**4.5 Heart failure**

Advanced congestive heart failure (New York Heart Association class III or IV), reduced left ventricular ejection fraction, or any history of congestive heart failure are independent predictors of CIN and contribute to a greater risk in patients who have diabetes or renal disease. The risk arises as a result of decreased renal blood flow due to low cardiac output in those patients. Moreover, the risk is enhanced by this population's use of specific medications such as aspirin, diuretics, and angiotensin converting enzyme (ACE) inhibitors [30].

## **4.6 Anemia**

Anemia can cause deterioration of renal ischemia which can be an acceptable explanation for the higher incidence of contrast-induced nephropathy in patients with a lower hematocrit level. A baseline hematocrit value of less than 39% for men and less than 36% for women is considered a risk that leads to a higher incidence of CIN. This relation was investigated in a prospective study of 6773 patients who underwent PCI [31]. A lower basal hematocrit value was an independent risk predictor of CIN; and every 3% decline in basal hematocrit resulted in a significant increase in the occurrence of CIN in patients with and without chronic kidney disease (11 and 23%, respectively). Dangas et al. showed that the basal hematocrit level is an independent risk factor for the occurrence of CIN among patients with chronic kidney disease (OR = 0.95, p < 0.00001) [17].

#### **4.7 Hyperuricemia**

Contrast media have a uricosuric effect, which is caused by increased renal tubular secretion of uric acid. Moreover, hyperuricemia is accompanied by an activated renin-angiotensin-aldosterone system, enhanced synthesis of reactive oxygen species, increased endothelin-1, tubular obstruction by uric acid, and an inhibited nitric oxide synthesis that provokes the development of CIN [32].

#### **4.8 Hypercholesterolemia**

Altered nitric oxide-dependent renal vasodilatation is common in hypercholesterolemia. Hypercholesterolemia enhanced the occurrence of CIN through the reduced production of nitric oxide [24].

#### **4.9 Hypovolemia**

Hypovolemia leads to active sodium reabsorption, which is an oxygen-dependent process, and increases neurohumoral vasoconstrictive stimuli that can diminish medullary oxygenation. The toxic actions of contrast media on the renal tubular lumen can be exaggerated in hypovolemia. Decreased circulatory volume and renal perfusion augment vasoconstriction of renal vasculature after administration of CM. Volume expansion decreases the activity of the renin-angiotensin system, increases the perfusion of the medulla, and minimizes the elevation in blood viscosity and osmolality. Currently, the most effective preventive measure against the development of CIN is proper hydration [33].

#### **4.10 Hypertension**

The alteration in intrarenal expression of vasoactive mediators, mainly reninangiotensin system and nitric oxide, is a common cause that ranks hypertension as

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considered.

**4.13 Acute myocardial infarction**

**4.14 Contrast medium-related risk factors**

accepted dose is four times the creatinine clearance.

*4.14.1 Increased dose of contrast medium*

*Contrast-Induced Nephropathy*

**4.11 Nephrotoxic drugs**

*DOI: http://dx.doi.org/10.5772/intechopen.90457*

an important risk factor for CIN. Impaired nitric oxide-dependent renal vasodilatation is common in individuals who are hypertensive. In addition, a decreased

Nephrotoxic drugs that inhibit the vasodilatory effects of prostaglandins make the kidneys extremely vulnerable to the toxic effect of contrast media. Aminoglycosides, sulfonamides, and their combinations with furosemide are very risky. Cyclosporin A may intensify medullary hypoxia, and cisplatin can bind to sulfhydryl groups. Mannitol can increase the metabolic load and the oxygen consumption of the kidney, and amphotericin B can cause the combined effect of mannitol and cyclosporine A. It has been demonstrated that nonselective NSAIDs and selective COX-2 inhibitors decrease the availability of vasodilatory prostaglan-

dins in the kidneys and enhance the vasoconstrictive effect of CM [34].

ACE inhibitors have been identified as a risk factor for CIN because of their ability to reduce renal function. On the contrary, some small studies have shown that the inhibition of angiotensin II can decrease renal vasoconstriction following the injection of contrast media. In a randomized controlled study including 71 patients with diabetes who underwent coronary angiography and randomized to captopril (25 mg thrice daily) or control, there was a significant decrease in CIN in the patients who received captopril compared with the control group (6 vs 29%, respectively, p < 0.02) [35]. A randomized controlled study was performed on 80 patients with serum creatinine less than 2 mg/dl who underwent coronary angiography where captopril was administered in 48 patients preceding coronary angiography. CIN occurred in five patients (10.4%) in the captopril group, compared with only one patient (3.1%) in the control group (p = 0.02) [36]. We can say that holding ACE inhibitor or ARB use before coronary angiography is to be

A study by Rihal and his colleagues pointed that acute myocardial infarction occurring within 24 h before administration of the CM is a risk predictor to CIN (OR = 1.85, p = 0.0006). This study showed that CIN represents a frequent complication in acute myocardial infarction. This can occur, as well, in patients with a normal baseline renal function [30]. In 2082 percutaneous interventions for acute myocardial infarction, a more than sevenfold (3.2 vs 23.3%) elevation in 1-year

Based upon multiple sources, the relatively unhazardous cutoff point of contrast amount ranges from 70 mL up to 220 mL. However, very small doses as much as 20–30 mL are capable of inducing CIN. In a study that included patients performing coro¬nary angiography, each 100 mL of contrast medium administered was linked to a significant increase of 12% in the risk of CIN (OR = 1.12, p = 0.02) [32]. A clear

mortality in patients who acquired CIN was acknowledged [37].

**4.12 ACE inhibitors and angiotensin receptor blockers**

nephron count could predispose hypertensive patients to CIN.

an important risk factor for CIN. Impaired nitric oxide-dependent renal vasodilatation is common in individuals who are hypertensive. In addition, a decreased nephron count could predispose hypertensive patients to CIN.
