5. Contrast-enhanced CT is one of the most commonly
used imaging methods for the diagnosis, staging, follow-
up and assessment of the response to therapy in
patients with cancer, and many patients are exposed to
contrast-enhanced CT many times.
Metabolic and obstructive problems, humoral changes
and therapy-induced renal toxicity may impair renal
functions in patients with advanced cancer. Therefore,
patients with cancer may have an increased risk of CIN.
6. Contrast-induced nephropathy (CIN) is defined as renal
injury that develops after the use of an intravascular
contrast agent (CA), provided that other likely causes
of renal failure are ruled out.
Nash et al. reported that CIN is the third leading cause
of hospital-acquired renal failure, with a rate of 11 %.
7. The prevalence of CIN varies depending on the physical
and chemical characteristics and volume of the CA,
patient risk factors and preventive measures
implemented prior to the procedure.
While the prevalence of CIN is less than 5% in those
with normal renal function, it may reach levels as high
as 50% in patients with various risk factors.
8. Oncology patients are exposed to multiple nephrotoxic
agents (cytotoxic drugs, antibiotics, analgesics and
drugs for supportive therapy).
In addition to drugs, issues such as anaemia,
hypercalcaemia and hyperuricacidemia may also cause
nephropathy in patients with cancer.
9. The development of renal failure either makes
impossible or impedes oncological treatments.
Thus, exposing the predictive factors for CIN would
contribute both to a reduction in the development of
renal failure and to the implementation of
oncological therapies under optimal conditions.
11. This prospective study involved 90 patients and was
carried out between October 2010 and September 2012 at
Trakya University Medical Oncology Clinic.
The study was approved by the ethics committee of the
institute, and written informed consent was obtained from
all patients.
Patients with cancer who were hospitalised for diagnostic
evaluation, chemotherapy or disease complications and
who underwent contrast-enhanced CT were examined.
12. Patients older than 18 years, and patients with a
glomerular filtration rate (GFR) of more than 50
ml/min were eligible for the study.
To definitively diagnose CIN and discriminate other
possible causes of nephropathy from CIN, patients
with a GFR less than 50 ml/min, patients with known
risk factors for ARF, and patients using nephrotoxic
drugs except chemotherapy agents were excluded
from the study.
13. Baseline data of the patients, including age, gender,
diagnosis and stage of cancer, number of chemotherapy
lines and cycles, chemotherapy drugs administered, time
between last chemotherapy and CT, comorbid diseases,
and nephrotoxic drugs used currently or in the past
were recorded.
Blood samples were examined before contrast-
enhanced CT to determine baseline urea, creatinine (Cr),
sodium, potassium, lactate dehydrogenase (LDH), and
haemoglobin (Hgb) values.
14. On the first, second, and third days following contrast-
enhanced CT, blood samples were drawn to examine only
Cr and urea.
The GFR was calculated by the Cockcroft-Gault formula.
CIN was defined as an increase in the serum Cr
concentration by 25 % or more, a 0.5-mg/dl or more
increase in the Cr level according to the baseline value, or
both, within 72 h after contrast-enhanced CT.
15. Iopromide (428 mOsmol/l) or iohexol (465 mOsmol/l) was
used as the CA.
The amount of CA used for the imaging of different body
regions was as follows:
50 ml for cranial CT, 75 ml for thoracic CT, 75 ml for
abdominal CT, 100 ml for thoracic and abdominal CT, and
100 ml for thoracic, abdominal, and cranial CT.
Before administration of the CA, all patients were hydrated
with 2,000-3,000 ml of oral or intravenous fluids to avoid
effects of possible dehydration on renal function.
Statistical analysis was performed.
16. Results
CIN was detected in 18/90 (20 %) patients.
CIN developed in 25.5 % patients who underwent
chemotherapy and in 11 % patients who did not.
CIN more frequently developed in patients who had
undergone CT within 45 days after the last chemotherapy;
it was also an independent risk factor.
CIN was significantly more after treatment with
bevacizumab/irinotecan and in patients with hypertension.
18. In this prospective observational study, authors
investigated the incidence of CIN in patients with cancer
admitted to the oncology clinic for various reasons and who
underwent contrast-enhanced CT, and evaluated the
potential predictive factors for CIN.
No relationship was found between the development of
CIN and the site of origin or stage of cancer. This indicates
that the site of origin has no effect on CIN development
unless there is an obstructive or metabolic disorder.
19. The risk for CIN development was 4.5- times higher in
patients who had undergone CT within 45 days after the
last chemotherapy compared with those who did not
undergo chemotherapy or those who had undergone CT
after 45 days from the last chemotherapy.
Patients who did not undergo chemotherapy and patients
who had undergone CT after 45 days from the last
chemotherapy had similar risks of CIN development.
20. These results suggest that contrast-enhanced CT performed
within a relatively short time after chemotherapy (within 45
days) increases the risk for CIN.
No relationship was found between the development of CIN
and the total number of chemotherapy cycles.
Among chemotherapy agents, only the combination of
bevacizumab/irinotecan was found to be associated with the
development of CIN.
21. Authors found no relationship between nephrotoxic
chemotherapy agents and CIN. This was an unexpected
finding, especially for cisplatin.
Bevacizumab was found to be a potential risk factor for CIN
development. Bevacizumab has remarkable effects on the
endothelial and vascular structures of the kidney.
22. Chemotherapeutic agents contribute to CIN development
by causing acute endothelial damage.
Chemotherapeutic agents may cause vasoconstriction,
arterial hypertension and tissue ischaemia with production
of oxygen free radicals and lipid peroxidation as well as
inflammation and endothelial damage due to thrombotic
events.
CAs decrease the GFR and renal medullary blood flow by
causing vasoconstriction in renal vessels.
23. In addition, they cause tissue ischaemia/hypoxia by
increasing adenosine and endothelin levels.
Development of tissue damage due to inflammation in
renal tissue and production of free oxygen radicals also
contribute to CIN development
24. The most important limitations of the present study was
the number of patients and the lack of a control group.
Nonetheless, the results serve as a warning, and
demonstrate the necessity for additional studies.
Inclusion of new outcomes would influence oncological
practice by defining chemotherapy as an independent risk
factor for CIN development.
26. To authors’ knowledge, the present prospective study is
the first to investigate the incidence and predictive factors
of CIN in patients with cancer.
The incidence of CIN was much higher in patients who
underwent chemotherapy.
27. This study demonstrated that the incidence of CIN
might be high in hospitalised patients with cancer
treated for any reason and who undergo CT within 45
days after the last chemotherapy.
Moreover, the presence of hypertension and
treatment with bevacizumab may be additional risk
factors for CIN development in patients with cancer.
