It appears that the molecular "shedding" of KIM-1 (Kidney injury Molecule-1) largely due to the actions of a metaloproteinase allows for reformation of the proximal tubule in areas of damage. The KIM goes thrrough a transmembrane potentiation of sorts and the simultaneous production of IL-18 allows the immunologic process to take part. Both molecules serve as early pre-creatinine,Glycosuria and proteinuria signs of kidney injury.
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