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Introduction
Contrast-induced nephropathy (CIN) is defined as the impairment of renal function and is measured as either a 25% increase in serum creatinine (SCr) from baseline or 0.5 mg/dL increase in absolute value, within 48-72 hours of intravenous contrast administration.(1)-(3)
CIN is an important cause of acute kidney injury (AKI) in hospitalized patients being reported as the third most common cause of kidney injury in patients who underwent interventional radiologic procedures. (4) However, the incidence of CIN is less than 2%(5) although, in patients with chronic kidney disease (CKD) the incidence is more than 12%, as well as in patients who developed an acute coronary syndrome (ACS) and underwent an urgent percutaneous coronary intervention (PCI). (6) Even more, is also associated with excess mortality and longer hospital stay. (7),(8)
The pathophysiology of CIN (Figure 1) is based on contrast media (CM) which act on distinct anatomic sites within the kidney and exert adverse effects via multiple mechanisms. They cause a direct cytotoxic effect on the renal proximal tubular cells, enhance cellular damage by reactive oxygen species, and increase resistance to renal blood flow. They also exacerbate renal vasoconstriction, particularly in the deeper portions of the outer medulla.(9),(10)
CIN is normally a transient process, with renal functions reverting to the baseline within 7-14 days of contrast administration.(9) Less than one-third patients develop some degree of residual renal impairment, and renal replacement therapy is required in less than 1% of patients, with a slightly higher incidence in patients with underlying AKI raising the mortality up to 17%, compared with just 3.9% in patients who don't develop AKI. (11)-(13) Preexisting renal impairment and diabetes mellitus appears to be primary risk factors for CIN.(13)
The presence of dehydration, anemia, congestive heart failure (New York Heart Association (NYHA) III-IV), age > 70 years, gout, the use of nephrotoxic and NSAID drugs, all these increase the risk for AKI. Patients undergoing primary PCI for myocardial infarction got some extra risk factors to develop CIN (hemodynamic instability, severe transient hypotension, use of intra-aortic balloon counterpulsation, undergoing emergency procedures and arterial contrast administration).(14)-(16)
The leading predictor for CIN is a pre-existent kidney injury, which increases more than 20 folds the risk for developing CIN, when glomerular filtration rate (GFR) is < 45 mL/min/1.73 m2. Furthermore, it has been found that not only decreased in the glomerular filtration rate predicts the appearance of contrast nephropathy; proteinuria plus a decreased GFR increases the incidence.(17)
There is few evidence in the literature review that evaluates the incidence and the risk factors that are associated with contrast media use in patients with ischemic cardiomyopathy that underwent a diagnostic or therapeutic PCI.
The objective of this study was to calculate the incidence of CIN and to describe the clinical and periprocedural risk factors for patients receiving contrast media and as a secondary objective was to compare mortality between patients who developed CIN and those who not. Our hypothesis is that the incidence and the risk factors of CIN is equal than the literature.
Material and methods
Study design
In a cohort, observational, descriptive and retrospective study, patients who were admitted to the hospital for diagnostic and/or therapeutic PCI between January 2014 to September 2015 and the serum creatinine and GFR were measured previous to the angiography (day 0) and 72 hours after contrast administration were included in the study. The GFR was calculated by the Modification Diet in Renal Disease (MDRD) formula. Risk factors to develop CIN and protective factors to prevent CIN were included in the study.
Inclusion criteria
1. Patients older than 18 years old who were admitted to the hospital Christus Muguerza Alta Especialidad, in Monterrey, Nuevo Leon, Mexico and underwent to PCI and had a serum creatinine measured prior to contrast administration, as well as 72 hours after the procedure.
Exclusion criteria
Patients who were in renal replacement therapy (peritoneal dialysis or hemodialysis).
Patients who did not complete a minimum 24-hours stay at the hospital.
Patients who did not have serum creatinine levels at the day of angiography (day 0) and 72 hours after the procedure.
Patients who had a previous AKI episode.
Statistics
Microsoft Excel and Medcalc® were used. Continuous variables were expressed with median and standard deviation, and qualitative variables as percentage. Continuous variables were analyzed with student's t test and categorical variables with χ2 test. Multivariate analysis was performed by logistic regression of the variables and results were expressed with odds ratio with confidence intervals of 95% and were expressed as a significant result when p < 0.05. It was calculated a given sample size of 64 patients to accomplish a significance of 0.05 and a beta error of 20%.
Conceptual definitions
Contrast-induced nephropathy: the impairment of renal function and is measured as either a 25% increase in serum creatinine (SCr) from baseline or 0.5 mg/dL increase in absolute value, within 48-72 hours of intravenous contrast administration.
Anemia: it was defined using the World Health Organization criteria as hemoglobin < 13 g/dL in men and < 12 g/dL in women.
Hypotension: blood pressure less than 90/60 mmHg.
Nephroprotective actions: hydratation, N-acetylcisteine or sodium bicarbonate use.
Results
During the period covered from January 2014 to September 2015, one hundred and four coronary angiographies were performed, of them 34 patients were excluded because did not meet the inclusion criteria. Seventy patients met the inclusion criteria; 10 patients developed AKI, with an incidence in our hospital of 14.2%. From these patients during the hospital stay, 3 (30%) died, and 1 (10%) required hemodialysis after angiography.
In patients who developed AKI (Table I), a predominance of males was observed, 7 out of 10 patients were men (70%), with a median age of 74.2 (± 8.10) years, however, in patients who did not develop AKI the mean age was lower at 59.18 (± 14.61) (p = 0.0024).
Among the demographic variables, patients with decreased renal function, 30% had diabetes mellitus type 2, 60% had high arterial hypertension and 10% had congestive heart failure. On admission, 6 (60%) patients with AKI had anemia compared with 10 (16.6%) patients without AKI (p = 0.0089).
The average baseline creatinine was similar in both groups with an average about 1 mg/dL, however showed difference at 72 hours; in the CIN group the mean was 1.87 (± 0.69) mg/dL, compared with 0.97 (± 0.29) in the group without CIN (p < 0.0001). This correlated with a reduced GFR at 72 hours in patients with AKI (42.88 [± 21.30] versus 90.92 [± 36.34], p < 0.0001).
It was found that intra-aortic balloon counterpulsation use (40% versus 3.33%, p = 0.0013) and the presence of periprocedural hypotension (40% versus 10% p = 0.043) was greater in patients with CIN, however in the multivariate analysis no significant difference was observed.
No difference was found in the type and amount of contrast media used between both groups, nevertheless patients who had a longer angiography time were more likely to develop AKI (112 min. [± 36.41] versus 71.86 min. [± 28.10], p = 0.0002).
By using the area under the curve analysis, time longer than 90 minutes showed a higher risk for development of AKI with an 80% sensibility and an 86.4% specificity, positive likelihood ratio of 6 (2.9-12.3) and a negative likelihood ratio of 0.52 (0.1-1.9). No difference was found in patients underwent to urgent procedure for develop CIN.
Also the area under the curve analysis for the amount of contrast media showed that more than 200 mL of contrast media was associated with further risk of development of CIN, with a sensibility of 80%, a specificity of 38%, a positive likelihood ratio of 1.33 (0.9-1.9) and a negative likelihood ratio of 0.52 (0.1-1.9).
Significant difference in mortality was found, being greater in those patients who developed CIN (30% versus 1.6%, p = 0.004). A 30-fold increase in mortality was documented in patients who developed CIN (OR 29.57; 95CI 2.7-323.7, p = 0.005).
A multivariate analysis was performed (Table II), showing a strong association to develop CIN in patients with age greater than 65 years (OR 12.6; 95CI 1.6-105.9, p = 0.03); anemia onset prior to the procedure (OR 7.5; 95CI 1.8-31.2, p = 0.006); and a median procedure time more than 90 minutes (OR 16; 95CI 3.1-85.3, p = 0.001).
Discussion
The major finding of this study was that the incidence of CIN media was 14.2%, higher than reported in similar studies such as that of Rihal et al;(11) showing that it is a common complication, even in patients with normal renal function. It is important the prevention and early diagnosis of this entity, because in our study it is associated with an increased mortality in hospitalized patients as Bouzas-Mosquera (6) had documented.
It is important to remember that although we had a high incidence of AKI and most patients in this study were at high risk, there are other causes besides the use of contrast media that could influence the decrease in renal function, as a atheroembolism, drug toxicity or hemodynamic changes; all these factors making it harder to differentiate the true cause of AKI, as Newhouse reported.(18)
In this study, it was documented that patients who developed CIN by definition were of older, had anemia or hypotension before the procedure, had the necessity for intra-aortic balloon counterpulsation for hemodynamic support and a longer angiography time. In the multivariate analysis used for risk factors, it was found that the angiography time greater than 90 minutes, followed by age and the presence of anemia, all these risk factors were the most strongly associated with CIN, that results are similar to other studies.
In the study population, no statistically significant difference in the use of nephroprotective measures between both groups was documented; nevertheless, the quantity of patients in which these measures were used was low, possibly creating a bias in our results. (19),(20)
As for weaknesses of this study we should emphasize that it is a retrospective study, with a small sample, single-center, where there is not influenced therapeutic measures, the cause for renal failure was not fully investigated, and it was not established that death was secondary to renal failure or has been a contributing factor.
This study is relevant because it is a rare entity described in our medical practice, leading to high morbidity and increases in-hospital costs. There are increasingly patients undergoing PCI due to ischemic heart disease, so it is necessary to stratify patients at high risk and carry out early preventive measures.
Conclusions
The reported incidence was higher than that mentioned in the literature. The most important risk factors were age > 65 years old, anemia and patients who underwent PCI procedures longer than 90 minutes. The early detection of risk factors and the development of the NIC is encourage as the present of this entity leads to increased mortality.
