Contrast-induced nephropathy (CIN) is acute kidney injury caused by intravenous contrast agents used in medical imaging. It is usually reversible and preventable through appropriate management before contrast exposure, such as hydration and checking for risk factors like pre-existing kidney disease. The risk of CIN increases with older age, poorer kidney function, larger volumes of contrast agent, and its higher osmolarity. Prevention focuses on hydration with intravenous fluids before and after exposure, along with potentially administering N-acetylcysteine or sodium bicarbonate.

1. Contrast Induced
Nephropathy
By
Mohammed Yaseen
(MNGH)

2. Introduction
CIN is decline of renal function shortly after
IV contrast
CIN is usually reversible and can be
preventable by appropriate management
before exposure
CIN is the 3 rd leading cause of hospital
acquired AKI and increasing length of
hospital stay.

3. Definition
Elevation of serum creatinine more than 0.5
above the baseline or more than 25% within 2
to 3 days after contrast( after exclusion of
other causes of AKI) .

4. Incidence
CIN is extremely low in normal renal function
CIN risk increase with increase of serum creatinine
Less than 1% of patients with CIN may need
haemodialysis (this percentage increase with high
risk patients).

5. Contrast agents
1st
generation: ionic- monomer-high
osmolarity(more than 1400 mosm/kg) e.g
diatrizoate
2nd
generation: ionic or non ionic – monomer
or diamer- low osmolarity(600-1000
mosm/kg) e.g ioxaglate and iohexol
The newest generation: non ionic-diamer- iso
osmolarity(290 mosm/kg) e.g iodixanol

6. The nephrotoxic effects of contrast agents are
changed by:
1- The osmolarity.
2- The volume.
3- The types.
4- The route of administration.

7. The nephrotoxic effect increase with:
1- the high osmolarity more than low
osmolarity more than iso osmolarity.
2- the larger volume( more than 100 ml).
3- the non ionic more than ionic.
4- intra-arterial more than intravenous.
5- Repeated dose less than 72 h .(better 2 w
between contrast exposure)

8. Pathophysiology
1- Direct toxicity
2- Osmotic load: increase o2 consumption and
blood viscosity with renal medullary
ischaemia .
3- Decrease anti oxidant activity with increase
of o2 free radicals.
4-Increase adenosine,endotheline and PGE2
and decrease of NO,PG E1 and PG12 lead
to vasoconstriction with renal ischaemia .

9. RISK FACTORS
A) Non modifiable:
1-Age
2-CKD
3-CHF
4-IABP
5-PVD

10. B) modifiable:
1- volume of contrast agent
2-Osmolarity of contrast agent
3-Anaemia and blood loss
4-Short duration between contrast media
exposure
5-intra arterial injection
6- BP
7-Nephrotoxic agents.

12. RISK SCORE PREDICTION
Hypotension…….5 points
CHF……………..5 points
IABP…………….5 points
Age above 75……4 points
Diabetes…………3 points
Volume of dye……1 point per 100ml
S.Creatinine above 1.5mg/dl………4 points or:
GFR: 40- 60…………2 points
GFR: 20-40………….4 points
GFR: less than 20……..6 points

13. Risk score :
Equal or less than 5:
Risk of CIN 7.5%
6- 10 :
Risk of CIN 14%
11-16:
Risk of CIN 26.1%
More than 16:
Risk of CIN 57.3%

14. Concomitant medications
1-Aminoglycosides,Amphotericin B,NSAIDS or
COX2 inhibitors must be stopped 24-48 h before
contrast.
2- oral and IV diuretics must be stopped if decrease the
effective circulatory volume or hypotension.
3-ACEIs and ARBs must be continued especially if
patient is euvolemic.
4- Cyclosporine and tacrolimus are adjusted(low
window) but not stopped (V.C.).

15. 5-Increase steroid dose and MMF dose .
6-Metformin must be stopped till 2-3 days
after contrast due to risk of lactic acidosis.
7- Statins should be continued as it may
has beneficial effect.

16. Clinical manifestations
-CIN most commonly manifest as non oliguric and
asymptomatic transient decline of renal function.
-The serum creatinine start to rise within 24 h after
contrast administration and peak reached 3-5 days and
return to baseline within 10-14 days
-oliguric presentation requiring haemodialysis can also
occurs within 24 h of dye and typically persist for 2-5
days with significant higher rate of morbidity and
mortality than non oliguric.

18. Investigations
- Low urinary sodium and fractional excretion of Na
less than 1%
- Urine epithelial cell cast, debris, urate and calcium
oxalate crystals(non specific)
- Abdominal ultrasound : to exclude other causes
(obstruction)
- Biopsy: not recommended except for further
evaluation.

20. Prevention

21. Prevention
Hydration
Goals of Hydration:
1- Correct any decrease in renal blood flow by
ensuring that intravascular volume is replete.
2- Establish adequate diuresis prior to contrast
media.
3- Avoidance of hypotension.

22. oral hydration:
Low risk patients should be instructed to take 1-2
liters of water 12 h before procedure. NPO 4 h
before procedure and I.V fluids may be started if
additional hydration is needed.
IV hydration:(high risk patients)
- 1-1.5 ml/kg/h of NSS(volume expander) 3-12h
before and 6-12 h after contrast exposure.
- Restriction of IV fluids to 0.5 ml/kg/h in
patients with poor systolic function or chronic
renal failure

23. NaHCO3
Alkalinization may protect against free radical
injury
3ml/kg bolus(maximum 300 ml) 1 hour prior
to procedure and 1ml/kg/h(maximum 100
ml/h) during and for 6 hours post procedure.
Isotonic NaHCO3: 150 meq in 850 ml
dextrose

24. N-acetylcysteine
- In conjugation with hydration.
- Antioxidant characters.
- Rare side effects.
- Oral dose: 600-1200 mg PO twice/day one day before
and one day after contrast.
- IV dose:600-1200 IV one dose over 15 minutes then
600-1200 mg PO twice/day for 4 doses after contrast.

25. Statins
Improve endothelial function.
Reduce arterial stiffness,inflammation and
oxidative stress.
NO sufficient data to use statins for prevention
of CIN.