During the last decade, conducting tests with the use of radiocontrast agents in CT diagnostics has increased by almost 800%, while the cardiac catheterization has increased by about 400%. For guidance as to which value is concerned, there is data that were actual some ten years ago when this figure was around eighty million doses of radiocontrast agent a year. We can assume that the risk of occurrence of kidney impairment will undoubtedly increase as a result of using radiocontrast agent not only because of an increased number of procedures, but also because of higher age of patients with significant and numerous associated diseases, of which diabetes is, of course, the most significant disease.

Patients with already impaired renal function, of whom there is 10% in the general population, are particularly vulnerable to contrast-induced nephropathy (CIN). Due to the undeniable connection between renal function impairment with an increased risk of cardiovascular events (1), these patients were more often exposed to diagnostic procedures with radiocontrast agent. This is supported by the fact that out of patients with chronic kidney disease that have not yet started dialy sis treatment there are 16% of them with stable, 5% with unstable angina pectoris, 18% of patients suffered from myocardial infarction, and in 35% of them heart failure was diagnosed (2, 3).

From the abundance of over a thousand of recent studies on CIN only some ninety of them can be taken into serious consideration after excluding irrelevant, experimental or review papers, while only some twenty randomized studies with a total of over 3.000 involved patients should be seriously accepted in the meta-analysis (4). The scope of shown incidence of CIN from 1% to 33% contributes to further consternation. We can notice discrepancy between occurrence of severe forms of CIN, treated by dialysis almost only after cardiac catheterization and the absence of clinically significant forms after contrast CT procedures (5).

A simple definition of CIN as an increase in creatinine by 25% or more from the initial value from 24 to 72 hours after the application of the contrast agent can explain the above discrepancy considering the complexity of cardiac patients who undergo procedures where contrast agent is used and the flow of time in which the event is placed, and during which the patient goes through the stages of adverse physiological events.

The pathophysiology of CIN mentions impairment of renal hemodynamics and hemorrhology of microcirculation, particularly of medullary microcirculation being particularly vulnerable, by the effect of iodine radiocontrast agent on the changes in tubular fluid due to an increase in osmolality and viscosity of contrast filtrate. Hyperosmolar contrast agents have an osmolality 1400-1800 mosmol/kg, hypoosmolar contrast agents 500-850 mosmol/kg, and isoosmolar contrast agents about 290mosmol/kg. Direct cytotoxic effect of iodine on cells of tubules and glomeruli is indisputable. Dose of 100 ml radiocontrast agent concentration 300 mg I/ml contains 30 g of iodine. Deposition of protein detritus as well as precipitation of uric acid may further damage the cells of renal tubules.

In animal models radiocontrast agent first causes vasodilatation followed by a persistent and intense vasoconstriction, but the cause of vasoconstriction stage is still unclear (6). The differences in occurrence of CIN considering the location of injecting the radiocontrast agent have been recorded, so any significant occurrence of nephropathy during intraarterial administration is greater, and the femoral access is more vulnerable compared to the radial access. It is believed that the reason is the need for a larger volume of contrast and potential embolization of renal microcirculation by atherosclerotic particles in previously impaired artery walls (7). Completely clear risk factors for the development of CIN such as pre-existing renal lesions, associated diabetes, advanced class of heart failure, older age, hypovolemia, large volume of radiocontrast agent, concomitant therapy with ACE inhibitors, nonsteroidal anti-inflammatory drugs or other known nephrotoxins are undisputable. Repeating the test within 72 hours causes a high risk of developing CIN (8). The use of those hypoosmolar contrast agents (iohexol, iopamidol) has undeniable advantage over hyperosmolar iodine radiocontrast agents.

In the cardiology literature, there is an attempt of making a simple calculation (risk score) in predicting the development of CIN and the risk of the need for dialysis treatment. The above mentioned score is available as Risk of Contrast- Induced Nephropathy Calculator (9). According to it, the basic clinical risk factors for the development of CIN in patients planned for coronary angiography and PCI are:

Prevention by isotonic fluid bolus injection seems to be rational because it reduces the time of contact of iodine radiocontrast with kidney cells, thus avoiding direct cytotoxicity, hypoxia and hypoperfusion due to vasoconstriction, as well as lowering the viscosity. The recommendation of 1 ml/kg/h of saline solution during 6-12 hours is widely and reasonably accepted, before and after the procedure. Correction of anemia due to potential blood loss is unavoidable in the prevention of occurrence of CIN (10).

There is no clear evidence of the benefits of preventive use of bicarbonate, diurertics, while the use of N-acetylcysteine is beneficial in preventing mild forms of CIN, but cannot stop the development of severe forms of the disease. Antioxidant effect of the drug is limited, but due to a simple application and low cost it should be taken at a dose of 1,200 mg/d before conducting the procedure, repeating the dose after the procedure. Statins proved to be beneficial in prevention in this case as well, whereas the 40 mg dose of atorvastatin is the most commonly recommended dose (11). Attempts with calcium channel blockers, dopamine, atrial natriuretic peptide, theophylline, or fenoldopam have not shown a clear therapeutic efficacy (12).

There is a need imposed for the usage of some other radiocontrast agents as to avoid CIN or allergies to iodine, so that gadolinium is used instead of iodine agents, but soon even this radio contrast agent proved to be causing kidney function impairment.

The first report on potential connection of contrast agents containing gadolinium ions and thus induced nephrogenic systemic sclerosis (NSS) was shown in 2006 (13). The syndrome includes the fibrosis in skeletal muscle, lungs, testicles and myocardium and it is often fatal. It is believed that the incidence of NSS is 2.9%-4.0% only in patients with pre-existing impairment of glomerular filtration rate of >30 ml/min /1.73m2, i.e. at the stage IV of chronic renal failure, and in severe acute renal failure (14).

Since there is no effective therapy for the NSS, it is necessary to avoid exposing patients with chronic renal failure to gadolinium, so alternative tests should be applied. Should it prove to be necessary, a preventive approach would mean the use of macrocyclic chelate (gadoteridol), the application of the least possible dose to avoid repetition of the test, planning on conducting hemodialysis after the test performed and during the next two days for patients who are already on dialysis, although there is no clear documented evidence that NSS is thus prevented. The recommendation is based on pharmacokinetics of gadolinium expecting the benefit from the removal of gadolinium by means of dialysis, of which clearance is >95%. Peritoneal dialysis is not an option due to its low clearance (15).

Renal impairments induced by using ions of iron, manganese and bromine as radiocontrast agents are not mentioned in the literature we have at our disposal.

To conclude, it is desirable to monitor the level of creatinine, urea and potassium on a daily basis during the period of three days in patients with clinical risk factors for the development of CIN and if the increase in residual nitrogen substances is progressive and exceeds 25% of the initial value, a nephrologist is to be consulted. In prevention it is recommended to prescribe 1ml/kg/h of saline during the 6-12 hours before and after the procedure, with statins as indicated above, and acetylcysteine as required in a dose of 1.200 mg.