Contrast induced nephropathy pathophysiology: Difference between revisions
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==Overview== | ==Overview== | ||
The pathophysiology of CIN is not clearly understood; however, several attempts have been made to explain the underlying mechanism. It is generally agreed that CIN is due to a combination of several influences brought on by contrast-media infusion rather than a single process. The most important mechanism thought to be involved in CIN is a reduction in renal perfusion and subsequent hypoxia. This has been attributed to several alterations in the renal microenvironment including activation of the tubuloglomerular feeback, local vasoactive metabolites including adenosine, prostaglandin, NO, and endothelin as well as increased interstitial pressure. <ref name="pmid21784541">{{cite journal| author=Wong PC, Li Z, Guo J, Zhang A| title=Pathophysiology of contrast-induced nephropathy. | journal=Int J Cardiol | year= 2012 | volume= 158 | issue= 2 | pages= 186-92 | pmid=21784541 | doi=10.1016/j.ijcard.2011.06.115 | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=21784541 }} </ref> Although sometimes considered controversial, studies have also proposed injury to renal tubular cells as another contributor both via a direct cytotoxic effect and via reactive oxygen species production. <ref name="pmid15954892">{{cite journal| author=Persson PB, Hansell P, Liss P| title=Pathophysiology of contrast medium-induced nephropathy. | journal=Kidney Int | year= 2005 | volume= 68 | issue= 1 | pages= 14-22 | pmid=15954892 | doi=10.1111/j.1523-1755.2005.00377.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?dbfrom=pubmed&tool=sumsearch.org/cite&retmode=ref&cmd=prlinks&id=15954892 }} </ref> | |||
==Pathophysiology== | ==Pathophysiology== | ||
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamed Moubarak, M.D. [2]
Overview
The pathophysiology of CIN is not clearly understood; however, several attempts have been made to explain the underlying mechanism. It is generally agreed that CIN is due to a combination of several influences brought on by contrast-media infusion rather than a single process. The most important mechanism thought to be involved in CIN is a reduction in renal perfusion and subsequent hypoxia. This has been attributed to several alterations in the renal microenvironment including activation of the tubuloglomerular feeback, local vasoactive metabolites including adenosine, prostaglandin, NO, and endothelin as well as increased interstitial pressure. [1] Although sometimes considered controversial, studies have also proposed injury to renal tubular cells as another contributor both via a direct cytotoxic effect and via reactive oxygen species production. [2]
Pathophysiology
Several mechanisims have been put forth to explain the development of nephropathy following contrast administration by exacerbating renal vasoconstriction, particularly in the deeper portions of the outer medulla, enhance cellular damage by reactive oxygen species, and increase resistance to renal blood flow. This is especially important in patients with chronic kidney disease, because their preexisting abnormal vascular pathobiology is made worse by the effects of CM.[3]
Renal Medullary Hypoxia Secondary to Renal Vasoconstriction
Vasoconstriction occurs following exposure to CM due to the release of adenosine and possibly endothelin, high osmolality of the contrast medium also have been associated.[4] [5] [6] The involvement of volume depletion and heart failure with renal vasoconstriction is a result of stimulation of the renin-angiotensin cascade and impaired nitric oxide generation. Taken together, these factors potentiate renal medullary ischemia.[7] [8] Normally, the oxygen consumption in the renal medulla is high due to high metabolic rate, and active salt reabsorption by the thick ascending limbs of Henle's loop. Hence then, the risk of intrarenal hypoxia and outer medullary hypoxic damage increase due to CM induced renal vasoconstriction, increased blood viscosity, and a leftward shift of the oxygen-hemoglobin dissociation curve.[9] [10]
Cytotoxic Effects of Contrast
Contrast Media can directly cause renal tubular injury.[11] Another mechanism had been described by 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. Also the oxidative and nitrosative effects mediated by these reactive species on the sulfhydrylic groups and aromatic rings of proteins, cellular membrane lipids and nucleic acids associated with the vasoconstriction. This occurs through the nitrosation of tyrosine residues of enzymes which are involved in the synthesis of medulla vasodilators, such as prostacycline synthase and nitric oxide synthase.[12] Other causes reported to contribute in this mechanism through studies have been done on animals are the mitochondrial injury, cytochrome-c release, and plasma membrane damage.[13] Creatinine clearence has also been seen reduced with increase in adenosine excreation on administration of low osmolality, non-ionic contrast, and with use of theophylline the fall in creatinine clearance declined.[5]
References
- ↑ Wong PC, Li Z, Guo J, Zhang A (2012). "Pathophysiology of contrast-induced nephropathy". Int J Cardiol. 158 (2): 186–92. doi:10.1016/j.ijcard.2011.06.115. PMID 21784541.
- ↑ Persson PB, Hansell P, Liss P (2005). "Pathophysiology of contrast medium-induced nephropathy". Kidney Int. 68 (1): 14–22. doi:10.1111/j.1523-1755.2005.00377.x. PMID 15954892.
- ↑ Lameire NH (2006). "Contrast-induced nephropathy--prevention and risk reduction". Nephrol Dial Transplant. 21 (6): i11–23. doi:10.1093/ndt/gfl215. PMID 16723348.
- ↑ 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) - ↑ 5.0 5.1 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) - ↑ Heyman SN, Rosen S, Brezis M (1994). "Radiocontrast nephropathy: a paradigm for the synergism between toxic and hypoxic insults in the kidney". Exp Nephrol. 2 (3): 153–7. PMID 7922266.
- ↑ 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)