Contrast induced nephropathy laboratory findings: Difference between revisions
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==Overview== | ==Overview== | ||
Revision as of 19:11, 11 September 2013
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Contrast Induced Nephropathy Microchapters |
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Differentiating Contrast induced nephropathy from other Diseases |
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Diagnosis |
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Treatment |
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Case Studies |
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Contrast induced nephropathy laboratory findings On the Web |
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American Roentgen Ray Society Images of Contrast induced nephropathy laboratory findings |
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Contrast induced nephropathy laboratory findings in the news |
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Directions to Hospitals Treating Contrast induced nephropathy |
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Risk calculators and risk factors for Contrast induced nephropathy laboratory findings |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamed Moubarak, M.D. [2]
Overview
The deterioration of renal function may be discovered by a measured decrease in urine output. Often, it is diagnosed on the basis of blood tests for substances normally eliminated by the kidney: urea and creatinine. Both tests have their disadvantages. For instance, it takes about 24 hours for the creatinine level to rise, even if both kidneys have ceased to function. A number of alternative markers has been proposed (such as NGAL, KIM-1, IL18 and cystatin C), but none are currently established enough to replace creatinine as a marker of renal function. Sodium and potassium, two electrolytes that are commonly deranged in people with acute kidney injury, are typically measured together with urea and creatinine.