Contrast induced nephropathy (CIN)- 6 Interesting Facts

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What is contrast induced nephropathy (CIN) and ?

Iodinated contrast media can lead to a usually reversible form of non oliguric acute kidney injury (AKI) that occurs typically 24 to 48 hours after intravenous (IV) or intra-arterial administration of contrast.

How does Contrast induced nephropathy occur?

Contrast induced nephropathy does not occur with oral delivery of contrast media because contrast is not absorbed through the gut.

Contrast media causes Acute Kidney Injury through two major mechanisms:

(1) renal vasoconstriction causing ischemia, and

(2) direct tubular epithelial toxicity from the contrast.

After contrast administration, there is an immediate transient increase in renal blood flow followed by a prolonged period of reduced flow resulting in renal ischemia.

Contrast media stimulates the release of vasoconstrictive mediators, such as endothelin, while blocking the release of vasodilators, such as prostaglandins and nitric oxide, which causes hypoperfusion.

The renal medulla, which is poorly oxygenated in normal conditions, is susceptible to injury from contrast-induced reductions in oxygen delivery.

This ischemic injury generates reactive oxygen species, which causes tubular injury by affecting renal endothelial cells.

Furthermore, contrast agents are directly toxic to renal epithelial cells, causing proximal tubular vacuolization, interstitial inflammation, and cellular necrosis.

6 Interesting Facts of Contrast induced nephropathy

1. Contrast media cause acute kidney injury through two major mechanisms: renal vasoconstriction and direct tubular epithelial toxicity.

2. In most cases, contrast-induced nephropathy (CIN) is characterized by an elevation (>0.5 mg/dL or 25%) of the baseline creatinine within 24 to 48 hours following exposure, reaching a peak within 3 to 5 days, usually followed by a return to baseline within 7 to 10 days. Most patients with CIN are non-oliguric. Typically, the urinalysis is characterized by coarse granular casts and renal tubular epithelial cells along with a high specific gravity and fractional excretion of sodium <1%.

3. The main predisposing factor for CIN is preexisting kidney disease with serum creatinine ≥1.5 mg/dL or estimated glomerular filtration rate <60 mL/min/1.73 m . Other risk factors include diabetes only when coupled with CKD, high contrast load, advanced age, proteinuria, hypotension, volume depletion, congestive heart failure, and nonsteroidal anti-inflammatory drug (NSAID) use.

4. Volume expansion, using minimal contrast volumes, and removal of nephrotoxins, including NSAIDs, are the principal prophylactic measures to reduce the risk for CIN. The recent demonstration in the PRESERVE Trial of a lack of prophylactic advantage of isotonic bicarbonate over normal saline results in our recommendation that the former solution should not be used and prophylactic hydration should be with normal saline only. The recommended infusion rates are:

• Outpatient: 3 mL/kg/hr for 1 hour pre-contrast administration and 1 to 1.5 mL/kg/hr for 4 to 6 hours after contrast

• Inpatients: 1 mL/kg/hr for 6 to 12 hours pre-procedure and intra-procedure, and 6 to 12 hours post-procedure

5. The recent PRESERVE Trial has demonstrated no prophylactic benefit to N-acetylsteine and we no longer recommend it as a prophylaxis.

6. Statins should be continued, but not routinely started before contrast exposure. We do not recommend discontinuing drugs that block the renin-angiotensin-aldosterone system prior to contrast administration. Prophylactic use of hemodialysis or hemofiltration is not recommended. Remote ischemic preconditioning remains an exciting option, but is not yet proven for CIN prophylaxis.

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