Quiz yourself on the 5 Pearls we will be covering!

Time Stamps

  • Are there diagnostic criteria for contrast-induced nephropathy (CIN)? (2:11)
  • Is there a difference between exposure to intra-arterial versus intra-venous contrast in terms of risk of CIN? (6:28)
  • What are the biggest risk factors for CIN? (14:48)
  • What preventive measures have been shown to best reduce the risk of CIN? (19:41)
  • Can ESRD patients on hemodialysis still suffer from CIN? (23:32)
  • Recap (25:49)

Show Notes

Pearl 1: Diagnostic criteria for Contrast-Induced Nephropathy (CIN)

  • Most research studies define CIN as a relative increase in serum creatinine of anywhere from 25-50% or, an absolute rise in serum creatinine of 0.5 to 1mg/dL within 48-72 hours after exposure to contrast with exclusion of other causes of acute kidney injury.
  • Other clues are signs of acute tubular necrosis and a fractional excretion of sodium (FeNA) less than 1.

Pearl 2: Intravenous vs Intra-arterial contrast

  • Most data suggest that CIN is a disease entity almost entirely reserved for patients undergoing intra-arterial contrast loads, and not intra-venous contrast loads.
    • The incidence of AKI after arterial contrast ranges anywhere from 5-30% depending on the other risk factors present.
    • The incidence of AKI following intravenous contrast exposure is much lower, in the ballpark of 2-10%
  • Issues often with studies of arterial contrast:
    • Retrospective
    • No control group
    • Selection Bias
    • Other variables: showering atherosclerotic emboli to kidneys or volume of contrast used
  • Issues often with studies of venous contrast:
    • Also retrospective
    • Controlled, but poorly
    • Selection bias

Pearl 3: Risk Factors

  • CKD
    • Patients with underlying CKD are at increased risk of developing CIN
    • Pinpointing the GFR at which the greatest risk occurs is very difficult because most studies lump patients into buckets with wide ranges of GFR
    • What we do know:
    • In patients undergoing studies with arterial contrast:
      • ~ 5% of patients with GFR 30-60 develop CIN
      • ~ 30% of patients with GFR <30 develop CIN
  • Proteinuria
    • GFR < 60 plus at least 1 g of proteinuria develop CIN at almost double the rate of patients with GFR <60 alone
  • Diabetes:
    • Patients with diabetes coupled with CKD demonstrated almost triple the rate of CIN compared to patients with CKD alone
  • Hypovolemia:
    • Given difficulty measuring volume status by exam or labs, there are no known randomized trials looking at rates of CIN in those hypovolemic vs. euvolemic
    • But given data with prophylactic hydration, low effect arterial blood volume and hypoperfusion to the kidneys are thought to constitute elevated risk.
  • High Osmolality Contrast
    • Older contrast agents are hyper-osmolar compared to serum and associated with much higher rates of CIN
    • Newer contrast agents are either iso-osmolar or hypo-osmolar and associated with rates that are lower relative to hyper-osmolar agents

Pearl 4: Prevention

  • Isotonic fluid pre and post contrast study:
    • Studies generally show that 24 hour of hydration with isotonic saline does in fact reduce risk of CIN compared to patients who did not receive it
      • Scrutinizing the data:
        • Could fluid administration just be preventing hypotension-induced AKI and not really represent a protective measure against contrast-induced AKI?
        • Are these studies findings true for patients with high risk features (CKD, proteinuria etc)?
  • Sodium bicarbonate pre and post contrast study:
    • Believed to work by alkalinizing the renal tubules and preventing free radical generation
    • Sodium bicarbonate is thought to be non-inferior to normal saline for risk of developing CIN
  • N-acetylcysteine (NAC)
    • Rationale is that NAC reduces free radicals generation adding back a reducing agent
    • Oral NAC demonstrated no reduction in CIN compared to placebo

Pearl 5: CIN in End Stage Renal Disease

  • ESRD patients who are oliguric still have some functioning nephrons
  • Residual kidney function has several beneficial effects
    • Still allows for filtration of uremic toxins
    • Still allows for some degree of volume and electrolyte regulation
    • Most importantly, has survival benefit
  • Patients with ESRD with some residual kidney function are thought to be at risk of CIN
    • Currently, the American College of Radiology (ACR) describes this as a ‘theoretical risk:’ “This remains speculative, as there are no conclusive outcome data in oliguric dialysis patients in this setting.”

References