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Biomarkers of Acute Renal Failure


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Potential Sources of Urinary Biomarkers

Slide 15

August 2009

In order talk about potential urinary biomarkers of kidney injury, it is first helpful to consider what their source might be. The glomerulus is usually a fairly effective barrier to filtration of proteins from the blood as long as they are >40 to 50 kDa in size. Therefore, much less than 1% of serum albumin ordinarily would make it past this filtration barrier into the urine. However, some albumin does make it through this filter. In addition, smaller molecular weight proteins are freely filtered. All proteins that are filtered into tubular fluid are reabsorbed in the proximal tubule and processed within lysosomes, as shown on the slide. Under conditions of proximal tubular injury, one might expect to find increased levels of these smaller molecular weight proteins, as well as some albumin. Cystatin C is another example of a small molecular weight protein that is metabolized in the kidneys by this mechanism, and, in fact, urinary cystatin C has been proposed as a sensitive biomarker of acute kidney injury. Other proteins are directly released in the urine by injured kidney epithelial cells. Examples include brush border enzymes such as NAG and GGT, as well as proteins that are upregulated in injured cells like NGAL and KIM 1. Finally, acute tubular necrosis is accompanied by some degree of inflammatory response in the region of cell damage and inflammatory markers such as IL18 have been identified in the urine of patients with acute kidney injury.

Potential Sources of Urinary Biomarkers


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