Multiple studies have suggested that in-hospital mortality is significantly higher in patients developing contrast induced kidney damage especially those who require hemodialysis.
1. Hx of Chronic Kidney Disease
2. Congestive heart failure
3. Older age
5. Volume depletion
6. Concomitant use of nephrotoxins such as nonsteroidal anti-inflammatory agents also increase the risk for contrast induced kidney damage.
In the majority of patients with contrast induced kidney damage, the serum creatinine value begins to rise within 24–48 hours after contrast media exposure, peaks within 3–5 days, and returns to baseline levels within 7–10 days. The majority of patients are nonoliguric and often have low urine sodium concentration. The urinalysis in patients with contrast induced kidney damage typically demonstrates coarse granular casts, renal tubular epithelial cells, and amorphous debris, findings characteristic of acute tubular necrosis.
Most studies, although not all, suggest that exposure to larger volumes of parenteral contrast causes greater predisposition to contrast induced kidney damage. In addition, the type of contrast material (specifically its osmolality) influences the development of contrast induced kidney damage. Contrast media formulations occur in three types: High-osmolar contrast media (also termed ionic), which have an osmolality of approximately 2000 mOsm/L, low-osmolar contrast media (also termed nonionic), which have an osmolality of 600–900 mOsm/L, and iso-osmolar contrast media (also a nonionic composition), which have an osmolality of 300 mOsm/L. Multiple studies in high-risk patients with CKD have demonstrated that low-osmolar contrast media results in less contrast induced kidney damage than high-osmolar contrast media, and there is some evidence that iso-osmolar contrast media may be less nephrotoxic than low-osmolar contrast media.
1. Acute Tubular Necrosis
2. Renal atheroembolism
3. Allergic interstitial nephritis
1. Begin an infusion of isotonic sodium bicarbonate at 1ml/kg/hr for 12 hours pre- and post-procedure
2. The most commonly employed dose of NAC is 600 mg by mouth twice daily the day prior to and the day of contrast administration. Initially, this finding was greeted with widespread enthusiasm and the use of NAC quickly became common in clinical practice. Subsequent studies of its efficacy have been mixed, as have meta-analyses of those studies. To date, it remains uncertain if NAC is an effective preventative measure, but it is nonetheless often used in clinical practice, based on its safety, simplicity, and low cost.
3. Although acute administration of diuretics has been shown to increase the risk of contrast-induced acute kidney injury, the discontinuation of chronic diuretic therapy has not been demonstrated to be beneficial.
4. Discontinuation of ACE Inhibitors has not been clearly shown to decrease the risk of contast induced acute kidney injury.
There is no specific therapy for contrast induced kidney damage once it occurs. The best strategy is one of prevention. Preemptive nephrologic consultation to ensure that optimal prophylactic strategies are provided may be of value in certain high-risk azotemic patients.
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