Contrast-Induced Nephropathy (CIN)

(also termed Contrast-Associated Acute Kidney Injury – CA-AKI in recent guidelines)

Definition

Contrast-induced nephropathy (CIN) is classically defined as an acute decline in renal function occurring after intravascular administration of iodinated contrast media, in the absence of an alternative cause.

Traditional definition :

• ↑ Serum creatinine ≥0.5 mg/dL OR
• ↑ Serum creatinine ≥25% from baseline
• Occurring within 48–72 hours after contrast exposure

Modern guideline term: Contrast-Associated AKI (CA-AKI)
– acknowledges that contrast may be a contributing rather than sole cause.

Pathophysiology (Why CIN occurs)

CIN results from a combination of hemodynamic and direct tubular effects:

1️⃣ Renal Hemodynamic Changes

• Contrast → afferent arteriolar vasoconstriction
• ↓ Renal blood flow (especially outer medulla)
• ↓ GFR
• Mediated by:
  • ↑ Endothelin
  • ↓ Nitric oxide & prostaglandins
  • Activation of RAAS

➡️ Leads to renal medullary ischemia

2️⃣ Direct Tubular Toxicity

• Contrast agents:
  • Disrupt tubular epithelial cell membranes
  • Cause mitochondrial dysfunction
  • Induce apoptosis & necrosis

➡️ Acute tubular injury

3️⃣ Oxidative Stress

• Contrast increases:
  • Reactive oxygen species (ROS)
  • Lipid peroxidation
• Medulla is especially vulnerable due to:
  • High oxygen demand
  • Low baseline oxygen tension

4️⃣ Increased Tubular Viscosity

• High-osmolar load → ↑ tubular fluid viscosity
• Sluggish tubular flow
• ↑ Intratubular pressure
• ↓ Effective filtration

Risk Factors for CIN

Patient-related

• Chronic kidney disease (most important)
  • eGFR <60 mL/min/1.73 m²
• Diabetes mellitus (especially with CKD)
• Elderly age
• Dehydration / volume depletion
• Heart failure, low cardiac output
• Hypotension / shock
• Anemia

Procedure-related

• Large contrast volume
• Repeated contrast exposure (<48–72 h)
• Intra-arterial contrast (higher risk than IV)
• High-osmolar contrast agents

Drug-related

• NSAIDs
• ACE inhibitors / ARBs (context-dependent)
• Diuretics
• Nephrotoxic antibiotics (aminoglycosides)

Clinical Course

• Rise in creatinine: 24–72 h
• Peak: 3–5 days
• Recovery: usually 7–10 days
• Most cases are non-oliguric
• Severe cases → dialysis (rare, but ↑ mortality)

Diagnosis

• Diagnosis of exclusion
• Temporal relationship with contrast exposure
• Rule out:
  • Sepsis-associated AKI
  • Hypovolemia
  • Obstruction
  • Drug-induced AKI

Urinalysis

• Usually bland
• Mild granular casts may be seen

Prevention (MOST IMPORTANT )

 Hydration – cornerstone

Isotonic saline (preferred):

• 0.9% NaCl
• 1–1.5 mL/kg/hr
• Start 3–12 h before and continue 6–12 h after

In ICU / heart failure patients:

• Tailored hydration (CVP/echo-guided)

 Contrast Strategies

• Use lowest possible contrast volume
• Prefer iso-osmolar or low-osmolar contrast
• Avoid repeat contrast within 48–72 h

 Pharmacologic Measures

 Not Recommended

• Prophylactic dialysis
• Loop diuretics for prevention
• Mannitol

Management

• Supportive care only
• Optimize hemodynamics
• Avoid further nephrotoxins
• Monitor creatinine & urine output
• Dialysis only if standard indications develop