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    <AnnotationProperty rdf:about="http://purl.obolibrary.org/obo/IAO_0000412"/>
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    <!-- http://purl.obolibrary.org/obo/HP_0032581 -->

    <Class rdf:about="http://purl.obolibrary.org/obo/HP_0032581">
        <rdfs:label>Abnormal renal insterstitial morphology</rdfs:label>
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    <!-- http://purl.obolibrary.org/obo/HP_0032948 -->

    <Class rdf:about="http://purl.obolibrary.org/obo/HP_0032948">
        <rdfs:label>Renal interstitial fibrosis</rdfs:label>
        <rdfs:subClassOf rdf:resource="http://purl.obolibrary.org/obo/HP_0032581"/>
        <rdfs:comment>Tubular atrophy (TA) is defined as loss of specialized transport and metabolic capacity and typically manifested by small tubules with cells with pale cytoplasm or dilated, thin tubules. TA is usually associated with IF, but probably has distinct mechanisms related to blood flow, glomerular filtration rate (GFR) or tubular continuity loss. However, IF and TA are separable, as shown by the profound TA in renal artery stenosis, which characteristically has little or no fibrosis (or inflammation).</rdfs:comment>
        <ns2:IAO_0000115>The accumulation of collagen and related extracellular matrix (ECM) molecules in the interstitium of the kidney. The interstitium is expanded by the presence of collagen that stain blue on trichrome. Tubules are not back to back, but rather separated by fibrosis and can be atrophic.</ns2:IAO_0000115>
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