ABSTRACT
It is important to note that patients who undergo PCI nowadays are usually discharged within <24 hours of the procedure, and they may develop this complication at home. Although the clinical importance of CIN may not be immediately obvious given the subclinical course and the high frequency of recovery of renal function, it is by no means a benign complication. CIN is no different from acute renal failure of any other etiology in terms of the symptoms, signs, complications that may ensue, and prognostic implications. It is the third most common cause of acute tubular necrosis in patients admitted to hospital. Some degree of residual renal impairment has been reported in as many as 30% of those affected and up to 7% may require temporary dialysis or progress to endstage renal failure.6-8 Proteinuria and oliguria may be observed in some patients, especially in those with prior renal insufficiency. However, CIN is usually non-oliguric and reversible. The serum creatinine level usually increases within 24-48 hours after contrast media administration, reaches a peak value at 3-5 days (generally an increase of 0.5-3.0 mgdl), and then returns to baseline within 7-10 days.9,10 Urinalysis is often compatible with acute tubular necrosis, demonstrating renal tubular epithelial cells and coarse granular casts.7 In high-risk patients, CIN may present as a more severe acute renal failure. In these patients, oliguria may develop within 24 hours of contrast administration, with peak levels of serum creatinine exceeding 5 mgdl, sometimes requiring dialysis. As discussed previously, permanent renal damage that requires dialysis replacement therapy is an unusual complication, but with dire consequences.1,11,12
In a study from the Washington Hospital Center, 0.7% of patients who underwent PCI required dialysis.These patients were usually older, female, diabetics, and 61% had prior history of chronic kidney disease.11 At 1-year follow-up, only 45% were alive and 75% of them required permanent dialysis replacement therapy. Similar results were described by McCullough et al, in which the in-hospital mortality of these patients was 35.7%.1 It is important to note that the majority of these patients suffer from generalized atherosclerotic vascular disease and may be at an increased risk to develop acute renal failure secondary to atheroembolic disease.12 Acute renal failure secondary to atheroembolic disease usually presents later, approximately 7 days to weeks; it is usually associated with a brief period of eosinophilia, hypocomplementemia, and other evidence of embolic phenomena, including livedo reticularis andor gastrointestinal ischemia or infarction. The course of this disease is more prolonged and usually there is no recovery of renal function.
