Biomedical subjects

Charles Davidson

Publications and source records attributed to Charles Davidson.

7 recordsLinked to original sources

PubMed2006

Strategies to reduce the risk of contrast-induced nephropathy.

In view of the clinical importance of contrast-induced nephropathy (CIN), numerous potential risk-reduction strategies have been evaluated. Adequate intravenous volume expansion with isotonic crystalloid (1.0-1.5 mL/kg per hr) for 3-12 hours before the procedure and continued for 6-24 hours afterward can lessen the probability of CIN in patients at risk. There are insufficient data on oral fluids (as opposed to intravenous volume expansion) as a CIN-prevention strategy. No adjunctive medical or mechanical treatment has been proved to be efficacious in reducing risk for CIN. Prophylactic hemodialysis and hemofiltration have not been validated as effective strategies. The CIN Consensus Working Panel considered that, of the pharmacologic agents that have been evaluated, theophylline, 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitors (statins), ascorbic acid, and prostaglandin E(1) deserve further evaluation. N-acetylcysteine is not consistently effective in reducing the risk for CIN. Fenoldopam, dopamine, calcium channel blockers, atrial natriuretic peptide, and l-arginine have not been shown to be effective. Use of furosemide, mannitol, or an endothelin receptor antagonist is potentially detrimental. Nephrotoxic drugs should be withdrawn before contrast administration in patients at risk for CIN.

Acute Kidney Injury↗

PubMed2006

Contrast medium use.

Various properties of iodinated contrast media (osmolality, ionic versus nonionic, and viscosity) may contribute to contrast-induced nephropathy (CIN). Therefore, the choice of contrast medium affects the risk for CIN. There is good evidence that low-osmolar contrast media are less nephrotoxic than high-osmolar contrast media in patients at increased risk for CIN who receive intra-arterial iodinated contrast. Current evidence suggests that nonionic isosmolar contrast presents the lowest risk for CIN in patients with chronic kidney disease (CKD), particularly in those patients with diabetes mellitus. Intra-arterial administration of contrast media may be associated with a greater risk for CIN above that observed with intravenous administration. The use of gadolinium or CO(2) as alternative contrast media to avoid the risk of nephrotoxicity cannot be substantiated by clinical trials and therefore cannot be recommended. Most studies show that, within a class, higher volumes (>100 mL) of iodinated contrast medium are associated with a higher risk for CIN. However, in patients at high risk, such as those with CKD and diabetes, even small volumes of contrast medium can have adverse effects on renal function.

Acute Kidney Injury↗

PubMed2006

Risk prediction of contrast-induced nephropathy.

In order to make appropriate decisions about clinical management, it is important for physicians to be able to stratify patients according to their risk for contrast-induced nephropathy (CIN). The most important risk marker for nephropathy after exposure to iodinated contrast media is preexisting renal impairment. The risk of CIN is elevated and becomes clinically important in patients with chronic kidney disease characterized by an estimated glomerular filtration rate <60 mL/min per 1.73 m(2). In patients with renal impairment, diabetes mellitus amplifies the risk of CIN and complicates postprocedure management. Other markers associated with an increased risk of CIN include cardiovascular disease, periprocedural hemodynamic instability, use of nephrotoxic drugs, and anemia. The effect of risk factors is additive, and the presence of multiple risk factors in the same patient can create a very high risk for CIN and acute renal failure requiring dialysis. Risk models incorporating baseline and periprocedural characteristics have been developed using data from large databases of percutaneous coronary intervention patients. These schemes are potentially valuable, but at present the most practical approach to risk prediction is based on a simple model incorporating renal function and diabetes mellitus.

Cardiovascular Diseases↗

PubMed2006

Baseline renal function screening.

Renal impairment at baseline (estimated glomerular filtration rate [eGFR] <60 mL/min/1.73 m(2)) is the most important risk marker to predict the risk of contrast-induced nephropathy (CIN) in patients receiving iodinated contrast media. Hence, it is important to assess renal function before administration of contrast medium to ensure that appropriate steps are taken to reduce the risk. Serum creatinine alone does not provide a reliable measure of renal function, hence the National Kidney Foundation Kidney Disease Outcome Quality Initiative (K/DOQI) recommends that clinicians should use an eGFR calculated from the serum creatinine as an index of renal function. The CIN Consensus Working Panel agreed that eGFR should be determined before contrast administration, using the abbreviated Modification of Diet in Renal Disease (MDRD) formula, recommended by K/DOQI as the preferred equation for the calculation of eGFR in adults. Where a serum creatinine measurement or eGFR is not available, a simple survey or questionnaire can be used before contrast agent administration to identify patients at higher risk for CIN compared with the general population. In emergency situations, where the benefit of very early imaging outweighs the risk of waiting, the CIN Consensus Working Panel agreed that the procedure can be performed without assessment of renal function.

Consensus Statements as Topic↗

PubMed2006

High-risk situations and procedures.

With the wider use of imaging and interventional techniques that require the use of iodinated contrast media in seriously ill patients, many clinical situations occur where patients may be at increased risk for contrast-induced nephropathy (CIN). There is little guidance for clinicians in these areas. The aim of this review is to assess the available literature. Acute renal failure is a common complication following coronary artery bypass surgery, and exposure to contrast medium may increase the risk for this condition, although there is insufficient evidence to make a definitive statement. Evidence is also limited for patients with liver disease: in those undergoing transarterial chemoembolization, cirrhosis may be a risk factor for renal failure. There is some evidence that periprocedural hypotension may be a risk factor for CIN after percutaneous coronary intervention, but no published information was identified on the significance of shock or hypotension in other groups of patients. The published evidence on the risk of CIN in renal transplant recipients is inconsistent. In emergency situations, the course of action is usually dictated by clinical circumstances; the renal status of a patient is likely to be unknown and it is important to ensure adequate volume expansion, especially after the procedure. In all clinical situations that are potentially associated with a high risk for CIN, the decision to administer contrast medium is a matter for clinical judgment, based on the clinical status of the patient and the expected benefits of the investigation or procedure.

Acute Kidney Injury↗

PubMed2006

Pathophysiology of contrast-induced nephropathy.

Contrast-induced nephropathy (CIN) is the third leading cause of acute kidney injury in hospitalized patients and is associated with significant patient morbidity. The pathogenesis of CIN is complex and not fully understood, but iodinated contrast agents induce intense and prolonged vasoconstriction at the corticomedullary junction of the kidney. Moreover, high-osmolar dyes directly impair the autoregulatory capacity of the kidney through a loss of nitric oxide production. These effects, coupled with direct tubular toxicity of contrast media, lead to overt acute tubular necrosis and the syndrome of CIN.

Acute Kidney Injury↗

PubMed2006

Epidemiology and prognostic implications of contrast-induced nephropathy.

Contrast-induced nephropathy (CIN), usually defined as an increase in serum creatinine of 0.5 mg/dL (44.2 mumol/L), or a 25% increase from the baseline value 48 hours after the procedure, is a common and potentially serious complication of the use of iodinated contrast media in patients at risk of acute renal injury. It is an important cause of hospital-acquired renal failure, responsible for approximately 11% of cases. CIN may be difficult to distinguish from cholesterol embolization, another cause of postprocedure renal impairment. The reported incidence of CIN varies depending on the patient population studied. The impact of postprocedural renal impairment on clinical outcomes has been evaluated most extensively in patients undergoing percutaneous coronary intervention. CIN is associated with increased mortality both in hospital and at 1 year. A higher incidence of in-hospital and late cardiovascular events, as well as longer hospital stays, has been reported in patients developing CIN. In a small proportion of patients, CIN is severe enough to require dialysis, and these patients have a particularly poor prognosis. Many of the risk markers for CIN are also predictive of a worse prognosis.

Acute Kidney Injury↗