Contrast induced nephropathy laboratory findings: Difference between revisions
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==Overview== | ==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 test]]s 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]], [[Interleukin 18|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. | Increase in the serum creatinine are generally observed within 24 to 48 hours after contrast exposure in most of patients, [[hyperkalemia]], [[acidosis]] and [[hyperphosphatemia]] may be present. | ||
==Laboratory Findings== | |||
The deterioration of renal function may be discovered by a measured decrease in urine output. Often, it is diagnosed on the basis of [[blood test]]s 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]], [[Interleukin 18|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. The absence of other findings on urinalysis such as [[white blood cells]] (wbc) or wbc casts or dysmorphic red blood cells (RBC`s) or RBC`s casts generally excludes other causes of [[AKI]] such as [[interstitial nephritis]] and [[glomerular diseases]]. | |||
Latest revision as of 09:17, 14 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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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mohamed Moubarak, M.D. [2]
Overview
Increase in the serum creatinine are generally observed within 24 to 48 hours after contrast exposure in most of patients, hyperkalemia, acidosis and hyperphosphatemia may be present.
Laboratory Findings
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. The absence of other findings on urinalysis such as white blood cells (wbc) or wbc casts or dysmorphic red blood cells (RBC`s) or RBC`s casts generally excludes other causes of AKI such as interstitial nephritis and glomerular diseases.