CIN is reported to be the third leading cause of in-hospital acute renal failure after hypotension and surgery. The incidence of CIN is reported to be 0.6-2.3% in general population who do not have any risk factor for CIN, but the incidence can be increased to 90% in patients at high risk for CIN ( Toprak, 2007).ĬIN may range in severity from asymptomatic, nonoliguric transient renal dysfunction to oliguric severe renal failure that necessitates permanent dialysis.

Cholesterol atheroemboli, volume depletion, and interstitial nephritis should consider in differential diagnosis of CIN. Urinary interleukin 18 and urinary liver-type fatty acid-binding protein are new potential biomarkers of CIN ( Perrin et al., 2012). Recent studies documented that serum and urine neutrophil gelatinase-associated lipocalin is an early predictive biomarker of CIN ( Shaker et al., 2010). Serum cystatin C may detect CIN one to two days earlier than creatinine. Serum cystatin C has been proposed as an alternative endogenous marker of GFR showing higher correlation to standard clearance methods such as inulin or iohexol clearance. Using the Cockcroft-Gault and the Modification of Diet in Renal Disease equations are useful in estimation of the GFR. The most commonly used definition for CIN is the elevation of serum creatinine by ≥0.5mg/dl or ≥25% occurring within 48 hours after administration of CM, and the absence of an alternative etiology. The strongly associated risk markers for CIN are pre-existing renal failure, diabetes mellitus, age greater than 70 years, concurrent use of nephrotoxic drugs, hypovolemia, use of a large amount of CM or an ionic hyperosmolar CM, and congestive heart failure.Īim of the present chapter is to summarize the knowledge about the risk factors and prophylactic treatments of CIN according to the ultimate clinical research and developments.Ī universally accepted definition of CIN does not exist. After the high-risk patient population has been identified and risk markers addressed, the next step in preventing CIN is the use of different prophylactic therapies. The occurrence of CIN is directly related to the number of pre-existing patient risk markers. No current treatment can reverse or ameliorate CIN once it occurs. Nearly one-third of the patients who require in-hospital dialysis because of CIN die prior to discharge. Patients who develop CIN have higher complication rates, longer hospital stays, and higher mortality than patients who not develop CIN. Tubular obstruction, apoptosis and oxidative damage, endothelial dysfunction, defective prostaglandin synthesis, and autonomic dysfunction are other proposed mechanisms. The proposed mechanisms are outer-medullary hypoxia due to decreased renal blood flow secondary to renal artery vasoconstriction.

Radiological procedures such as coronary angiography require intravascular administration of iodinated CM is becoming a great source of an iatrogenic disease known as contrast-induced nephropathy (CIN). Many complex interventions are lengthy and require large dosages of contrast medium (CM). Diagnostic and therapeutic angiographic procedures are increasingly performed.

Dr omer toprak