Lights and shadows on the pathogenesis of contrast-induced nephropathy: state of the art
Author(s) -
Simona Detrenis,
Michele Meschi,
Sabrina Musini,
G Savazzi
Publication year - 2005
Publication title -
nephrology dialysis transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.654
H-Index - 168
eISSN - 1460-2385
pISSN - 0931-0509
DOI - 10.1093/ndt/gfh868
Subject(s) - medicine , pathogenesis , contrast (vision) , nephropathy , contrast induced nephropathy , pathology , artificial intelligence , endocrinology , diabetes mellitus , computer science
A recent report has suggested that contrast mediainduced nephropathy (CMIN) is the third highest cause of hospital-acquired acute renal failure [1]. In nearly half of these patients, CMIN occurred during cardiac diagnostic or interventional procedures such as percutaneous coronary intervention. However, considering the amount of contrast media (CM) used today in extracardiac diagnostic procedures, the incidence of nephropathy still remains relatively low. This low incidence may be attributed to the introduction and use of nonionic, lowor iso-osmolal compounds, to the use of smaller volumes of CM and to an increasing awareness of patients who may be at risk for impairment of renal function. The latter is especially true in patients with pre-existing renal failure, diabetes, or both. Understandably, the reason a number of patients develop acute renal failure following a cardiac procedure is the necessity to perform these procedures in the presence of pre-existing, and often non-modifiable, risk factors for renal impairment. Permanent impairment of renal function requiring dialysis can occur in up to 10% of patients with preexisting renal failure who develop further reduction in renal function after coronary angiography [2], or in <1% of all patients who undergo percutaneous coronary intervention using CM [3]. In-hospital mortality after acute renal failure requiring dialysis in these patients could reach 36% [3], even if this rate might be due to the effects of eventually coexisting comorbidities [4,5]. In most studies, CMIN is defined as an acute decrease in renal function after intravascular administration of CM in the absence of other causes. It is expressed as an increase in serum creatinine levels of 0.5mg/dl (or 44 mmol/l) or a 25% or greater relative increase from baseline 48–72 h after a diagnostic or interventional procedure [6], even if the clinical significance of this definition in the absence of preexisting chronic renal failure is questionable. Nonionic and ionic iodinated contrast media are currently classified, at the concentrations required for diagnostic or interventional radiologic and cardiac procedures, according to their osmolality compared with the osmolality of plasma. The high-osmolal contrast media (osmolality 1500–1800mOsm/kg) are first generation agents. In fact, the so-called low-osmolal contrast media still have an increased osmolality compared with plasma (600–850mOsm/kg), while the newest nonionic radiocontrast agents have a lower osmolality, 290mOsm/kg, iso-osmolal to plasma (Table 1).
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