Contrast induced nephropathy pathophysiology
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
Several mechanisims have been put forth to explain the development of nephropathy following contrast administration:
Renal medullary hypoxia secondary to renal vasoconstriction
It has been hypothesized that vasoconstriction occurs due to contrast induced release of adenosine and possibly endothelin as well as the high osmolality of the contrast medium [1] [2] [3]. Volume depletion and heart failure may also be associated with renal vasoconstriction as a result of stimulation of the renin-angiotensin cascade and impaired nitric oxide generation. Taken together, these factors potentiate renal medullary ischemia [4] [5]. Normally the metabolic rate and thereby oxygen consumption in the renal medulla is high as a result of active salt reabsorption by the thick ascending limbs of Henle's loop. Hence renal vasoconstriction, increased blood-contrast viscosity, and a leftward shift of the oxygen-hemoglobin dissociation curve may all contribute to intrarenal hypoxia, with an imbalance between oxygen demand and supply thereby playing a major role in radiocontrast-induced outer medullary hypoxic damage[6]
Cytotoxic effects of contrast
Contrast agents themselves can directly cause renal tubular injury [7]. Contast agents can also cause the generation of free oxygen radicals such as superoxide anions, hydrogen peroxide, hydroxyl radicals and hypochlorous acid. The endothelial dysfunction discussed above is also partly due to oxygen free-radical generation during post ischemic reperfusion as they decrease bioavailibility of nitric oxide leading to vasoconstriction. These reactive species also exerts their oxidative and nitrosative effects on the sulf hydrylic groups and aromatic rings of proteins, cellular membrane lipids and nucleic acids and contribute to vasoconstriction. This occurs through the nitrosation of tyrosine residues of enzymes, such as prostacycline synthase and nitric oxide synthase, which are involved in the synthesis of medulla vasodilators [8]. Mitochondrial injury/cytochrome-c release and plasma membrane damage may be other causes of renal injury as shown in animal experiments [9]. Reduction in creatinine clearence was also seen with increase in adenosine excreation on administration of low osmolality, non-ionic contrast and with use of theophylline the fall in creatinine clearance declined [2].
References
- ↑ Cantley LG, Spokes K, Clark B, McMahon EG, Carter J, Epstein FH (1993). "Role of endothelin and prostaglandins in radiocontrast-induced renal artery constriction". Kidney International. 44 (6): 1217–23. PMID 8301922. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ 2.0 2.1 Katholi RE, Taylor GJ, McCann WP, Woods WT, Womack KA, McCoy CD, Katholi CR, Moses HW, Mishkel GJ, Lucore CL (1995). "Nephrotoxicity from contrast media: attenuation with theophylline". Radiology. 195 (1): 17–22. PMID 7892462. Retrieved 2011-03-06. Unknown parameter
|month=ignored (help) - ↑ Pflueger A, Larson TS, Nath KA, King BF, Gross JM, Knox FG (2000). "Role of adenosine in contrast media-induced acute renal failure in diabetes mellitus". Mayo Clinic Proceedings. Mayo Clinic. 75 (12): 1275–83. PMID 11126837. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ Rosenstock JL, Gilles E, Geller AB, Panagopoulos G, Mathew S, Malieckal D, DeVita MV, Michelis MF (2010). "Impact of heart failure on the incidence of contrast-induced nephropathy in patients with chronic kidney disease". International Urology and Nephrology. 42 (4): 1049–54. doi:10.1007/s11255-010-9798-. PMID 20602168. Retrieved 2011-03-06. Unknown parameter
|month=ignored (help) - ↑ Agmon Y, Peleg H, Greenfeld Z, Rosen S, Brezis M (1994). "Nitric oxide and prostanoids protect the renal outer medulla from radiocontrast toxicity in the rat". The Journal of Clinical Investigation. 94 (3): 1069–75. doi:10.1172/JCI117421. PMC 295165. PMID 8083347. Unknown parameter
|month=ignored (help);|access-date=requires|url=(help) - ↑ Heyman SN, Reichman J, Brezis M (1999). "Pathophysiology of radiocontrast nephropathy: a role for medullary hypoxia". Investigative Radiology. 34 (11): 685–91. PMID 10548380. Retrieved 2011-03-06. Unknown parameter
|month=ignored (help) - ↑ Heinrich MC, Kuhlmann MK, Grgic A, Heckmann M, Kramann B, Uder M (2005). "Cytotoxic effects of ionic high-osmolar, nonionic monomeric, and nonionic iso-osmolar dimeric iodinated contrast media on renal tubular cells in vitro". Radiology. 235 (3): 843–9. doi:10.1148/radiol.2353040726. PMID 15845795. Retrieved 2011-03-08. Unknown parameter
|month=ignored (help) - ↑ Detrenis S, Meschi M, Musini S, Savazzi G (2005). "Lights and shadows on the pathogenesis of contrast-induced nephropathy: state of the art". Nephrology, Dialysis, Transplantation : Official Publication of the European Dialysis and Transplant Association - European Renal Association. 20 (8): 1542–50. doi:10.1093/ndt/gfh868. PMID 16033768. Retrieved 2011-03-08. Unknown parameter
|month=ignored (help) - ↑ Zager RA, Johnson AC, Hanson SY (2003). "Radiographic contrast media-induced tubular injury: evaluation of oxidant stress and plasma membrane integrity". Kidney International. 64 (1): 128–39. doi:10.1046/j.1523-1755.2003.00059.x. PMID 12787403. Retrieved 2011-03-08. Unknown parameter
|month=ignored (help)