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Saudi Journal of Kidney Diseases and Transplantation
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ORIGINAL ARTICLE Table of Contents   
Year : 2009  |  Volume : 20  |  Issue : 2  |  Page : 240-245
Risk score for contrast induced nephropathy following percutaneous coronary intervention


1 Nephrology Department, Mubarak Al Kabeer Hospital, Kuwait
2 Cardiology Department, Al- Sabah Hospital, Ministry of Health, Kuwait

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   Abstract 

Contrast-induced nephropathy (CIN) is an important cause of acute renal failure. Identification of risk factors of CIN and creating a simple risk scoring for CIN after percutaneous coronary intervention (PCI) is important. A prospective single center study was conducted in Kuwait chest disease hospital. All patients admitted to chest disease hospital for PCI from March to May 2005 were included in the study. Total of 247 patients were randomly assigned for the development dataset and 100 for the validation set using the simple random method. The overall occurrence of CIN in the development set was 5.52%. Using multivariate analysis; basal Serum creatinine, shock, female gender, multivessel PCI, and diabetes mellitus were identified as risk factors. Scores assigned to different variables yielded basal creatinine > 115 µmol/L with the highest score(7), followed by shock (3), female gender, multivessel PCI and diabetes mellitus had the same score (2). Patients were further risk stratified into low risk score (< 4), moderate (5-8), high (9-12), and, very high risk score (>_ 12). The developed CIN model demonstrated good dis­criminative power in the validation population. In conclusion, use of a simple risk score for CIN can predict the probability of CIN after PCI; this however needs further validation in larger multi­center trials.

Keywords: Contrast, Nephropathy, Risk score, Coronary intervention

How to cite this article:
Ghani AA, Tohamy KY. Risk score for contrast induced nephropathy following percutaneous coronary intervention. Saudi J Kidney Dis Transpl 2009;20:240-5

How to cite this URL:
Ghani AA, Tohamy KY. Risk score for contrast induced nephropathy following percutaneous coronary intervention. Saudi J Kidney Dis Transpl [serial online] 2009 [cited 2019 Dec 9];20:240-5. Available from: http://www.sjkdt.org/text.asp?2009/20/2/240/45571

   Introduction Top


Contrast-induced nephropathy (CIN) has become a significant source of hospital morbidity and mortality with the ever-increasing use of iodinated contrast media. It is the third most common cause of hospital-acquired acute renal failure, after surgery and hypotension. [1],[2]

CIN is defined as a 25% increase in serum creatinine from the baseline value, or an abso­lute increase of at least 0.5 mg/dL (44.2 µmol/ L), within 48 hours after the administration of radiographic contrast media that is not attributable to other causes. [3],[4],[5],[6],[7],[8]

CIN represents a combination of toxic and ischemic injury to the kidney, predominantly in the medulla. A decrease in medullary blood flow and oxygen tension following exposure to contrast, the increases in vasoconstrictor hor­mones, such as endothelin and adenosine, and loss of vasodilatory factors such as nitric oxide, may contribute to the vasoconstriction that reduces medullary blood flow. [9],[10] Variety of characteristics may predispose to a higher incidence of CIN, most importantly, pre-exis­ting renal impairment and diabetes mellitus. [11],[12],[13],[14]

The aim of the present study was to identify the risk factors and to create a risk scoring for CIN after PCI.


   Patients and Methods Top


A prospective single center study was con­ducted in chest disease hospital of Kuwait from March to May 2005. All patients admitted for PCI were included in the study. Pa­tients on regular dialysis for chronic renal fai­lure, patients with acute renal failure, patients requiring planned pre or postprocedure hemo­dialysis for intractable pulmonary edema, or hyperkalemia, patients exposed to contrast within 14 days before the study and, patients developing complications during PCI were ex­cluded. Written consent was taken before the study.

All patients underwent the procedure using same non ionic contrast media, serum create­nine was assessed before, immediately after and, 48 hours after the procedure. Patients' age, body mass index, hematocrit value, cholesterol level was assessed before the procedure. All patients were hydrated with dextrose half nor­mal saline with sodium bicarbonate at a rate of 1 mL/kg/hr for 4 hours before and 24 hours after the procedure. Those with renal impair­ment before the procedure (serum creatinine above 115 µmol/L) were given N-acetyl cysteine 600 mg twice a day 24 hours before and 48 hours after the procedure.

CIN was defined as an increase in serum creatinine concentration of > 44.2 µmol/L with­in 48 hours after the procedure. 153 patients were excluded based on the exclusion criteria. 247 patients were randomly assigned for the development dataset and 100 were randomly assigned for the validation set.

Statistical Methods

Results are presented as mean ± SD (conti­nuous variables) and percentage of the total (categorical variables). Risk factors were iden­tified by univariate analysis, followed by the forward stepwise logistic selection approach to clarify the risk factors with the strongest in­fluence on CIN using analysis of deviance. Finally, multivariate binary logistic regression model was created and results represented as the regression coefficients, odds ratio (ORs) with 95% CIs. Goodness of fit of the model was tested using Chi-square test. The predicted value of CIN post PCI was calculated. Finally the five variables of the model were assigned a weighted integer coefficient value. The final risk score represented the sum of integer co­efficient.

The risk score was tested in the validation data set and finally, the prognostic significance of risk score on rates of post PCI dialysis was evaluated. Data were analyzed using SPSS for windows version 13 (SPSS, Inc, Chicago, IL).


   Results Top


500 patients underwent PCI during the study period. 153 patients were excluded and a total of 247 patients were included in the develop­ment data set. Patient's demographic data and clinical characteristics were shown [Table 1]. Majority was males, diabetics, over weight and mean age of 63.3 ± 10.2 years. Basal serum creatinine, diabetes, emergency procedure, age above 65, low ejection fraction, heart failure, shock at presentation, multivessel PCI and female gender were the most significant risk factors associated with the development of CIN by univariate analysis [Table 1].

Data of 247 patients; 13 (5.52%) developed CIN; with no missing values was used for mul­tivariate model of predictors of CIN. Basal serum creatinine > 115 µmol/L, shock, female gender, multivessel PCI, and diabetes were iden­tified as risk factors [Table 2]. Goodness of fit of the model was Chi-square = 5.35 (p= 0.37) indicating that the model was appropriate.

The predicted values of CIN post PCI for each variable and corresponding score were estimated. [Table 3] where basal creatinine > 115 µmol/L score was the highest (7) followed by shock (3) while female gender, multivessel PCI and diabetes had the same score of (2).

Patients were further categorized into four groups; low risk score (< 4), moderate (5-8), high (9-12), very high risk score ( > 12).

Validation of the risk score

CIN occurred in (5.0%) of the validation set patients. The rates of CIN in the validation set were close to the rates in the development set in all risk groups [Figure 1]. The developed CIN model demonstrated good discriminative power in the validation population (c_ statistic = 0.61). The ability of the risk score to predict the rates of post- PCI dialysis was evaluated in the development and validation sets. Signifi­cant increases in rates of post- PCI dialysis were reported in those with moderate, high and very high risk scores.

The observed incidence of CIN after PCI was related to the baseline creatinine concentration and the presence of diabetes [Table 4]. Dia­betic patients had significantly higher risk than non diabetics in those with preprocedural serum Cr < 115 µmol/L (3.46% versus 1.46% p value 0.025), while patients with baseline Cr > 115 µmol/L had similar risk (8.12% versus 7.36% p value 0.447)


   Discussion Top


Diagnostic and therapeutic cardiac catheteri­zation has increased remarkably over the recent years and the problem of CIN is similarly faced more frequently. [15] The pathogenesis of CIN is likely complex [16] and a variety of cha­racteristics may predispose to the higher incidence of CIN. [16],[17]

In the present study, we proposed a CIN risk stratification score based on five variables: pre­procedure renal impairment, diabetes mellitus, presence of shock, female gender, and multi­vessel PCI.

Pre-existing renal impairment in our study was the most important risk factor for CIN confirming previous results. [13],[18],[21] This is probably due to a decreased vasodilatory response and a slower clearance of contrast media com­pared to normal subjects. [18] In the present study, the incidence of CIN more than doubled from 2.76%to 8.0% in those with serum creatinine above 115 µmol/L. Similar results were reported by Moore et al [22] and Barrett et al. [23]

Diabetes mellitus similar to previous reports was found as an independent risk factor for CIN. [13],[24],[25] Various mechanisms including altered nitric-oxide dependent renal vasodilata­tion, [26] endothelial dysfunction and decreased vasodialtory response, [27] and presence of pre­existing diabetic nephropathy may all increase the risk of CIN. [28],[29]

The present study showed that females were independently at higher risk of CIN by uni­variate analysis consistent with other studies, [13],[30],[31] while male gender was found to be at a higher risk of CIN in another study. [32] This could be attributed to the effect of ovarian hormones on the renin-angiotensin system and the renal blood flow. [30]

We also found multivessel PCI with increa­sing incidence of CIN. This may be related to the use of high volumes of contrast media [33],[34],[35],[36] and already compromised renal vessels due to atherosclerosis. [37]

Shock due to its hemodynamic effect, reflec­ting the acuteness of the study and probable use of larger volumes of contrast media, was a risk factor associated with CIN in our study. [38] This needed to be included in the risk stratifi­cation since the emergency nature of the study would influence the other variables and pre­ventive measures become a secondary consideration. Adequate risk assessment prior to procedure offers a greater opportunity to prevent CIN. In the absence of effective thera­peutic measures for CIN and greater cost and associated morbidity prevention remains the best option. [39],[40] CIN risk scoring could be used to predict the outcome after contrast injection and help in increasing awareness as well as initiate preventive measures.

In conclusion a simple risk score for CIN can be utilized to predict the probability of CIN after PCI and therefore more vigilance in applying preventive measures.


   Acknowledgment Top


We would like to express our deepest thanks to Dr. Nadra-elwgoud M.I. Abdou, lecturer of Infectious diseases and Epidemiology, Faculty of Veterinary Medicine, Cairo University, for statistical analysis.

 
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Correspondence Address:
Amal Abdel Ghani
Nephrology Unit, Mubarak Al Kabeer Hospital, P.O. Box 43787, Code 3205 Hawally
Kuwait
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