Quiz yourself on the 5 Pearls we will be covering!

Time Stamps

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

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.”


What are the diagnostic criteria for Contrast-Induced Nephropathy (CIN)?
Trick question! There is no guideline-based diagnostic criteria for CIN. There is no diagnostic lab, imaging or biopsy finding diagnostic of CIN. CIN has been defined for research purposes as a rise in Cr by at least 25% within 48-72 hours after contrast and exclusion of other likely causes of AKI.

What is the proposed mechanism for contrast-induced nephropathy?
Animal models suggest that the strongest element of CIN is from hypoxic and cytotoxic ATN (acute tubular necrosis)

What lab findings might you expect in a patient with CIN?
1. Rising Cr 2. Urine microscopy with muddy brown casts and a FENa <1 (in the literature the average FENa in CIN is quite low, around 0.3-0.7). NOTE: you may be surprised CIN is correlated with a low FENa. CIN is thought to damage the kidneys via an ATN-like mechanism, which is associated with a FENa >1.

Does the risk for CIN change depending on how the contrast is delivered?
Most data suggest that CIN is a disease almost entirely seen with intra-arterial contrast loads. This is after accounting for numerous confounders (i.e. differences in severity of illness, volume of contrast used, rate of complications such as plaque emboli, study type and selection bias).

There is evidence to support that intravenous contrast does not cause CIN. In very broad strokes, what does the evidence show?
Studies compared patients undergoing contrast vs. non-contrast intravenous studies and found no differences in: 1. The development of CIN; 2. Need for eventual HD; 3. Mortality. This remained true after stratifying by traditional CIN risk factors (chronic kidney disease, diabetes, and heart failure).

The risk of CIN in intra-arterial studies varies depending on other risk factors. What are they? (Hint: think about both the patient and the contrast agent!)
PATIENT CHARACTERISTICS: 1) CKD with or without proteinuria (with proteinuria a greater risk factor) 2) Diabetes 3) Hypovolemia CONTRAST CHARACTERISTICS: 1) Greater volume and 2) High osmolarity formulations (now uncommon)

How does diabetes alter the risk of CIN?
Works synergistically with CKD to raise risk of developing CIN. People with diabetes and CKD demonstrated almost triple the rate of CIN compared to patients with CKD alone.

What is an easy way to estimate risk of CIN in patients undegoing intra-arterial contrast?
By GFR and proteinuria!  GFR 30-60: about 5% risk of CIN. GFR less than 30: about 30% risk of CIN. Protienuria greatly increases risk! For example, GFR < 60 and > 1 g of proteinuria equates to double the risk of CIN versus those with GFR < 60 and < 1 g proteinuria.

What preventive measures have been shown to reduce the risk of CIN?
Achieve euvolemia – ideally via 1mL/kg/hr of prophylactic hydration 12 hours before/during/after intra-arterial contrast. Caveat: data to support IV fluids prior to intra-artieral contrast varies.

What fluid should be used to prophylactically hydrate and reduce the risk of CIN?
Chose either NaHC03 or NS (no difference in outcomes). Note: do not give NAC – no better than placebo!

Attempts to prevent CIN are important in which patients with end stage kidney disease (ESKD)?
Patients with ESKD who still make urine. Why? They still have residual nephron function that could be threatened/compromised by development of CIN! Residual nephron function has importance clinical benefits (some filtration of uremic toxins, volume removal and survival benefit).

You have a patient with ESKD on HD who is scheduled to undergo cardiac catheterization. She is oliguric. Should you give her prophylactic IV fluids?
Yes, however there is limited data to support this practice. Because the patient can tolerate volume expansion, best practice is likely to give IV fluids.


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