Chronic Kidney Disease: CT or MRI? - Medscape

Contrast-induced Nephrotoxicity

Nephrotoxicity of contrast media - Oxford Journals

In contrast, nephrotoxic reactions to iodinated contrast reagents are more predictable and, with a high enough dose, would be seen in everyone. Increased levels of serum creatinine can be detected 24 hours after a contrast CT in approximately 1% of the healthy outpatient population, returning to baseline within 1-2 weeks. Nephrotoxic reactions are much more likely in patients with impaired renal function. In one study, increased levels of serum creatinine were detected in 23% of those with a baseline serum creatinine > 2 mg/dl and almost 100% of patients with serum creatinine levels > 4.5 mg/dl and diabetes. Fortunately, permanent renal damage is rare. However, contrast medium nephrotoxicity can prolong the patient’s stay in hospital and increase the risk of non-renal complications.

Contrast nephrotoxicity: A randomized controlled trial of a nonionic and an ionic radiographic contrast agent

Drug-Induced Nephrotoxicity - American Family Physician

The use of low-osmolar nonionic monomeric and, more recently,isosmolar nonionic dimeric contrast media has been recommended inhigh-risk patients to reduce the risk of contrast medianephrotoxicity. A multicenter study of 129 patients with renalimpairment and diabetes mellitus (serum creatinine between 1.5 and3.5 mg/dL) undergoing angiography with either the isosmolar dimeriodixanol or the nonionic monomer iohexol showed that CMINdeveloped only in 3% of the patients after the dimer and in 26%after the monomer.47The study concluded that the isosmolar dimer iodixanol issignificantly less nephrotoxic in comparison with the nonionicmonomers. In another study of patients with nephropathy due tovarious causes, CMIN developed in 4% after the isosmolar nonionicdimer and in 10% after a low-osmolar nonionic monomer.48In a further study, CMIN developed in 17% of patients with severerenal impairment who received intravenous injection of either anonionic monomer or an isosmolar dimer for body or cranial CT. Nodifference in the incidence of CMIN between the monomer and dimerwas found in this study.49Further studies are required to elucidate whether there is asignificant difference in the nephrotoxic effects of the nonionicdimer in comparison with nonionic monomers.50

A randomized prospective trial to assess the role of saline hydration on the development of contrast nephrotoxicity.

Contrast Nephrotoxicity (CN) remains an important complication in cardiac and vascular imaging studies. Although the renal effects are usually reversible, the development of acute renal failure (ARF) is associated with longer hospital stays, need for dialysis, and mortality. Traditionally, contrast ARF has been defined as plasma creatinine (PCr) elevations of 25% or more in the 48 hours after administration of intravenous contrast.1,2 It follows from this definition that most cases of CN are subclinical and have little effect on the subsequent disease course. However, in certain cases, it can represent a major complication. Incidence varies according to series, and can be as high as 10%.1-7

Contrast medium–induced nephrotoxicity (ie, contrast nephrotoxicity [CN]) remains an important complication of angiographic procedures.


ABBREVIATIONS
ANP: atrial natriuretic peptide
ARF: acute renal failure
CN: contrast nephrotoxicity
EF: ejection fraction
PCr: plasma creatinineAlthough the incidence of contrast agent nephrotoxicity is low in patients with normal renal function, it is a significant concern for those with poor renal function, diabetes, congestive heart failure, dehydration, or the concurrent use of nephrotoxic drugs. Contrast Nephrotoxicity (CN) remains an important complication in cardiac and vascular imaging studies. Although the renal effects are usually reversible, the development of acute renal failure (ARF) is associated with longer hospital stays, need for dialysis, and mortality. Traditionally, contrast ARF has been defined as plasma creatinine (PCr) elevations of 25% or more in the 48 hours after administration of intravenous contrast.1,2 It follows from this definition that most cases of CN are subclinical and have little effect on the subsequent disease course. However, in certain cases, it can represent a major complication. Incidence varies according to series, and can be as high as 10%.1-7Aminoglycosides have long been one of the commonest causes of drug-induced nephrotoxicity (). Although a clear recognition of the patient- and treatment-related risk factors (), combined with the once-a-day schedule and effective monitoring procedures (), have definitely improved the situation over what prevailed in the early 1980s (), we are still short of having brought the safety of aminoglycosides to that of the main other wide-spectrum antibiotics. Chemical research aimed at obtaining intrinsically less toxic compounds has met with only modest success, and few of the other approaches proposed to reduce the toxicities of the available agents have reached practical clinical applications. Yet, because aminoglycosides are very effective antibiotics well suited to the treatment of severe infections (), it seems important to maintain and even develop efforts to improve their therapeutic indices. The present minireview tries to present in a prospective way the status of both the basic and the clinical research on aminoglycoside nephrotoxicity in order to clarify the main issues and to pinpoint strategies that may eventually lead to their safer use. Ototoxicity, which is the second main adverse effect of aminoglycosides and which, in contrast to nephrotoxicity, is irreversible, will not be considered here since it has already been reviewed in this journal () and elsewhere (). A companion minireview () examines and discusses the recent research dealing with the activities of aminoglycosides and bacterial resistance. ABBREVIATIONS
ANP: atrial natriuretic peptide
ARF: acute renal failure
CN: contrast nephrotoxicity
EF: ejection fraction
PCr: plasma creatinine