Radiographic contrast media associated nephrotoxicit",
|Full paper||Not Available|
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.