Contrast media I.CM) is a general term used to
describe substances of low or high atomic weight
which help to visualize certain structures in the body
or to produce information about organ function
(Grainger, 1982). Radio contrast-medium induced
nephropathy (RCIN) or Contrast-associated
nephropathy (CAN) has been defined as an acute
impairment of renal function following exposure to
radiographic contrast materials after excluding of
other causes of renal impairment (Berkseth and
Kjellstrand, 1984). Also, RCIN is defined as a
proportional rise in serum creatinine, e.g. 25% or
50%. or an absolute rise in serum creatinine, e.g. 0.5
mgicIL or 1.0 mggiL. or a combination of both, after
exposure to contrast media, that is within 48 or 72
hours (Cheryl et aL, 1998).
The contribution of RCIN to all, hospital-acquired
acute renal failure has increased from 5% in a 1977
study to 32% in a 1987 study (Anderson et al., 1977
and Shusterman et aL, 1987). The incidence of
RCIN depends on a number of risk factors: preexisting
renal. insufficiency, diabetes mellitus, heart
failure, volume depletion, patients with multiple
myeloma, and the dose of contrast media; all
increase the risk of RCIN (Barret, 1994). RCIN is not
benign. It can result in increased hospital stay,
occasional need for dialysis, and perhaps increased
mortality in inpatients with pre-existing co-morbid
conditions (Cheryl et al., 1998). Besides. Levy et al.
(1996) concluded that RCIN increased the risk of
developing severe non-renal complications that can
lead to death.
The pathogenesis of RCIN involves ischemic injury
to the medulla with a fall in total renal blood flow, i.e.
a medullary steal syndrome which might be a final
common pathway induced by imbalance of
vasodilator and vasoconstrictive forces operating
independently in the cortex and medulla (Caldkott et
al., 1970). A number of potential vasoconstrictive
factors as angiotensin, endothelin, adenosine,
thromboxanes, and evidence of increased lipid
peroxidation (reactive oxygen species) have all been
implicated in the pathogenesis of RCIN (Margulies et
al.. 1991 and Cheryl et al., 1998). Evidence also
indicates that contrast media are directly toxic to
renal tubular cells. In human studies, a variety of
proximal tubular enzymes such as N-acetyl-beta-Dglucosaminidase
(NAG) and a lysosomal enzyme as
alanine-amino-peptidase (AAP) and gamma glutamyl
transferase (GOT) are released into the urine
following contrast media exposure (Parvez et al.,
1990). Small-molecular-weight proteins such as
alpha- 1 -microglobulin and beta-2-microglobulin are
also excria— :ncreased amounts following contrast
medium exposure (Carraro et al., 1996). The aim of
the present work is to study early detection of
asymptomatic radio-contrast media nephropathy and
its possible effect on gjomerular and tubular function. |
