|ECR 2013 / C-2148|
|Contrast-induced nephropathy: Preventive measures.|
Contrast induced nephropathy (CIN) is a generally reversible decrease in renal function, defined as an increase a rise of 25% in the serum creatinine when the baseline is less than 1,5 mg/dl, or an absolute rise of 0.5 mg/dl when the baseline is greater than 1,5 mg/dl in serum creatinine within 3 days of the intravascular administration of a iodinated contrast medium (ICM) in the absence of an alternative aetiology for the renal impairment.
CIN is the third most common cause of hospital-acquired renal failure. The incidence of the NCI varies widely depending on renal function prior to the administration of contrast, the presence or absence of risk factors, the amount and type of radiocontrast agent administered and the exact radiologic procedure. In patients with preserved renal function the incidence is between 2 - 3 %, and those who present values of serum creatinine greater than 1.5 or creatinine clearance less than 50 the incidence increases to 13% (50% in high-risk patients).
CIN is usually mild, transient and nonoliguric although it may persist in patients with pre-existing advanced underlying disease, particularly in diabetics. It usually begins within 12 – 24 hours of contrast administration, with creatinine peaks at 3-5 days and normalization with 1-3 weeks.
It is important to make the differential diagnosis with renal atheroembolic disease, in these cases the presence of other embolic lesions, transient eosinophilia e hypocomplementemia and a delay in the onset of renal failure and the prolonged course of renal alteration are frequent.
There is no etiological treatment of this pathology, so it it should be managed as any cause of acute tubular necrosis, focusing on fluid maintenance and electrolyte balance.
There are intrinsic factors of the renal physiology responsible for renal susceptibility to contrasts iodinated injury such as the corticomedullary gradient (the renal cortex receives 90% of the renal flow and performs 10% metabolic work, instead these percentages are reversed in the renal medulla), medullary hypoxia (PaO2 in the cortex is 50 mmHg in the medulla of 10-20 mmHg) and the small diameter of the vasa recta (reduction in medullary blood flow occur due to contrast media, that increase blood viscosity).
The exact pathogenic mechanism of CIN is not well understood. The two major theories that have been suggested include:
1) Renal hemodynamic changes (vasoconstriction), resulting in medullary hypoxia, possibly mediated by vasoactive mediators such as endothelin and adenosine, and by reduction of the release of vasodilators factors (nitric oxide, prostaglandins). Diabetes mellitus and heart failure increase the risk of contrast-induced kidney injury in humans and these disorders are associated with impaired nitric oxide generation, which could contribute to the susceptibility to contrast agents
2) Direct tubular toxicity, as a direct result of the cytotoxic effects of the contrast agents or by the release of oxygen-free radicals.
In addition, it is possible that prerenal factors or intratubular obstruction contribute to the pathogenesis.
TYPES OF RADIOCONTRAST AGENTS
Iodinated radiocontrast agents are either ionic or nonionic and, at the concentrations required for different imaging techniques, are of variable osmolality:
First generation agents are ionic monomers; they are highly hyperosmolal (1400 to 1800 mosmol/kg) compared with the osmolality of plasma.
Second generation agents, such as iohexol, are nonionic monomers with a lower osmolality than the first generation radiocontrast media; however, they still have an increased osmolality (500 to 850 mosmol/kg) compared with plasma. There is an ionic low osmolal contrast agent (ioxaglate).
The newest nonionic contrast agents are iso-osmolal, being dimers with an osmolality of approximately 290 mosmol/kg (iodixanol is the first such agent).
RISK FACTORS FOR CONTRAST MEDIUM-INDUCED NEPHROPATHY
There are several factors that are associated with an increased risk of CIN: pre-existing renal failure (particularly as a result of diabetic nephropaty), dehydration, class III/IV congestive heart failure, age > 70 years, gout, administration of nephrotoxic drugs, the use of hyperosmolal ionic contrast agents, high total dose of contrast agent, or multiple contrast studies within a 72 hour period. The risk of CIN associated with intravenous CM administration may be lower than with intra-arterial administration.
Several potential new markers of CIN risk have been identified in patients undergoing coronary intervention. These include metabolic syndrome, prediabetes, hyperuricemia, hypertriglyceridemia, impaired fasting glucose and women ≥65 years of age.
Thematically related posters
ECR 2013 / C-0823
Procedure to prevent adverse reactions in patients in treatment with metformin that receive yodinated contrast
ECR 2013 / C-1555
Prevalence of contrast induced nephropaty (CIN) in preemptive living renal donor recipients after enhanced CT with CIN prophylaxis