Contrast induced nephropathy pathophysiology: Difference between revisions
Rim Halaby (talk | contribs) |
Rim Halaby (talk | contribs) |
||
| Line 11: | Line 11: | ||
====Vascular Resistance ==== | ====Vascular Resistance ==== | ||
The renal vascular bed is supplied by small capillaries known as the vasa recta. While these small vessels have a diameter similar to that of other capillaries, their length is usually several times longer, creating higher vascular resistance. To offset that, viscosity needs to be maintained at its lowest demonstrated in Poiseuille’s law: | The renal vascular bed is supplied by small capillaries known as the vasa recta. While these small vessels have a diameter similar to that of other capillaries, their length is usually several times longer, creating higher vascular resistance. To offset that, viscosity needs to be maintained at its lowest demonstrated in Poiseuille’s law: | ||
[[Image:Poiseuille's_Law.png|thumb|width 400px| ]] | [[Image:Poiseuille's_Law.png|thumb|width=400px| ]] | ||
====Cytotoxic Effects of Contrast==== | ====Cytotoxic Effects of Contrast==== | ||
Revision as of 04:04, 1 October 2013
|
Contrast Induced Nephropathy Microchapters |
|
Differentiating Contrast induced nephropathy from other Diseases |
|---|
|
Diagnosis |
|
Treatment |
|
Case Studies |
|
Contrast induced nephropathy pathophysiology On the Web |
|
American Roentgen Ray Society Images of Contrast induced nephropathy pathophysiology |
|
Directions to Hospitals Treating Contrast induced nephropathy |
|
Risk calculators and risk factors for Contrast induced nephropathy pathophysiology |
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 mechanisms have been put forth to explain the development of nephropathy following contrast administration. Broadly, the pathophysiology can be divided into renal vascular compromise and cytotoxic tubular cell injury.
Renal Vascular Compromise and Hypoxia
Vascular Resistance
The renal vascular bed is supplied by small capillaries known as the vasa recta. While these small vessels have a diameter similar to that of other capillaries, their length is usually several times longer, creating higher vascular resistance. To offset that, viscosity needs to be maintained at its lowest demonstrated in Poiseuille’s law:
Cytotoxic Effects of Contrast
Contrast Media can directly cause renal tubular injury.[3] 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.[4] 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.[5] 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.[6]
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.
- ↑ 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) - ↑ 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 2011-03-08. Unknown parameter
|month=ignored (help)