mannheim, Germany) on a Hitachi Modular analyzer. The reference values for the upper limits of normal were 1.2 mg/L for serum cystatin C and 1.14 mg/dL for plasma creatinine.

We used the plasma creatinine values to estimate GFR with the modification of diet renal disease equation (MDRD): GFR = 175 x plasma creatinine level (mg/dL) –1.154 x age –0.203 x 0.742 (if female), GFR in mL · minute–1 · (1.73 m2)–1 [20]. To determine the degree of renal failure after surgery we used the risk, injury, failure, loss, end-stage kidney disease (RIFLE) criteria [21]. According to these criteria we divided AKI into three levels based on plasma creatinine levels or calculated GFR: (1) R = risk (increased PCrea by 1.5-fold or GFR decrease > 25%); (2) I = injury (increased PCrea by twofold or GFR decrease > 50%); (3) F = failure (increased PCrea by threefold or GFR decrease ≥ 75% or PCrea ≥ 4 mg/dL). Urine output was measured on the first postoperative day to detect AKI according to the RIFLE criteria, in which an output less than 0.5 mL · kg–1 · hour–1 during 6 or more hours is considered a risk. In this study, all the patients who had an AKI according to urine output also had decreased GFR that met the criteria. We determined the RIFLE status every morning days 1 to 5 after surgery.

Statistical Analysis
The patient data and results are reported as median and interquartile ranges (IQRs) for continuous variables, and as counts or percentages for categoric data. We compared the groups using the Mann-Whitney U test or independent samples t test and categoric variables using the {chi}2 test, followed by the Fisher exact test when appropriate. The proportional changes of creatinine and cystatin C values over the time in patients of the AKI group we tested with a repeated measures analysis of variance (ANOVA), with values over time (five time points) as within factors, the marker for AKI (cystatin C or creatinine) as the between factor and the interactions of these two markers over time. The appropriate F value as a measure of variance and p values for testing for statistical significance of the factors were calculated. We used receiver operating characteristics (ROC) curves with the respective areas under the curve (AUC) to visualize the discriminative ability of creatinine and cystatin C to predict the later occurrence of AKI, as defined by the presence of any of the RIFLE categories, at different time points. The time points studied were before surgery, and on the first and second postoperative days. The generated ROC curves and the AUC values were compared using a nonparametric method. Statistical analyses were performed with statistical software (SPSS package, version 13.0; Chicago, IL and Analyse-it software Ltd, Leeds, UK).


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Comment
 References
 
Baseline characteristics and intraoperative data are presented in Table 1. Of the 110 enrolled patients 20 (18.2%) had preoperative creatinine levels above the normal limit [median 1.39 (1.21 to 1.63) mg/dL]. Among all the patients, 48 (43.6%) did not have any deterioration in renal function and 62 (56.4%) developed AKI according to the RIFLE classification; with 48 at the risk level, 12 at the injury level, and 1 at the failure level. The majority of AKI incidences (47 patients of 62) occurred during the first three days after surgery. Patients with diabetes and peripheral arteriosclerosis were more prone to develop AKI after surgery (Table 1).


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  		Table 1 Demographic and Intraoperative Data. Results Are Presented as Medians and the Interquartile Range, Counts, and Percentages
 
Creatinine increased over 50% in 30 (48.3%) patients on the postoperative days 1 to 3 in the AKI group and cystatin C increased over 50% in 17 (27.4%) patients in the AKI group. The 50% increase of creatinine occurred in 7 (23%) patients on day 1, in 8 (27%) patients on day 2, and in 15 (50%) patients on day 3 postoperatively. Cystatin C increased in 3 (18%) patients on the day 1, in 9 (53%) patients on the day 2, and in 5 (29%) patients on day 3 postoperatively. Both creatinine and cystatin C peaked on postoperative day 3 (see Table 2). The ANOVA analysis indicated that in the AKI group there was an effect of time (both markers changed over time), there was a significant difference between the two markers (ie, the magnitudes of the proportional changes were different) but the interaction over time was not significant (thus the proportional changes occurred in a similar way in the two markers over time) (Fig 1).


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  		Table 2 Median and Interquartile Range Values of Plasma Creatinine, Serum Cystatin C, and GFR Before Surgery and on Postoperative Days 1 to 3
 

Figure 1
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  		Fig 1. The proportional change of creatinine (•) and cystatin C ({blacksquare}) after cardiac surgery in patients with acute kidney injury as defined by the risk, injury, failure, loss, and end-stage kidney disease criteria. The change is relative to the preoperative creatinine or cystatin C value, respectively.

 
The ROC curves for the absolute values of creatinine and cystatin C at different time points showed equal correlation with AKI defined by the later presence of the RIFLE criteria. Before the creatinine and cystatin C peaked on postoperative day 3, the AUCs of cystatin C and creatinine were not significantly different from one another (Fig 2A,B). There was no difference in the change of values over the first postoperative day between creatinine and cystatin C; the {Delta} AUC for both of them was 0.77 (0.69 to 0.86), p = 0.93.


Figure 2
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  		Fig 2. Receiver operating characteristic curves for the absolute values of creatinine (light grey line) and cystatin C (dashed line) on postoperative days 1 (A) and 2 (B).

 
There was no significant difference between the AKI and non-AKI groups in the cardiac index in different time points. In addition, the AKI and non-AKI groups did not differ in the use of perioperative and postoperative inotropes and loop-diuretics, fluid balance, blood loss, and red blood cell transfusions (data not shown). During the hospital stay three patients required RRT. The renal failure patient in the AKI group had complications during the surgery and RRT was started on day 2 postoperatively. One patient, who received RRT but did not have AKI during the study period, had a late cardiac tamponade on day 6 and developed renal failure. The other patient had an ischemic colon and multiorgan failure a week after cardiac surgery and received RRT but later died of complications. Four patients had an intraaortic balloon pump postoperatively, and one of them also had renal replacement therapy. The 30-day mortality was 2.7% (3 of 110).


   Comment
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
References
 
The incidence of AKI (56.4%) in this study was higher than in other studies (7% to 25%) performed in elderly cardiac surgery patients [22, 23]. However, the incidence of AKI after cardiac surgery depends highly on the diagnostic criteria. We chose to use the RIFLE criteria as it has been recently shown to be applicable for the assessment of postcardiac surgery renal failure [24]. Although the golden standard for GFR measurement is based on the clearance of inulin, its use is complex, expensive, and impractical in the clinical use of cardiac surgical patients or in large clinical trials [25]. In the absence of any other validated measures, we used changes in estimated GFR calculated with the MDRD formula to determine the development of AKI. The MDRD formula is most commonly calculated from serum creatinine levels, which are prone to extrarenal factors explained previously. Furthermore, real time changes in GFR may not be observed with using creatinine because it requires time to accumulate before abnormal levels are detected [9].

Could serum cystatin C be used for the assessment of postoperative renal injury in elderly cardiac surgery patients? Cystatin C has a lower variability of measurements, a shorter half life, and a lower distribution volume than creatinine, which make cystatin C an attractive tool for assessment of AKI [25]. In elderly patients with chronic renal insufficiency, cystatin C based on MDRD equations have been more accurate then creatinine-based estimates [25].

However, only a few studies have assessed cystatin C in acute kidney injury so far. In the ICU setting cystatin C has correlated better with GFR than creatinine, when patients had only mild renal dysfunction [26]. With more severe renal impairment cystatin C has been comparable with creatinine, but in one study with 85 ICU patients cystatin C revealed AKI 1 to 2 days earlier than creatinine [27, 28]. Abu-Omar and colleagues [17] found a good correlation between cystatin C and creatinine in 60 patients after coronary artery surgery but could not demonstrate any superiority of cystatin C to creatinine. Zhu and colleagues [19] determined serum cystatin C, serum creatinine, and 24-hour creatinine clearance rate in 60 patients undergoing heart valve replacement. They showed that cystatin C not only correlated better with creatinine clearance rate, but it also peaked a day earlier than creatinine. We have now shown that the diagnostic performance of cystatin C is similar to plasma creatinine to detect postoperative AKI in patients over 70 years of age. In patients with AKI, both creatinine and cystatin C increased significantly, reaching the peak on postoperative day 3. Even though there was no significant difference between these two markers, creatinine increased over 50% most often on the third postoperative day as cystatin C increased over 50% mostly on the second postoperative day in the AKI group.

There is evidence to suggest that cystatin C levels could be useful for identification of patients developing AKI after cardiac surgery. In a recent single center study of patients undergoing cardiac surgery, GFR as estimated with cystatin C was an independent risk factor for hospital morbidity and mortality and for one year mortality, while GFR estimated with creatinine did not reveal a similar association [29]. Haase-Fielitz and colleagues [18] reported recently that plasma neutrophil gelatinase-associated lipocalin, a novel biomarker of kidney injury, and serum cystatin C revealed renal dysfunction earlier compared with creatinine and urea. In patients who developed AKI, cystatin C levels in serum were already significantly more elevated 6 hours after surgery than those of creatinine and urea but 24 hours after surgery all measured renal tests were equally increased [18]. In our study the first postoperative measurements of cystatin C and creatinine were performed at 15 to 18 hours after the arrival to ICU, which may have been too late to detect any difference between them. We did not measure urinary cystatin C, which has been shown to increase rapidly in patients with AKI after cardiac surgery [30]. Further studies are needed to clarify the optimal timing to measure cystatin C concentrations after cardiac surgery.

Old age, male sex, larger body size, current cigarette smoking, and higher serum C-reactive protein levels have been suggested to associate independently with higher serum cystatin C levels [31]. Cystatin C may also be a marker of inflammation, which might explain the association with C-reactive protein, a fact which may even be taken into consideration when cystatin C levels are measured right after CPB [31, 32]. Finally, both thyroid hormone disorders and corticosteroid therapy affect serum cystatin C concentration, but in studies conducted in the ICU and among cardiac surgery patients neither have had any significant influence on cystatin C [19, 28]. In the present study the preoperative use of thyroxin or corticosteroids was not associated with elevated cystatin C.

Cystatin C has been described to detect mild to moderate renal dysfunction earlier than creatinine, but the number of included patients in these studies has been relatively small [18, 19, 28]. The sample size of the present study was not formally assessed because no information was available for the variance of serum creatinine or cystatin C in elderly patients after cardiac surgery. Therefore, 110 patients were included in this study and were decided to post hoc compare confidence intervals of the creatinine and cystatin C AUC values and their difference, as a surrogate measure of power of the study.

The current study was underpowered to assess the relationship between creatinine or cystatin C and severe renal failure, requiring renal replacement therapy. This needs to be addressed in large-scale prospective trials.

In summary, AKI remains a major complication after cardiac surgery in elderly patients, and in the absence of specific methods for preventing this injury, early recognition of kidney dysfunction is crucial. In this study with elderly cardiac surgery patients serum cystatin C could not detect mild renal injury earlier than plasma creatinine and did not produce further aid to the diagnosis of AKI. Further studies are needed to establish the role of serum and urinary cystatin C in the assessment of renal deterioration during and after heart surgery.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Comment
 References
 

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