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 Radiocontrast-induced nephropathy

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Male Number of posts : 53
Age : 36
location : Qatar
Registration date : 2006-12-08

PostSubject: Radiocontrast-induced nephropathy   Sun Jan 14, 2007 1:18 am

- Radiocontrast-induced
nephropathy is the 3rd most common cause of in-hospital acute renal
failure after hypotension and surgery. Radiographic contrast media are
used at a pregressive rate for several diagnosis and therapeutic
applications as catherter. Prevention of radiocontrast-induced
nephropathy will become more important, including risk of patient
impairment and costs.

Radiocontrast-induced nephropathy (RCIN) defined as an acute
deterioration of renal function occurring after exposure to
radiocontrast media (RCM). Its incidence varies depending on how it is
defined in terms of increase in serum creatinine, on prophylactic
measures employed, and on the basal risk profile of the population
studied. The greatest impact of RCIN is in severe cases that may
require treatment with renal replacement therapy "the frequency of need
for dialysis" and on other cases may cause other complications as
increase morbidity, extended length of hospital stay, total cost of
care, and an association with increased mortality risk. Because there
is no medical treatment for established RCIN, much interest has been
directed at approaches to renal protection and prophylaxis. Saline
hydration has been the most widely used approach, and is believed to be
at least partially effective. In recent years, N-acetylcysteine (NAC),
an inexpensive agent with multiple biologic actions, has been
extensively studied, with some reports indicating outstanding efficacy
in the prevention of RCIN. The drug was initially introduced into
clinical medicine as a mucolytic agent, which led to its use in
pulmonary diseases complicated by obstructive mucous production. Later
its antioxidant properties led to use in treatment of acetaminophen
overdose and in ischemic cardiac diseases.

Risk factors for RCIN, which include: volume depletion, salt depletion,
renal insufficiency, heart failure, age, gender, diabetes,
atherosclerosis, intra-arterial injection of contrast, and previous
history of contrast nephropathy.

- The processes invoked are (1)
renal ischemic injury (secondary to changes in arterial blood flow and
altered distribution of intrarenal blood flow, endothelial cell
function, tubuloglomerular feedback, and red blood cell deformities); (2) tubular epithelial cell toxicity (secondary to disruption of cell integrity, oxygen radical generation, and apoptosis); (3) intratubular obstruction; (4) hemoglobin oxygen saturation curve shifts; and (5) immunologic reactions.

- NAC for prevention of RCIN was greatly stimulated by the publication by Tepel et al. in
2000 of study results indicating outstanding efficacy. In this section,
we explore NACís potential therapeutic role in RCIN by examining its
relevant biologic actions. It must be noted that, although NAC has had
a multitude of biologic effects reported, we will focus on those
effects most likely to be relevant to RCINís pathogenesis. Recently,
there has been a great increase in interest regarding NACís antioxidant
properties. Oxidative stress occurs as a result of an imbalance between
ROS and the bodyís native antioxidant systems. NAC is one of a large
group of exogenous antioxidant drugs that may protect against oxidative
tissue injury. The antioxidant effects of NAC may be directly related
to the drug itself or to the secondary induction of glutathione
production. Among direct effects of NAC are reactions with hydroxyl
radicals (∑OH), resulting in their inactivation A secondary antioxidant
effect of NAC is indirect via the induction of glutathione synthesis.
Glutathione (GSH) plays a key role in the cellular defense against
oxidative damage.

Selecting appropriate patients for treatment should follow a careful
clinical evaluation for known RCIN risk factors such as diabetes
mellitus, renal insufficiency, older age, dehydration, congestive heart
failure, need for greater contrast volumes, multiple myeloma, and
hypoalbuminemia. It would seem that the Tepel administration protocol
(600 mg orally twice daily on the day before and on the day of the
procedure) is a reasonable treatment approach. Intravenous hydration
was used in most of the studies and is felt to be an important
treatment component. If time permits and the patient can tolerate a
volume load, then 0.45% or 0.9 saline may be administered at 1 ml/kg
per h for 12 h before and after the procedure. It should be noted that
most NAC studies included a full course of intravenous hydration.

Last edited by on Fri Jun 08, 2007 10:39 am; edited 4 times in total
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Number of posts : 112
Registration date : 2006-12-09

PostSubject: Re: Radiocontrast-induced nephropathy   Fri Jan 19, 2007 1:57 am

its nice and simple
By the way N-acetylcysteine was one of the exam questions
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Number of posts : 34
Registration date : 2006-12-09

PostSubject: Re: Radiocontrast-induced nephropathy   Mon Jan 22, 2007 12:10 am

yes indeed
there was an article on this issue in the medscape with full details
on the rule of N-acetylcysteine nephropathy

it is really sooooo important
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Number of posts : 112
Registration date : 2006-12-09

PostSubject: Re: Radiocontrast-induced nephropathy   Mon Jan 22, 2007 3:44 am

Its one of malak hand maded articles.
Its really soooooo important;)
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