Team:Brasil-SP/Project/Cystatin

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<b>This page and all its content are provisional!</b>
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<h3 align="center">Cystatin C</h3>
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<p>What is the cystatin role on the CKD? How it works? Why it is a good biomarker? These are some points to be clarified on this page.</p>
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<p><div align="justify">Cystatin C, an inhibitor of cysteine proteases, has 120 amino acid residues and it is produced by all nucleated cells. It is an excellent biomarker for renal dysfunction due to its constant rate in the blood and its independence of the aforementioned variables (diet, gender, ethnicity, age, muscle mass, and others). Several scientific studies showed that Cystatin C has inhibitory activity against Papain and Calpain II.
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Cystatin C, likewise other low molecular weight proteins, is freely filtered by the glomeruli and it is almost completely reabsorbed in the proximal tubules. The level of Cystatin C remain constant when its production is equivalent to the nonreabsorbed portion. In patients with renal dysfunction, the GFR is lower because a smaller amount of filtered blood is filtered; as a consequence, a smaller amount of Cystatin C is reabsorbed by the proximal tubules, resulting in lower levels of excreted Cystatin C. Logically, a decrease in GFR implies an increase of Cystatin C concentration in the blood. Thus, the Cystatin C concentration in the blood is totally dependent on the GFR.</div></p>

Revision as of 18:16, 26 September 2014

Cystatin C

Cystatin C, an inhibitor of cysteine proteases, has 120 amino acid residues and it is produced by all nucleated cells. It is an excellent biomarker for renal dysfunction due to its constant rate in the blood and its independence of the aforementioned variables (diet, gender, ethnicity, age, muscle mass, and others). Several scientific studies showed that Cystatin C has inhibitory activity against Papain and Calpain II. Cystatin C, likewise other low molecular weight proteins, is freely filtered by the glomeruli and it is almost completely reabsorbed in the proximal tubules. The level of Cystatin C remain constant when its production is equivalent to the nonreabsorbed portion. In patients with renal dysfunction, the GFR is lower because a smaller amount of filtered blood is filtered; as a consequence, a smaller amount of Cystatin C is reabsorbed by the proximal tubules, resulting in lower levels of excreted Cystatin C. Logically, a decrease in GFR implies an increase of Cystatin C concentration in the blood. Thus, the Cystatin C concentration in the blood is totally dependent on the GFR.