Contrast induced nephropathy (CIN)
- is acute kidney dysfunction occurring after exposure to intravascular contrast media that is not attributable to other causes.
- is the third most common cause of hospital-acquired renal failure and has significant prognostic implications on patient outcomes
Definition - is defined as increase in serum creatinine concentration by 0.5 mg/dl or 25% than the baseline value within 48 to 72 hours of administration of contrast agent.
Pathophysiology of CIN-
Natural History of CIN -
Most CIN is self-limited. Serum creatinine typically increases over 1 to 3 days, peaks at 4 to 5 days, and returns to baseline in 7 to 14 days.
Risk factors indentified for CIN –
The major risk factor for developing CIN is preexisting renal dysfunction, particularly in association with diabetes.
Patients are considered to be at risk when estimated glomerular filtration rate (eGFR) or estimated creatinine clearance (eCCr) is less than 60.
5.Chronic kidney disease
6. Age>75 yrs
8. Contrast volume
1. Dose <4ml> 1.5mg/dl ).
2. Adequate hydration with 0.9% normal saline ( at rate of 1ml/kg/hr for 12 hours before and after the procedure.
3. Low or Iso-osmolar contrast agents.
5. N-acetylcysteine (mucomyst)
6. Sodabicarb infusion
7. Ultrafitration dialysis has shown some benefit.
8. Fenoldopam,a dopamine agonist has been tried but has not shown any benefit.
1. Patients with impaired renal function sr.cr.>1.5 mg/dl & GFR< 60ml> 2. Effect is more pronounced on kidneys when contrast agents are given near renal arteries.
3.Low osmolar,non-ionic,agents are preferred
4.Contrast agents are:-
High osmolar, ionic = Diatrizoate(hypaque)
Low osmolar, ionic = Ioxaglate
Low osmolar, non ionic = iohexol (omnipaque)
ISO osmolar, non ionic = Iodixanol(visipaque)
Strategies for renal protection -
1. Hydration – Normal Saline
2. IV fluid hydration with normal saline is the mainstay of practice in the prevention of CIN. It is low-risk, carries few side effects, and is cost-effective.
3. It increases intravascular volume, promotes diuresis, dilutes the overall intravascular contrast load, induces vasodilation, suppresses the renin–angiotensin–aldosterone axis, and suppresses the release of antidiuretic hormone.
4. Sodium bicarbonate – Decreases acidification of urine and renal medullary environment which reduces free radical injury.
5. N-acetylcysteine:mechanism- antioxidant and vasodilatory effects
6.Discontinuation of nephrotoxic drugs - NSAIDS , loop diuretics and all other should be stopped 24 to 48 hours before a contrast study to reduce the risk of CIN.
9.Procedural Techniques for Minimizing Iodinated Contrast - Dilution is often the easiest and most effective method for contrast dose reduction.